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On-pump vs. off-pump coronary artery bypass grafting (CABG)

Off-pump CABG avoids complications that can arise with the cardiopulmonary bypass and manipulation of the aorta. Thus, off-pump CABG appears to provide superior short-term outcomes specifically by reducing the risk of perioperative stroke, renal dysfunction, blood transfusion, wound infection, respiratory failure, atrial fibrillation, ventilation time, and ICU and hospital length of stay.1 However, the trade-off may be reduced graft patency and increased risk of cardiac re-intervention and death.1 While the literature is a bit muddled,2,3 on-pump, or traditional, CABG seems to be associated with better long-term outcomes than off-pump CABG.4,5 Despite these trade-offs and a fair bit of controversy6, off-pump CABG is a valid approach for select (usually high risk) patients, especially when precise and complete revascularization is prioritized.

Risk factors for perioperative myocardial infarction following CABG are unclear

Unfortunately, it is still clinically challenging to determine which patients are best suited to off-pump CABG. One of the major barriers to accurate risk assessment is the high rate of perioperative myocardial infarction associated with CABG, either on-pump or off-pump. Perioperative MI (Type 5) may occur in as many as 3 in 10 patients who undergo CABG.7 Sadly, this risk of perioperative MI makes the risk-based decision between on-pump and off-pump CABG even more difficult.

Obstructive sleep apnea is an independent risk factor for MI following off-pump CABG

A recent study prospectively followed 147 consecutive patients at a single hospital scheduled to have off-pump CABG.8 In addition to the extensive bloodwork required before surgery, each study participant underwent portable cardiorespiratory polygraphy with a device similar to one used for at-home sleep apnea testing. This testing identified 62 patients with obstructive sleep apnea (42.2% of the cohort). Of the 147 patients who then had off-pump CABG, 24 were diagnosed with perioperative MI, 17 patients had obstructive sleep apnea, and 7 patients did not, which was a significant difference (P = 0.002). Furthermore, multivariate logistic regression revealed that apnea-hypopnea index (AHI, a measure of sleep apnea severity) was significantly associated with perioperative MI following off-pump CABG. Similar associations were discovered for high-sensitivity c-reactive protein (hs-CRP) and SYNTAX (SYNergy between PCI with TAXUS and Cardiac Surgery9,10) score, which were also independent risk factors for patients with perioperative MI after off-pump CABG.8

Possible mechanistic links between obstructive sleep apnea and perioperative MI

The authors of this prospective study speculated on the pathophysiologic mechanisms that would undergird their clinical findings. They pointed out that patients with obstructive sleep apnea showed signs of increased systemic inflammation, which promote the formation of atheromatous lesions, including within coronary arteries.11,12 Certainly the strong association with hs-CRP levels seen in the current study would support that putative link. Furthermore, patients with obstructive sleep apnea have enhanced platelet activation and rates of aggregation13 and diminished fibrinolytic capacity.14

The role of CPAP for CABG patients with obstructive sleep apnea

Indirect evidence suggests CPAP treatment for patients with obstructive sleep apnea could have a beneficial effect on this patient population. CPAP appears to correlate with lower levels of inflammation,15 improvements in markers of atherosclerosis,16 and reduced coagulability.17 Cassar et al. (32) found that screening for and treating obstructive sleep apnea with CPAP decreased cardiac death in patients who underwent percutaneous coronary intervention (PCI). Admittedly, these data do not get to the heart of whether CPAP can reduce the apparent increased risk of perioperative MI in patients with obstructive sleep apnea; prospective interventional studies are needed for that. However, until that question is answered, CPAP treatment poses little risk and potentially substantial reward for these individuals.

Practice implications for cardiologists and cardiothoracic surgeons

Now that obstructive sleep apnea, hs-CRP, and SYNTAX score are known independent risk factors for perioperative MI after off-pump CABG, these variables should be quantified prior to surgery and factored into the overall risk assessment. Since SYNTAX score is calculated with an algorithm based on angiography results—available in all patients destined for CABG—determining this value adds negligibly to the workflow. The same is true for the hs-CRP blood assay. While formal polysomnography could add substantially to pre-surgical planning, at-home sleep apnea testing is relatively inexpensive and convenient for patients. Surgeons can order the study for patients directly and the results are interpreted remotely by a sleep medicine specialist. Perhaps most importantly, at-home sleep apnea testing has comparable sensitivity and specificity with polysomnography or in laboratory sleep study testing.18-20 In fact, home sleep apnea testing was  used in the current study.8 Thus, cardiologists and cardiothoracic surgeons can feasibly integrate these three critical risk factor assessments into every patient’s pre-CABG surgical evaluation workflow.


1. Puskas JD, Martin J, Cheng DC, et al. ISMICS Consensus Conference and Statements of Randomized Controlled Trials of Off-Pump Versus Conventional Coronary Artery Bypass Surgery. Innovations (Phila). 2015;10(4):219-229. 10.1097/IMI.0000000000000184

2. Diegeler A, Borgermann J, Kappert U, et al. Off-pump versus on-pump coronary-artery bypass grafting in elderly patients. N Engl J Med. 2013;368(13):1189-1198. 10.1056/NEJMoa1211666

3. Lamy A, Devereaux PJ, Prabhakaran D, et al. Five-Year Outcomes after Off-Pump or On-Pump Coronary-Artery Bypass Grafting. N Engl J Med. 2016;375(24):2359-2368. 10.1056/NEJMoa1601564

4. Smart NA, Dieberg G, King N. Long-Term Outcomes of On- Versus Off-Pump Coronary Artery Bypass Grafting. J Am Coll Cardiol. 2018;71(9):983-991. 10.1016/j.jacc.2017.12.049

5. Shroyer AL, Hattler B, Wagner TH, et al. Five-Year Outcomes after On-Pump and Off-Pump Coronary-Artery Bypass. N Engl J Med. 2017;377(7):623-632. 10.1056/NEJMoa1614341

6. Gaudino M, Angelini GD, Antoniades C, et al. Off-Pump Coronary Artery Bypass Grafting: 30 Years of Debate. J Am Heart Assoc. 2018;7(16):e009934. 10.1161/JAHA.118.009934

7. Thielmann M, Sharma V, Al-Attar N, et al. ESC Joint Working Groups on Cardiovascular Surgery and the Cellular Biology of the Heart Position Paper: Perioperative myocardial injury and infarction in patients undergoing coronary artery bypass graft surgery. Eur Heart J. 2017;38(31):2392-2407. 10.1093/eurheartj/ehx383

8. Fan K, Gao M, Yu W, et al. Obstructive Sleep Apnea Increases the Risk of Perioperative Myocardial Infarction Following Off-Pump Coronary Artery Bypass Grafting. Front Cardiovasc Med. 2021;8:689795. 10.3389/fcvm.2021.689795

9. Farooq V, Girasis C, Magro M, et al. The CABG SYNTAX Score – an angiographic tool to grade the complexity of coronary disease following coronary artery bypass graft surgery: from the SYNTAX Left Main Angiographic (SYNTAX-LE MANS) substudy. EuroIntervention. 2013;8(11):1277-1285. 10.4244/EIJV8I11A196

10. Ishiwata S, Tomita Y, Ishiwata S, Narui K, Daida H, Kasai T. Association between Obstructive Sleep Apnea and SYNTAX Score. J Clin Med. 2020;9(10). 10.3390/jcm9103314

11. Ryan S. Mechanisms of cardiovascular disease in obstructive sleep apnoea. J Thorac Dis. 2018;10(Suppl 34):S4201-S4211. 10.21037/jtd.2018.08.56

12. Ryan S, Taylor CT, McNicholas WT. Selective activation of inflammatory pathways by intermittent hypoxia in obstructive sleep apnea syndrome. Circulation. 2005;112(17):2660-2667. 10.1161/CIRCULATIONAHA.105.556746

13. Bokinsky G, Miller M, Ault K, Husband P, Mitchell J. Spontaneous platelet activation and aggregation during obstructive sleep apnea and its response to therapy with nasal continuous positive airway pressure. A preliminary investigation. Chest. 1995;108(3):625-630. 10.1378/chest.108.3.625

14. Rangemark C, Hedner JA, Carlson JT, Gleerup G, Winther K. Platelet function and fibrinolytic activity in hypertensive and normotensive sleep apnea patients. Sleep. 1995;18(3):188-194. 10.1093/sleep/18.3.188

15. Yokoe T, Minoguchi K, Matsuo H, et al. Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure. Circulation. 2003;107(8):1129-1134. 10.1161/01.cir.0000052627.99976.18

16. Drager LF, Bortolotto LA, Figueiredo AC, Krieger EM, Lorenzi GF. Effects of continuous positive airway pressure on early signs of atherosclerosis in obstructive sleep apnea. Am J Respir Crit Care Med. 2007;176(7):706-712. 10.1164/rccm.200703-500OC

17. Phillips CL, McEwen BJ, Morel-Kopp MC, et al. Effects of continuous positive airway pressure on coagulability in obstructive sleep apnoea: a randomised, placebo-controlled crossover study. Thorax. 2012;67(7):639-644. 10.1136/thoraxjnl-2011-200874

18. Hedner J, White DP, Malhotra A, et al. Sleep staging based on autonomic signals: a multi-center validation study. J Clin Sleep Med. 2011;7(3):301-306. 10.5664/JCSM.1078

19. Hedner J, Pillar G, Pittman SD, Zou D, Grote L, White DP. A novel adaptive wrist actigraphy algorithm for sleep-wake assessment in sleep apnea patients. Sleep. 2004;27(8):1560-1566. 10.1093/sleep/27.8.1560

20. Kasai T, Takata Y, Yoshihisa A, et al. Comparison of the Apnea-Hypopnea Index Determined by a Peripheral Arterial Tonometry-Based Device With That Determined by Polysomnography- Results From a Multicenter Study. Circ Rep. 2020;2(11):674-681. 10.1253/circrep.CR-20-0097

Morbidity HF post

Sleep-disordered breathing and heart failure appear to have a bidirectional relationship.1 Obstructive sleep apnea is an independent risk factor to develop heart failure2. Of patients with known heart failure, most have sleep-disordered breathing (both reduced and normal ejection fraction3-5).  Sleep-disordered breathing appears to adversely affect heart failure outcomes.6 This bidirectional relationship signifies importance of connection however until now the impact of sleep disordered breathing on heart failure prognosis has been unclear.  . Fortunately, a recent meta-analysis provides some clarity.

TST90 predicts mortality in ambulatory heart failure patients

In May 2021, researchers at the University of Toronto presented the results of a systematic review and meta-analysis at the American College of Cardiology conference in Atlanta, GA.7 The authors screened more than 100,000 citations and identified 10 studies that included results of nearly 9,000 ambulatory heart failure patients. They reported that sleep-disordered breathing was not significantly associated with mortality or hospital admission. Likewise, apnea-hypopnea index, or AHI, was not significantly associated with mortality either. However, minutes spent under 90% oxygen saturation, also known as TST90, was significantly associated with mortality. This suggests TST90 may be able to identify which heart failure patients are at particular risk for premature mortality.

Implications for cardiology practice

These results reinforce previous findings that sleep-disordered breathing is a risk factor for death in ambulatory patients with heart failure. In the absence of additional studies, cardiologists can lean on quantitative measures of TST90 as a way to identify those at risk from a notoriously heterogeneous patient population.7 While additional work is needed, this metric may help cardiologists select which heart failure patients may benefit from CPAP or other sleep apnea treatments, a process that has proven difficult based on clinical trial results alone.8,9 At the very least, worsening sleep-disordered breathing parameters may indicate worsening heart failure,10,11 which would allow early heart failure treatment optimization prior to a full exacerbation with hospitalization. Of course, evaluation of  TST90 and other sleep-disordered breathing indicators can be accomplished with unobtrusive, convenient, at-home sleep apnea testing and monitoring.

WatchPAT®️ provides convenient, at-home monitoring of TST90 and AHI 

In-laboratory sleep apnea testing, i.e., polysomnography, is considered the gold standard for sleep-disordered breathing diagnosis; however, formal polysomnography is impractical for ongoing monitoring. Fortunately, at-home sleep apnea testing devices are now available which reliably correlate with in-laboratory polysomnography. WatchPAT®️ is an at-home sleep apnea testing device that detects peripheral arterial tone, heart rate, oximetry, actigraphy, body position, snoring, and chest motion through small, unobtrusive sensors worn on the wrist, chest, and finger. Clinical studies have shown that WatchPAT®️ testing achieves an 89% correlation with in-laboratory polysomnography.12 It provides instant, easy-to-interpret reporting of AHI, oxygen levels including desaturations (i.e., TST90), heart rate, sleep cycle, and body position information. The Central PLUS Module provides detailed information on central sleep apnea, which is particularly prevalent and problematic in patients with chronic heart failure. Perhaps most importantly, cardiologists can prescribe and implement this at-home sleep testing without a referral to a sleep center or sleep medicine specialist.

More research is needed, but cardiologists can act now

The full extent of the interactions between sleep-disordered breathing and heart failure is still unknown. Clearly, additional prospective studies are needed to determine the role of CPAP in the treatment of heart failure-related morbidity and mortality. Nonetheless, the adverse consequences of obstructive and central sleep apnea in people with heart failure are clear. If specific measures of sleep-disordered breathing severity can identify heart failure patients at particular risk for exacerbation or death, at-home sleep apnea testing is a convenient means for cardiologists to gather those clinical data.


1. Pietrock C, von Haehling S. Sleep‐disordered breathing in heart failure: facts and numbers. In: Wiley Online Library; 2017.

2. Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;163(1):19-25. 10.1164/ajrccm.163.1.2001008

3. Oldenburg O, Lamp B, Faber L, Teschler H, Horstkotte D, Topfer V. Sleep-disordered breathing in patients with symptomatic heart failure: a contemporary study of prevalence in and characteristics of 700 patients. Eur J Heart Fail. 2007;9(3):251-257. 10.1016/j.ejheart.2006.08.003

4. Sekizuka H, Osada N, Miyake F. Sleep disordered breathing in heart failure patients with reduced versus preserved ejection fraction. Heart Lung Circ. 2013;22(2):104-109. 10.1016/j.hlc.2012.08.006

5. Bitter T, Faber L, Hering D, Langer C, Horstkotte D, Oldenburg O. Sleep-disordered breathing in heart failure with normal left ventricular ejection fraction. Eur J Heart Fail. 2009;11(6):602-608. 10.1093/eurjhf/hfp057

6. Javaheri S, Shukla R, Zeigler H, Wexler L. Central sleep apnea, right ventricular dysfunction, and low diastolic blood pressure are predictors of mortality in systolic heart failure. J Am Coll Cardiol. 2007;49(20):2028-2034. 10.1016/j.jacc.2007.01.084

7. Sterling LH, Lalonde S, Alba AC. Sleep Disordered Breathing as a Predictor of Morbidity and Mortality in Ambulatory Patients with Heart Failure: A Systematic Review and Meta-Analysis. Journal of the American College of Cardiology. 2021;77(18):673-673. 10.1016/s0735-1097(21)02032-5

8. Cowie MR, Woehrle H, Wegscheider K, et al. Adaptive Servo-Ventilation for Central Sleep Apnea in Systolic Heart Failure. N Engl J Med. 2015;373(12):1095-1105. 10.1056/NEJMoa1506459

9. Bradley TD, Logan AG, Kimoff RJ, et al. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med. 2005;353(19):2025-2033. 10.1056/NEJMoa051001

10. McDonald K, O’Hanlon R, Savage HO, et al. Sleep-disordered breathing in chronic heart failure is highly variable when measured remotely using a novel non-contact biomotion sensor. European journal of heart failure. 2017;19(5):688-690. 

11. Defaye P, de la Cruz I, Marti-Almor J, et al. A pacemaker transthoracic impedance sensor with an advanced algorithm to identify severe sleep apnea: the DREAM European study. Heart Rhythm. 2014;11(5):842-848. 10.1016/j.hrthm.2014.02.01112. Epstein M, Musa T, Chiu S, et al. Use of the WatchPAT to detect occult residual sleep-disordered breathing in patients on CPAP for obstructive sleep apnea. J Clin Sleep Med. 2020;16(7):1073-1080. 10.5664/jcsm.8406

Jul29 OSA prevalence in cardiac patients revised

2021 AHA Recommendations on Obstructive Sleep apnea

The American Heart Association released a new Scientific Statement on Obstructive Sleep Apnea (OSA) and Cardiovascular Disease on June 21, 2021.1 This article concisely reviews the core recommendations from the statement as they affect cardiology practice with a focus on patients who require OSA screening.

Obstructive sleep apnea and cardiovascular complications are interrelated

Apneic events during sleep lead to periods of hypercapnia with recurrent cycles of hypoxemia and reoxygenation. In addition to disrupting sleep, patients endure wide changes in intrathoracic pressure and autonomic dysregulation including increased sympathetic activation. As the article points out, these changes lead to or are associated with hypercoagulability, endothelial dysfunction, left atrial enlargement, metabolic dysregulation, and atherosclerosis. Not surprisingly, OSA has been associated with hypertension, atrial fibrillation and other arrhythmias, heart failure, coronary artery disease, stroke, pulmonary hypertension, metabolic syndrome, diabetes, and cardiovascular mortality. Indeed, the process seems to act via a feed-forward mechanism; OSA begets cardiovascular complications which begets worsening OSA.

Obstructive sleep apnea is underrecognized and undertreated in cardiovascular practice

Despite the strong connection between OSA and poor cardiovascular states and outcomes, the disease is shockingly underdiagnosed. About a third of patients had moderate or severe OSA in a racially and ethnically diverse sample of 2,230 adults, but only 1 out of 10 of these patients with clinically significant OSA had previously received a diagnosis.2 The high prevalence of OSA in middle age and older adults, low case surveillance rates, and significant cardiovascular risks of OSA are almost certainly contributing to suboptimal cardiovascular care for millions of patients nationally.

OSA screening triggered by cardiovascular disease state rather than OSA symptoms

The core signs and symptoms of OSA include excessive daytime sleepiness, morning headaches, memory impairment, decreased libido, changes in mood, nocturia, and poor concentration. To be fair, few patients present to a cardiologist with these chief complaints. So, to some extent, cardiologists can be forgiven for not immediately considering OSA as part of the larger constellation of cardiovascular risk factors. However, the AHA makes clear in their new Scientific Statement that patients with certain cardiovascular conditions should be referred for OSA screening. In some cases, this referral should be made simply based on cardiovascular diagnosis, apart from signs, symptoms, or exam findings related to OSA.

AHA screening recommendations for OSA: Practice-changing Recommendations for cardiologists

The AHA now recommends OSA screening for all patients with;

  • Treatment-resistant or poorly controlled hypertension
  • Pulmonary hypertension
  • Recurrent atrial fibrillation status post cardioversion or ablation

This list alone likely encompasses a large number of patients in any cardiology practice, but the AHA goes on to recommend OSA screening for patients with other cardiovascular diagnoses under certain circumstances.

  • A sleep study is recommended for patients with NYHA class II, III, or IV heart failure who have symptoms of sleep apnea. In these patients, the major diagnostic concern is whether the symptoms are caused by central sleep apnea or obstructive sleep apnea.
  • The threshold for sleep apnea screening should be low in patients with tachy-brady syndrome, sick sinus syndrome, ventricular tachycardia, and those who have survived cardiac arrest.
  • Patients with angina that tends to occur at night, a history of myocardial infarction, and those who have received appropriate cardiac stimulations (“shocks”) from implanted cardioverter-defibrillators should be sent for screening, according to the AHA.

At-home sleep apnea testing for at-risk cardiology patients

A common, lingering misconception is that OSA screening requires formal polysomnography in a sleep laboratory. Unfortunately, this misconception has real-world consequences. Patients have notoriously low adherence rates with formal polysomnography testing given the lack of providers and the onerous nature? of in-laboratory testing. Fortunately, in-home sleep apnea testing provides a convenient, accurate, and reliable alternative to formal polysomnography.

At-home sleep apnea testing has advanced considerably over the past 10 to 15 years. Indeed, this same AHA Scientific Statement mentions, “Diagnostic [sleep apnea] testing can be performed by overnight in-laboratory, multichannel polysomnography, or home sleep apnea tests.”1 Various studies indicate at-home sleep apnea testing tightly correlates with “gold standard” sleep laboratory testing for a wide variety of adult patients.3-5 Newer at-home sleep apnea testing systems, such as the WatchPAT ® HSAT from Itamar Medical, even have “self-scoring” algorithms that provide clinically reliable information on OSA diagnosis and severity.

With at-home testing, cardiologists now have the ability to directly offer at-risk patients a convenient way to screen for OSA. This should enable most cardiologists to increase the detection and treatment of OSA in their practices by an order of magnitude. This, in turn, should vastly improve cardiovascular outcomes for patients who currently suffer from occult OSA.

The award-winning WatchPAT® ONE and WatchPAT® 300 HSATs from Itamar Medical go far beyond standard HSAT metrics —including both OSA and central sleep apnea identification —to provide comprehensive sleep data that can facilitate the accurate diagnosis of sleep apnea in your cardiac patients.


1.           Yeghiazarians Y, Jneid H, Tietjens JR, et al. Obstructive Sleep Apnea and Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2021;144(3):e56-e67. 10.1161/CIR.0000000000000988

2.           Chen X, Wang R, Zee P, et al. Racial/Ethnic Differences in Sleep Disturbances: The Multi-Ethnic Study of Atherosclerosis (MESA). Sleep. 2015;38(6):877-888. 10.5665/sleep.4732

3.           Zancanella E, do Prado LF, de Carvalho LB, Machado Junior AJ, Crespo AN, do Prado GF. Home sleep apnea testing: an accuracy study. Sleep Breath. 2021. 10.1007/s11325-021-02372-6

4.           Suzuki M, Furukawa T, Sugimoto A, Kotani R, Hosogaya R. Comparison of diagnostic reliability of out-of-center sleep tests for obstructive sleep apnea between adults and children. Int J Pediatr Otorhinolaryngol. 2017;94:54-58. 10.1016/j.ijporl.2017.01.015

5.           Yalamanchali S, Farajian V, Hamilton C, Pott TR, Samuelson CG, Friedman M. Diagnosis of obstructive sleep apnea by peripheral arterial tonometry: meta-analysis. JAMA Otolaryngol Head Neck Surg. 2013;139(12):1343-1350. 10.1001/jamaoto.2013.5338

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Gestational diabetes can have short- and long-term consequences for the health of the mother and the fetus. Mothers are more likely to experience preeclampsia during pregnancy and to develop cardiovascular disease.1 While dietary interventions may be enough to control blood sugars in some women, many with gestational diabetes must adapt to a complex and expensive exogenous insulin regimen. Emerging research suggests CPAP may be an effective, intermediate treatment for some women with gestational diabetes between nutritional interventions and pharmacological treatments. If CPAP may help pregnant women with sleep-disordered breathing and gestational diabetes control their blood glucose levels without pharmacological agents, then it would stand to reason that testing for sleep apnea would be a good first step with this patient population.

Gestational diabetes is increasingly common and potentially deadly

Gestational diabetes is a state of glucose intolerance that emerges during pregnancy. Unfortunately, gestational diabetes is common; the prevalence of gestational diabetes is around 15%, a rate that has been increasing over the past three decades.2 While most women with gestational diabetes return to a state of euglycemia within hours to days after delivery, maternal hyperglycemia is associated with preeclampsia, neonatal metabolic abnormalities and macrosomia, which lead to increased rates of cesarean section, birth injury, or perinatal mortality.3 Despite being a transient disease that will resolve on its own, maternal hyperglycemia requires tight control during the pregnancy for the health of the mother and the baby. 

Gestational diabetes is often treated on a two tier system

As with type 2 diabetes mellitus, the treatment of gestational diabetes begins with patient education and dietary management. Unless glucose levels are so high that they are unlikely to resolve with dietary interventions alone, women are prescribed nutritional therapy and exercise. For those who can adhere to the diet and exercise regimen, the approach does keep glucose levels under control and tends to avoid macrosomia, polyhydramnios or oligohydramnios and preeclampsia. As is also seen in type 2 diabetes, however, patients are not often able to adhere to a diet that will control blood glucose levels. In these cases, insulin or an antihyperglycemic drug are required.

The risks and burdens of pharmacologic therapy for gestational diabetes

Pregnant women with gestational diabetes who fail to achieve glucose control through diet and exercise are offered insulin, which is usually the first choice, or either metformin or glyburide.4 Each comes with risks and drawbacks. Patients must successfully administer the appropriate amount of insulin to avoid hypoglycemia, which requires point of care glucose monitoring, dosage calculations, and self-administered subcutaneous injections. Not surprisingly, insulin refusal or non-adherence is high, and quality of life suffers with insulin treatment.5 Oral medications are easier to self-administer, but come with potential risks to the fetus. The fetal drug levels of glyburide and metformin are 70 and 200 percent of the maternal levels, respectively. The long-term effects of this exposure, if any, are not known. Nevertheless, as many as one in four women fail to achieve glucose control with their oral diabetes medications alone.6 

The link between sleep-disordered breathing and gestational diabetes

Sleep-disordered breathing may occur in nearly 50% of pregnancies and, if present, triples the risk of gestational diabetes even after controlling for obesity.7,8 Likewise, sleep-disordered breathing during pregnancy increases nocturnal blood glucose levels.9 Certainly increased weight and decreased functional capacity during pregnancy contribute to sleep apnea, though pregnancy is also associated with upper airway narrowing, vascular and nasal congestion that appear to increase the risk of sleep apnea as well.10 Indeed, the prevalence and severity of sleep-disordered breathing during pregnancy argues for greater use of CPAP during pregnancy, but the argument is even more persuasive if CPAP could prevent or even treat gestational diabetes. 

CPAP significantly lowers nocturnal glucose levels in women with gestational diabetes

A research group at McGill University in Montreal, Canada published intriguing results at the 2020 American Thoracic Society International Conference.11 In the pilot randomized controlled trial, the researchers showed that in 45 pregnant women with sleep-disordered breathing and gestational diabetes, CPAP treatment (n = 22) significantly lowered nocturnal blood glucose levels compared to control (n = 23; adhesive nasal dilator strips) by 0.9 mmol/L or 16.2 mg/dl measured by continuous glucose monitoring. 

Should we try CPAP for gestational diabetes before pharmacological antihyperglycemic treatments?

It is important to keep in mind this is a pilot trial presented in abstract form. Also, mean CPAP adherence was only 3.3±2.4 hours per night (though that suggests better CPAP adherence may lead to more robust decreases in blood glucose levels). It will be interesting to see if follow-up studies confirm this finding. We know from previous work that CPAP is a safe and well-tolerated therapy in pregnant women with sleep-disordered breathing and improves maternal and fetal outcomes.12  What this work suggests is that CPAP may also help pregnant women with sleep-disordered breathing and gestational diabetes control their blood glucose levels without pharmacological agents. Future work could give women with gestational diabetes another treatment option in addition to diet and exercise but before starting metformin, glyburide, or insulin. 

At-home sleep apnea testing should be offered to pregnant women at risk for gestational diabetes

It is likely too onerous to expect pregnant women to have a formal sleep study in a sleep laboratory and then a second study to titrate CPAP levels, if sleep apnea is detected. Pregnant women with or at risk for gestational diabetes would seem like an ideal patient population to use at-home sleep apnea testing in lieu of polysomnography in a lab. Compliance with testing and titration would likely be higher with at-home sleep apnea testing and could also reduce healthcare costs. Given the potential benefits for blood sugar reduction and stabilization, it is reasonable for clinicians to offer testing for sleep apnea at home to all pregnant women at risk for gestational diabetes.


1. Tobias DK, Stuart JJ, Li S, et al. Association of History of Gestational Diabetes With Long-term Cardiovascular Disease Risk in a Large Prospective Cohort of US Women. JAMA Intern Med. 2017;177(12):1735-1742. 10.1001/jamainternmed.2017.2790

2. Halperin IJ, Feig DS. The role of lifestyle interventions in the prevention of gestational diabetes. Curr Diab Rep. 2014;14(1):452. 10.1007/s11892-013-0452-2

3. Buchanan TA, Xiang AH. Gestational diabetes mellitus. J Clin Invest. 2005;115(3):485-491. 10.1172/JCI24531

4. ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstet Gynecol. 2018;131(2):e49-e64. 10.1097/AOG.0000000000002501

5. Marchetti D, Carrozzino D, Fraticelli F, Fulcheri M, Vitacolonna E. Quality of Life in Women with Gestational Diabetes Mellitus: A Systematic Review. J Diabetes Res. 2017;2017:7058082. 10.1155/2017/7058082

6. Nachum Z, Zafran N, Salim R, et al. Glyburide Versus Metformin and Their Combination for the Treatment of Gestational Diabetes Mellitus: A Randomized Controlled Study. Diabetes Care. 2017;40(3):332-337. 10.2337/dc16-2307

7. Pamidi S, Meltzer SJ, Garfield N, et al. A Pilot Randomized-Controlled Trial on the Effect of CPAP Treatment on Glycemic Control in Gestational Diabetes: Study Design and Methods. Front Endocrinol (Lausanne). 2018;9(659):659. 10.3389/fendo.2018.00659

8. Pien GW, Pack AI, Jackson N, Maislin G, Macones GA, Schwab RJ. Risk factors for sleep-disordered breathing in pregnancy. Thorax. 2014;69(4):371-377. 10.1136/thoraxjnl-2012-202718

9. Newbold R, Benedetti A, Kimoff RJ, et al. Maternal Sleep-Disordered Breathing in Pregnancy and Increased Nocturnal Glucose Levels in Women with Gestational Diabetes Mellitus. Chest. 2021;159(1):356-365. 10.1016/j.chest.2020.07.014

10. Edwards N, Middleton PG, Blyton DM, Sullivan CE. Sleep disordered breathing and pregnancy. Thorax. 2002;57(6):555-558. 10.1136/thorax.57.6.555

11. Newbold R, Meltzer S, Benedetti A, et al. CPAP Treatment Reduces Nocturnal Glucose Levels in Gestational Diabetes: A Pilot Randomized-Controlled Trial (RCT). In: A97. SRN: NEW INSIGHTS INTO THE CARDIOMETABOLIC CONSEQUENCES OF INSUFFICIENT SLEEP.A2524-A2524.12. Izci Balserak B. Sleep disordered breathing in pregnancy. Breathe (Sheff). 2015;11(4):268-277. 10.1183/20734735.009215

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CPAP Reduces Long-Term Cardiovascular Risk in Patients with Obstructive Sleep Apnea

Multiple lines of research show patients with moderate to severe obstructive sleep apnea are at significantly increased risk of suffering a cardiovascular event.1-5 It is also clear that over the short term, continuous positive airway pressure (CPAP) treatment significant reduces sleepiness, blood pressure, and motor vehicle accidents, and enhances sleep-related quality of life in this population.6 What has been missing is evidence of long term cardiovascular risk benefit, if any, on sustained CPAP use.7 Work presented at the virtual SLEEP 2021 annual meeting in June may finally provide some of the evidentiary support cardiologists have been waiting to see.

CPAP therapy decreased the risk of a cardiovascular event by 44%

Dr. Diego Mazzotti and colleagues analyzed the large and detailed Kaiser Permanente Southern California health system electronic health records over a period of nearly two years and identified 45,927 patients with apnea-hypopnea index (AHI) results.8 The researchers assorted the records into three groups; 11,145 without sleep apnea, 13,898 with sleep apnea and any CPAP use, and 20,884 patients with sleep apnea and no record of CPAP use. Importantly, “any CPAP use” was defined broadly; in this group, the median CPAP use was 2.5 hours per day with an interquartile range of 0.7 to 5.0 hours per day. Rather modest CPAP use, to be sure, but in line with other real world studies examining CPAP adherence. All patients included in the analysis had reasonably continuous insurance coverage had no evidence of cardiovascular disease for at least 1 year prior to diagnosis of obstructive sleep apnea. Cox proportional hazards model accounted for age, sex, BMI, race, Charlson comorbidity index, and the use of hypertension or hyperlipidemia medications. Cardiovascular events of interest were myocardial infarction, stroke, unstable angina, heart failure or death from a cardiovascular cause.

Over a median of 262 days, patients with moderate to severe obstructive sleep apnea had a 71% higher likelihood of experiencing a cardiovascular event than those without obstructive sleep apnea (p=0.016). This result was expected from many previous retrospective and prospective studies. However, if patients with any severity of obstructive sleep apnea used a CPAP device for any length of time, their risk of an incident cardiovascular event was essentially reduced by a third (p=0.016). When the same analysis was restricted to patients with moderate or severe obstructive sleep apnea, any CPAP use reduced the risk of a cardiovascular event by an impressive 44% (p=0.002).8

Identifying patients with obstructive sleep apnea must be a priority for cardiologists

While this is an observational study, its large size and long duration highlight the importance of treating as many patients with obstructive sleep apnea as possible. Untreated moderate to severe sleep apnea is clearly a major risk factor for a cardiovascular event. The cardiovascular benefits of CPAP treatment are increasingly clear for patients with any degree of sleep apnea, but especially so for those with moderate or severe disease. Moreover, CPAP therapy is cost effective in patients with moderate or severe obstructive sleep apnea and is generally regarded as safe.9,10

Overcoming the barriers to CPAP implementation: A Role for home sleep apnea testing?

Unfortunately, implementing CPAP can be clinically challenging. Poor CPAP adherence is a common problem, as these recent data also indicate, yet even modest CPAP use appears to confer a cardiovascular benefit. The initial and often most difficult barrier to overcome is to get patients to undergo polysomnography in a sleep laboratory. Traditionally patients must spend one night (e.g., 9 pm to 7 am) in a sleep center for diagnostic purposes and a second night to titrate CPAP (or bilevel positive airway; BPAP) settings. However, the number of sleep centers and the number of testing and titration slots within those centers are limited. This creates geographical and scheduling barriers that only very motivated patients will overcome. If patients do schedule and attend their appointment at the sleep lab, sleeping “normally” in a sleep center is its own challenge.

Home sleep apnea testing, which tends to be much more favorable to patients for comfort, convenience, and logistical reasons, correlates very well with in-laboratory, “gold standard” polysomnography studies11 for sleep apnea diagnosis. Patients can receive an accurate diagnosis and titration with unattended sleep apnea monitoring in the comfort of their own bedrooms. Home sleep apnea testing is certainly something to consider for any patient who complains of daytime sleepiness, nighttime gasping events, or snoring.  


1.           Valham F, Mooe T, Rabben T, Stenlund H, Wiklund U, Franklin KA. Increased risk of stroke in patients with coronary artery disease and sleep apnea: a 10-year follow-up. Circulation. 2008;118(9):955-960. 10.1161/CIRCULATIONAHA.108.783290

2.           Lee CH, Sethi R, Li R, et al. Obstructive Sleep Apnea and Cardiovascular Events After Percutaneous Coronary Intervention. Circulation. 2016;133(21):2008-2017. 10.1161/CIRCULATIONAHA.115.019392

3.           Uchôa CHG, de Jesus Danzi-Soares N, Nunes FS, et al. Impact of OSA on cardiovascular events after coronary artery bypass surgery. Chest. 2015;147(5):1352-1360.

4.           Wang H, Parker JD, Newton GE, et al. Influence of obstructive sleep apnea on mortality in patients with heart failure. J Am Coll Cardiol. 2007;49(15):1625-1631. 10.1016/j.jacc.2006.12.046

5.           Costa LE, Uchoa CH, Harmon RR, Bortolotto LA, Lorenzi-Filho G, Drager LF. Potential underdiagnosis of obstructive sleep apnoea in the cardiology outpatient setting. Heart. 2015;101(16):1288-1292. 10.1136/heartjnl-2014-307276

6.           Patil SP, Ayappa IA, Caples SM, Kimoff RJ, Patel SR, Harrod CG. Treatment of Adult Obstructive Sleep Apnea With Positive Airway Pressure: An American Academy of Sleep Medicine Systematic Review, Meta-Analysis, and GRADE Assessment. J Clin Sleep Med. 2019;15(2):301-334. 10.5664/jcsm.7638

7.           Drager LF, McEvoy RD, Barbe F, Lorenzi-Filho G, Redline S, Initiative I. Sleep Apnea and Cardiovascular Disease: Lessons From Recent Trials and Need for Team Science. Circulation. 2017;136(19):1840-1850. 10.1161/CIRCULATIONAHA.117.029400

8.           Mazzotti D, Chen A, An J, et al. 439 Continuous Positive Airway Pressure and Cardiovascular Risk in a Large Clinical Sample of Obstructive Sleep Apnea Patients. Sleep. 2021;44(Supplement_2):A173-A174. 10.1093/sleep/zsab072.438

9.           Ayas NT, FitzGerald JM, Fleetham JA, et al. Cost-effectiveness of continuous positive airway pressure therapy for moderate to severe obstructive sleep apnea/hypopnea. Arch Intern Med. 2006;166(9):977-984. 10.1001/archinte.166.9.977

10.         Catala R, Villoro R, Merino M, et al. Cost-effectiveness of Continuous Positive Airway Pressure Treatment in Moderate-Severe Obstructive Sleep Apnea Syndrome. Arch Bronconeumol. 2016;52(9):461-469. 10.1016/j.arbres.2016.02.005

11.         Zancanella E, do Prado LF, de Carvalho LB, Machado Junior AJ, Crespo AN, do Prado GF. Home sleep apnea testing: an accuracy study. Sleep Breath. 2021. 10.1007/s11325-021-02372-6

Cardio May Blog1 Afib
Cardio May Blog1 Afib

Optimal management of OSA may be considered to reduce AF incidence, progression, recurrences, and symptoms.

Screening for AF should be considered in patients with OSA.

The newly revised European Society of Cardiology (ESC) guidelines for the diagnosis and management of atrial fibrillation (AF) recommend that screening for AF should be considered in patients with obstructive sleep apnea (OSA).

Furthermore, screening for OSA and OSA treatment for patients with symptomatic AF prior to the start of rhythm control therapy is recommended because treatment for OSA may reduce the need for rhythm control therapy as well as the recurrence, progression, and symptoms of AF. 

The revised guidelines emphasize that addressing the combination of cardiovascular risk factors as well as a range of comorbidities is found to reduce the lifetime risk of developing AF. 

The specific comorbidities include hypertension, heart failure, coronary artery disease, diabetes mellitus, and sleep apnea, as these may contribute to atrial remodeling, cardiomyopathy, and development of AF. 

OSA is the most common form of sleep-disordered breathing. OSA is highly prevalent in patients with AF, heart failure, and hypertension and is associated with increased risk of mortality and major cardiovascular events.

The revised recommendations regarding OSA screening are based upon the following:  

  • A high prevalence of OSA found among patients with AF
  • A well-defined mechanism by which OSA contributes to AF development
  • OSA, when present, can reduce the success of the treatment of AF
  • Availability of effective and reliable in-home methods for OSA screening and treatment  

High Prevalence of OSA in AF Patients

The basis of  the ESC clinical recommendations for screening for OSA in patients with AF is due to the high prevalence. One prospective study examined  consecutive patients undergoing electrocardioversion for AF (n=151) with  patients without past or current AF who were referred to a general cardiology practice (n=312).2 Patients in both groups were similar in age, gender, body mass index, diabetes rates, hypertension, and congestive heart failure. The results show a significantly higher  proportion of OSA in the AF group (49% [95% CI, .41%-57%] versus the general cardiology group (32% [95% CI, 27%-37%]; P<0.0004.)2 Additionally, the Sleep Heart Study demonstrated a risk of AF 4 times greater in patients with sleep-disordered breathing (both OSA and central sleep apnea) compared with patients with no sleep-disordered breathing.3

Well-Defined Pathophysiological Mechanism 

The pathophysiological mechanisms by which OSA promotes AF include repeated intermittent episodes of nocturnal hypoxia and hypercapnia, triggering a chemoreflex and enhancement of sympathetic nerve activity. The chemoreflex and sympathetic nerve activity can lead to tachycardia and elevated blood pressure which increase myocardial oxygen demand under hypoxic conditions, resulting in repeated myocardial and atrial ischemia during sleep, leading to AF.

OSA Screening and Treatment May Ameliorate AF Recurrence

The presence of OSA is shown to reduce success rates of antiarrhythmic drugs, electrical cardioversion, and catheter ablation in AF.4 Individuals with untreated OSA have a higher recurrence of AF after cardioversion than individuals without OSA. However, appropriate treatment of OSA with continuous positive airway pressure (CPAP) therapy is associated with lower recurrence of AF, and recent studies show that CPAP treatment for OSA reverses atrial remodeling in OSA.

Several methods of screening for OSA are available, including an in-home device for use during sleep to detect periods of apnea. The gold standard for OSA therapy is CPAP. The positive pressure keeps the pharyngeal area from collapsing and thus helps alleviate the airway obstruction.4 Data show that the treatment of OSA with CPAP may ameliorate OSA effects on the recurrence of AF and may improve rhythm control in patients with AF.5 

In conclusion, based upon the revised 2020 ESC guidelines, optimal management of OSA (see also: home sleep apnea testing) may be considered to reduce AF incidence, progression, recurrence, and symptoms. Consequently,  screening for AF should be considered in patients with OSA.1


  1. Hindricks G, Potpara T, Nikolaos D, et al; ESC Scientific Document Group. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2020;42(5):373-498. doi: 10.1093/eurheartj/ehaa612
  2. Gami AS, Pressman G, Caples SM, et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation. 2004;110(4):364-367. doi: 10.1161/01.CIR.0000136587.68725.8E
  3. Mehra R, Benjamin EJ, Shahar E, et al. Association of nocturnal arrhythmias with sleep-disordered breathing: the sleep heart health study. Am J Respir Crit Care Med. 2006;173(8):  910-916. doi: 10.1164/rccm.200509-1442OC
  4. Goudis CA, Ketikoglou DG. Obstructive sleep and atrial fibrillation: pathophysiological mechanisms and therapeutic implications. Int J Cardiol. 2017;230:293-300. doi: 10.1016/j.ijcard.2016.12.120 
  5. Linz D, McEvoy RD, Cowie MR, et al. Associations of obstructive sleep apnea with atrial fibrillation and continuous positive airway pressure treatment: a review. JAMA Cardiol. 2018;3(6):532-540. doi: 10.1001/jamacardio.2018.0095

Patients with severe obstructive sleep apnea (OSA) are five times more likely to experience cardiovascular mortality than those without sleep disordered breathing.1 OSA is strongly associated with hypertension, atrial fibrillation, stroke, coronary heart disease, myocardial ischemia and infarction.2 So why do clinical trials repeatedly show that treating OSA with continuous positive airway pressure (CPAP) makes little meaningful difference in cardiovascular outcomes? The answer, as Drs. Noah and Cook point out in a recent review article3, is in the details.

If RCT authors report it, it must be true, right?

We tend to take the results of randomized clinical trials (RCTs) as sacrosanct. And if we still have questions, a meta-analysis of RCTs quickly puts to rest any residual doubts to rest. In this regard, CPAP has been beaten up pretty badly. The largest RCT of its kind in published in the New England Journal of Medicine reported, “Therapy with CPAP plus usual care, as compared with usual care alone, did not prevent cardiovascular events in patients with moderate-to-severe obstructive sleep apnea and established cardiovascular disease.”4 If that was not enough, meta-analyses that included the results of nearly a half dozen similarly designed RCTs have come to the same conclusion: CPAP does not appreciably improve cardiovascular outcomes in patients with OSA.5-9

CPAP adherence in RCTs has been very low

Drs. Noah and Cook, specialists in sleep medicine and cardiovascular health, respectively, point out that despite several RCTs and corresponding meta-analyses reporting a lack of benefit, those same studies also report very low CPAP adherence rates. For instance, the authors of the NEJM paper came to their conclusions about the lack of effect while reporting “the mean duration of adherence to CPAP therapy was 3.3 hours per night” and only 42% of participants used CPAP for greater than 4 hours per night.4 In a way, that is like saying atorvastatin failed to change cardiovascular outcomes in patients with hyperlipidemia when the participants in the treatment arm took a dose of  1/3 of a pill per day, or, a full dose of the statin only 2-3 times per week. This poor adherence plagues all CPAP RCTs and their corresponding meta-analyses, which means we need to take a closer look at them.

Secondary analyses of three RCTs and a considerable number of observational studies (although they are not as highly regarded as RCTs, note they can be as informative in certain contexts) show a dose-dependent effect of CPAP usage on CVD in patients with OSA.2,3,7 Despite reporting results in patients with “severe” OSA (and therefore those who should benefit most from CPAP), RCTs often excluded certain at-risk groups due to the fact that investigators discouraged the practice. Their determination was that it would be a poor ethical choice to withhold CPAP in those patients with the most severe symptoms.3 Secondary analyses consistently show that patients who do manage to adhere to CPAP for more than 4 hours a night for months to years do reap a benefit in cardiovascular outcomes.3 This indicates that if patients with OSA can somehow be encouraged to adhere to CPAP, they would reap the long-promised CVD benefits of the treatment.

Current real world CPAP adherence is low, and that is a problem

There is a reason why CPAP adherence in RCTs was very low—it is low in real world settings. Perhaps as few as 1 in 3 patients with OSA actually adhere to treatment.3,10 The RCTs taken at face value may give  the impression that there is of little to no benefit, if physicians do refer their patients for polysomnography, only small fraction will use CPAP enough to even hope to benefit.  But this does not have to be the case.

CPAP adherence can be improved, substantially

Studies have shown that close, short term follow-up after CPAP deployment can improve adherence, e.g., working with a patient to choose the right type and size of mask, for example.6 Adherence can be further increased by targeted interventions such as motivational enhancement and cognitive behavioral therapy.11,12 Unfortunately, the incentives in the system do not currently reward healthcare providers for patient adherence, as Drs. Noah and Cook point out.3 The sleep specialist and the sleep center receive a large reimbursement for the sleep study itself, regardless of later patient adherence. Likewise, medical device providers make their biggest money on initial deployment and only need to hit almost absurdly low adherence rates—roughly 2.8 hours of use per night—to continue receiving reimbursements for supplying CPAP consumables. Drs. Noah and Cook suggest a change of incentive structure may be needed to combat this problem, one that focuses on more clinically relevant adherence targets.

What is at stake?

Secondary analyses of the CPAP RCTs found significant reductions in blood pressure, daytime sleepiness, and quality of life—despite poor adherence. However, we do not give up the struggle of trying to enhance medication adherence in patients with cardiovascular risk factors—that same risk factors that are exacerbated by OSA. 

The book is not closed on CPAP for cardiovascular outcomes. It would be an extreme disservice to patients for physicians to fail to refer at-risk patients for sleep studies. Obtaining and maintaining CPAP is a problem, but it is a solvable problem with a little time and effort. Considering that untreated OSA carries the same mortality risk as a middle-aged patient with a total cholesterol of over 300 why would we only treat the latter and ignore the former?

Itamar Medical is a global medical device manufacturer specializing in the WatchPAT home sleep apnea testing device.


1. Young T, Finn L, Peppard PE, et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin sleep cohort. Sleep. 2008;31(8):1071-1078. 

2. Drager LF, McEvoy RD, Barbe F, Lorenzi-Filho G, Redline S, Initiative I. Sleep Apnea and Cardiovascular Disease: Lessons From Recent Trials and Need for Team Science. Circulation. 2017;136(19):1840-1850. 10.1161/CIRCULATIONAHA.117.029400

3. Noah WH, Cook JL. “Using CPAP” Improves Cardiovascular Outcomes: Physicians Must Look Behind the RCT Veil and Focus on Long-Term Adherence. J Cardiol Clin Res. 2021;9(1). 

4. McEvoy RD, Antic NA, Heeley E, et al. CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea. N Engl J Med. 2016;375(10):919-931. 10.1056/NEJMoa1606599

5. Abuzaid AS, Al Ashry HS, Elbadawi A, et al. Meta-Analysis of Cardiovascular Outcomes With Continuous Positive Airway Pressure Therapy in Patients With Obstructive Sleep Apnea. Am J Cardiol. 2017;120(4):693-699. 10.1016/j.amjcard.2017.05.042

6. Patil SP, Ayappa IA, Caples SM, Kimoff RJ, Patel SR, Harrod CG. Treatment of Adult Obstructive Sleep Apnea With Positive Airway Pressure: An American Academy of Sleep Medicine Systematic Review, Meta-Analysis, and GRADE Assessment. J Clin Sleep Med. 2019;15(2):301-334. 10.5664/jcsm.7638

7. Peker Y, Balcan B. Cardiovascular outcomes of continuous positive airway pressure therapy for obstructive sleep apnea. J Thorac Dis. 2018;10(Suppl 34):S4262-S4279. 10.21037/jtd.2018.11.48

8. Wang X, Zhang Y, Dong Z, Fan J, Nie S, Wei Y. Effect of continuous positive airway pressure on long-term cardiovascular outcomes in patients with coronary artery disease and obstructive sleep apnea: a systematic review and meta-analysis. Respir Res. 2018;19(1):61. 10.1186/s12931-018-0761-8

9. Yu J, Zhou Z, McEvoy RD, et al. Association of Positive Airway Pressure With Cardiovascular Events and Death in Adults With Sleep Apnea: A Systematic Review and Meta-analysis. JAMA. 2017;318(2):156-166. 10.1001/jama.2017.7967

10. Chervin RD, Rosen IM, Watson NF. CPAP in Obstructive Sleep Apnea. N Engl J Med. 2016;375(23):2301-2302. 10.1056/NEJMc1613219

11. Bakker JP, Wang R, Weng J, et al. Motivational Enhancement for Increasing Adherence to CPAP: A Randomized Controlled Trial. Chest. 2016;150(2):337-345. 10.1016/j.chest.2016.03.019

12. Andry JM, Jr., Toban G, Chafin C, Noah W. Positive airway pressure therapy supplied by an integrated sleep practice associated with greater adherence among pre-Medicare-aged patients with sleep-disordered breathing. J Clin Sleep Med. 2021;17(1):31-36. 10.5664/jcsm.8786 

13. Ho PM, Bryson CL, Rumsfeld JS. Medication adherence: its importance in cardiovascular outcomes. Circulation. 2009;119(23):3028-3035. 10.1161/CIRCULATIONAHA.108.768986

14. Prospective Studies C, Lewington S, Whitlock G, et al. Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths. Lancet. 2007;370(9602):1829-1839. 10.1016/S0140-6736(07)61778-4

*This material is subject to a disclaimer available here.

April Dr Collaboration

Review of Pollak and Povitz’s Editorial on Obstructive Sleep Apnea and Cardiovascular Disease1

In an editorial in the Candian Journal of Cardiology, Drs. Timothy Pollack and Marcus Povitz ask if cardiologists are failing to recognize obstructive sleep apnea in patients with atrial fibrillation and heart failure. In 2018, the Canadian Cardiovasular Society updated their guidelines on the management of atrial fibrillation to specifically recommend the aggressive treatment of cardiovascular risk conditions such as sleep apnea, as they have been shown to reduce the burden of atrial fibrillation and improve quality of life.2

And while there are a number of clinical symptom-based questionnaires that have been proposed (e.g., Epworth Sleepiness Scale) to identify patients with sleep apnea, Drs. Pollack and Povitz ask if enough is being done in cardiac patients given the impact that sleep disordered breathing (SBD) can potentially have on a patient’s cardiac condition. 

The Connection between Atrial Fibrillation and Sleep-Disordered Breathing

Atrial Fibrillation (AF) is the most common arrhythmia diagnosed in clinical practice, and AF may be an unrecognized consequence of SDB / obstructive sleep apnea (OSA). Many patients that are referred to AF clinics have had unsuccessful attempts at managing their condition at primary clinics. It is not uncommon for practitioners at these AF clinics to discover that these patients have either been diagnosed with OSA or have risk factors that suggest they have OSA. 

The authors suggest that much like a stroke triggers screening for AF, that AF should trigger screening for the presence of OSA / SBD. 

Neurocirculatory Consequences of Sleep-Disordered Breathing

SDB not only can affect the cardiovascular system but also the nervous and circulatory systems as well. SDB caused by OSA can lead to repeated nocturnal hypoxia, which can contribute to many ailments, such as cognitive dysfunction, hypertension, and stroke. It can also lead to a distortion of the heart’s electrophysiologic environment, which can lead to arrhythmia. With studies showing that OSA treatment can help prevent such neurocirculatory conditions, treating SDB is essential.

Detecting a Patient’s Risk for SDB: The Importance of Sleep Screening 

While questionnaires like the Epworth Sleep Scale and SNOOZE AF have been developed as an assessment tool to help predict the probability of SDB in patients, many of the available questionnaires are not effective. As a result, Drs. Pollack and Povitz suggest that the best strategy for screening might be to screen all AF and heart failure patients with an at-home sleep apnea test. They note that home sleep apnea testing is relatively inexpensive and sensitive and specific enough to screen this high-risk patient group. 

Recommendations for the Future

Should SDB be considered a cardiovascular risk factor? What benefit does a sleep apnea diagnosis provide to a cardiac patient? The authors recognize that they – and many of their peers – are seeing an increase in patients with AF and heart failure – both diagnoses that are associated with SDB.  But cardiologists can’t do it alone – and neither can respirologists.

The review goes on to make recommendations that cardiologists and sleep medicine specialists work together to better serve their combined patient population. They raise the point that the inconsistent application of tools like the clinical questionniares mentioned above will likely not solve the issues around the rising prevalence of SBD-associated cardiac disease. Rather, they suggest that we need to raise awareness of the implications of SBD-associated cardiac disease and that cardiologists should push for easier access to home sleep apnea testing to help overcome some of the barriers to traditional sleep-laboratory polysomnography. 

Bridging the Gap Between Cardiology and Sleep

What review articles like this tell us is that the linkage between cardiovascular health and sleep cannot be ignored. Cardiologists need to ensure that sleep screening solutions are offered at their practice as common sleep disorders like OSA can attribute to a patient’s heart condition. In doing so, cardiologists will be better equipped to diagnose and treat their patients effectively. 


  1. Pollak PT, Povitz M. Asleep at the Switch? Are We Failing to Recognize Obstructive Sleep Apnea in Patients with Atrial Fibrillation and Heart Failure?. Can J Cardiol. 2019;35(11):1426-1429. doi:10.1016/j.cjca.2019.09.005
  2. Andrade JG, Verma A, Mitchell LB, et al. 2018 focused update of the Canadian Cardiovascular Society guidelines for the management of atrial fibrillation. Can J Cardiol Can J Cardiol 2018;34:1371-92.

*This material is subject to a disclaimer available here.

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In 2018, nearly half a million deaths in the United States included hypertension as a primary or contributing cause.1 Its prevalence is undeniable as nearly one out of two adults in the country suffer from this condition.2 We know that hypertension can contribute to many health ailments, such as heart disease and stroke, which is why we focus on the many factors that can lead to its development. However, when it comes to hypertension, one such factor often overlooked is abnormal sleep. This week is the National Sleep Foundation’s National Sleep Awareness Week, and since many individuals suffer from sleep disorders, it is important to know the association between sleep disorders and hypertension.  

Sleep Disorders and Hypertension 

The American Academy of Sleep Medicine and the Sleep Research Society recommend that adults sleep at least seven hours each night for well-being.3 As reported by the Centers for Disease Control and Prevention, one out of three American adults do not meet this criteria.4 One  primary reason is the prevalence of sleep disorders in American society. The Cleveland Clinic states that about 70 million people in the United States suffer from sleep disorders.5 

With many Americans not getting adequate sleep, the health repercussions that can follow are important to decipher. Seeing that high blood pressure is one of the most common conditions in the United States, compelling evidence links hypertension and sleep. According to a study by Daniel J. Gottlieb that involved 5,910 participants, it was found that the prevalence of hypertension was increased for participants who had less than the median mean of seven to eight hours of sleep per night, with a pronounced increase in prevalence seen in individuals who slept six hours or less per night.6 In fact, in a Mayo research study involving healthy adults, nightly sleep was restricted to four hours for nine nights and nine hours for nine nights—it was found that during the nine nights of four hours of sleep, participants had an average systolic blood pressure reading that was 10 millimeters of mercury (mm Hg) higher than the nine-hour sleep phase.7                           

For many people, a lack of adequate sleep is caused by sleep disruption from obstructive sleep apnea—a condition where there is a blockage of the upper airway that can lead to cessations of breathing during sleep. Patients who suffer from obstructive sleep apnea have elevated blood pressure during the night and are more likely to suffer from hypertension.  

But how can an apnea disorder like obstructive sleep apnea induce hypertension? What is the etiology behind it? We are continuing to understand the intricacies of this relationship, but there are certain elements that we know to be relevant. During normal sleep, our blood pressure typically decreases by 10% to 20% than that of our daytime blood pressure.8 This decrease is often referred to as nocturnal dipping. Since sleep apnea can cause disturbances in this natural dipping phenomenon, blood pressure can stay higher for longer periods of time. It is also thought that since sleep helps regulate stress hormones, a lack thereof could lead to high blood pressure due to inadequate regulation.7

Why Sleep Should Be Discussed With Patients

As a cardiologist, you are aware of the implications that hypertension can have on the heart. With millions of people suffering from sleep disorders, such as sleep apnea, it is possible that many patients who have hypertension may be suffering from sleep apnea or a lack of adequate sleep in general. The association between improper sleep and hypertension is important; therefore, sleep health must become a priority. Sleep apnea screening benefits your patients as sleep apnea is a relevant cardiac co-morbidity. However, discussing and screening for sleep apnea with your patients is not only important for hypertension but also for other conditions that can affect the heart. For example, atrial fibrillation is the most common arrhythmia diagnosed in clinical practice, and sleep disorders—especially sleep apnea –  have been discovered to be a significant risk factor. Learn more about that specific link in our upcoming article on the relationship between sleep apnea and atrial fibrillation as we take a deeper dive into this relation.

Also, if you are looking for a remote sleep apnea management solution for your practice, check out our WatchPAT® TurnKey Program, where we provide a seamless pathway to ensure cardiovascular patients with sleep apnea are diagnosed effectively and can be treated in less than 2 weeks on average. 


  1. Facts About Hypertension. Centers for Disease Control and Prevention. Published September 8, 2020. Accessed March 1, 2021. 
  2. Estimated Hypertension Prevalence, Treatment, and Control Among U.S. Adults. Million Hearts. Published February 5, 2020. Accessed March 1, 2021. 
  3. Watson NF, Badr MS, Belenky G, et al. Recommended Amount of Sleep for a Healthy Adult: A Joint Consensus Statement of the American Academy of Sleep Medicine and Sleep Research Society. SLEEP. 2015;38(6):843-844. doi:10.5665/sleep.4716 
  4. 1 in 3 adults don’t get enough sleep. Centers for Disease Control and Prevention. Published February 16, 2016. Accessed March 1, 2021. 
  5. Common Sleep Disorders: Symptoms, Causes & Treatment. Cleveland Clinic. Accessed March 1, 2021. 
  6. Gottlieb DJ, Redline S, Nieto FJ, et al. Association of Usual Sleep Duration With Hypertension: The Sleep Heart Health Study. Sleep. 2006;29(8):1009-1014. doi:10.1093/sleep/29.8.1009 
  7. Torborg L. Mayo Clinic Q and A: Lack of sleep and risk of high blood pressure. Mayo Clinic. Published January 28, 2017. Accessed March 1, 2021. 
  8. Yano Y, Kario K. Nocturnal blood pressure and cardiovascular disease: a review of recent advances. Hypertension Research. 2012;35(7):695-701. doi:10.1038/hr.2012.26 
  9. Calhoun DA, Harding SM. Sleep and hypertension. Chest. 2010;138(2):434-443. doi:10.1378/chest.09-2954 
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March hosts both National Sleep Awareness Week and National Sleep Day. Therefore, it is appropriate to explore the connection between sleep and heart health.  In our article, “Can Sleep Disorders Lead to Hypertension?”, we examined the relationship between sleep disorders and hypertension and how important it is to discuss sleep with your patients and conduct sleep screenings. We know that a lack of proper sleep, especially caused by sleep disorders like sleep apnea, is linked to poor heart health.

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figure 1

As seen in figure 1 above , a lack of quality sleep can be harmful to the heart in various ways, and as cardiovascular disease is the leading cause of death in the United States, clinicians are constantly treating patients for heart conditions and unraveling risk factors that can lead to heart disease. With atrial fibrillation (AF) being the most common arrhythmia diagnosed in clinical practice, it is important that we thoroughly analyze the factors that can lead to its occurrence. One relevant factor that we have found to be associated is atrial fibrillation.   

The Relationship Between Sleep and Atrial Fibrillation

Sleep itself is a vital component of life, and although sleep apnea has been linked to heart conditions like AF, a lack of adequate sleep, independent from sleep disorders, can also lead to issues. A study that analyzed participants from various heart studies found that sleep quality itself, independent of sleep apnea, was a determinant of AF, with less REM sleep and sleep disturbances being highlighted risks.1 However, with millions of people suffering from sleep disorders, diagnosing and treating such disorders can also be the gateway to improving sleep and decreasing the chance for AF. Sleep apnea, in particular, has been revealed to be a major risk factor for AF.

Sleep Apnea and Atrial Fibrillation

Experimental data and epidemiologic studies show both central and obstructive sleep apnea are associated with atrial fibrillation.2 Studies, such as the Sleep Heart Study and the Outcomes of Sleep Disorders in Older Men Study, have found a two to fivefold increased chance of AF for those with a moderate to severe degree of sleep-disordered breathing.2 Furthermore, in examining the etiology behind sleep apnea and AF, experiments with animals have been conducted. In one experiment, obstructive sleep apnea was mimicked in rats using a mechanical ventilator. It was found that the rats with chronically repeated episodes of obstructive sleep apnea exhibited characteristics such as AF-promoting cardiac remodeling, atrial conduction slowing, and increased atrial fibrous tissue content.3 Similar characteristics have been found in human subjects with obstructive sleep apnea as well, with studies showing AF-promoting cardiac remodeling characterized by changes like atrial enlargement and a reduction in cardiac voltage.4, 5

In light of the findings mentioned above, there are studies that show that treating sleep apnea decreases AF recurrence. In a study by Abe et al. consisting of 1300 patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), it was found that continuous positive airway pressure (CPAP) treatment significantly reduced episodes of paroxysmal AF in patients with moderate to severe OSAHS.6 In another study, Kanagala et al. further investigated the effect of CPAP treatment for OSAHS patients with AF and found an 82% increased chance of AF recurrence in the patients who did not receive CPAP compared to the 42% chance of recurrence when CPAP therapy was administered. With further studies continuing to validate sleep apnea as a notable risk factor for AF, the importance of incorporating sleep apnea screening in your practice can be the key to treating patients with AF. 

The WatchPAT® TurnKey Program: A Sleep Apnea Management Solution for Your Practice 

Undoubtedly, quality of sleep is an essential factor to assess when consulting patients. As a cardiologist, an effective yet efficient screening method for sleep apnea can be the difference-maker in a diagnosis and treatment plan. Whether patients are dealing with AF or other conditions, you want to ensure that sleep apnea does not go unnoticed, as up to 80% of moderate and severe cases are.8 This is the reason why we provide clinicians the WatchPAT® TurnKey Program. The program is a seamless solution that ensures cardiovascular patients with sleep apnea are diagnosed and can be brought to a treatment plan in less than two weeks on average.

Contact us today to learn more about our TurnKey Program and how WatchPAT® provides sleep screening solutions for your practice. 


  1. Poor sleep quality linked to atrial fibrillation. ScienceDaily. Published June 26, 2018. Accessed March 2, 2021. 
  2. Ayache MB, Mehra R, Mayuga KA. Should I Evaluate My Patient With Atrial Fibrillation for Sleep Apnea? Consult QD. Published March 9, 2020. Accessed March 2, 2021. 
  3. Iwasaki YK, Kato T, Xiong F, et al. Atrial fibrillation promotion with long-term repetitive obstructive sleep apnea in a rat model. J Am Coll Cardiol. 2014;64(19):2013-2023. doi:10.1016/j.jacc.2014.05.077
  4. Dimitri H, Ng M, Brooks AG, et al. Atrial remodeling in obstructive sleep apnea: implications for atrial fibrillation. Heart Rhythm. 2012;9(3):321-327. doi:10.1016/j.hrthm.2011.10.017
  5. Müller P, Grabowski C, Schiedat F, et al. Reverse Remodelling of the Atria After Treatment of Obstructive Sleep Apnoea with Continuous Positive Airway Pressure: Evidence from Electro-mechanical and Endocrine Markers. Heart Lung Circ. 2016;25(1):53-60. doi:10.1016/j.hlc.2015.05.004
  6. H. Abe, M. Takahashi, H. Yaegashi, S. Eda, H. Tsunemoto, M. Kamikozawa, et al. Efficacy of continuous positive airway pressure on arrhythmias in obstructive sleep apnea patients.
  7. R. Kanagala, N.S. Murali, P.A. Friedman, N.M. Ammash, B.J. Gersh, K.V. Ballman, et al.Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation, 107 (2003), pp. 2589-2594
  8. Heart Vessels, 25 (2010), pp. 63-69Lee W, Nagubadi S, Kryger MH, Mokhlesi B. Epidemiology of Obstructive Sleep Apnea: a Population-based Perspective. Expert Rev Respir Med. 2008;2(3):349-364. doi:10.1586/17476348.2.3.349
POST1 REVISEDsimple 7 1080X1080 2

In 2010 the American Heart Association coined the term Life’s Simple 7, referring to the seven most important predictors of heart health. The Simple 7 included four behaviors that patients could modify (smoking, weight, diet and exercise) as well as three biometric measures (blood pressure, cholesterol and blood glucose)1.

The AHA also classified these seven factors into three categories (ideal, intermediate and poor)2 to help create a common standard.

Screen Shot 2021 02 24 at 17.30.16

Along with identifying these seven factors and establishing metrics to track what ‘good’ looked like, the AHA also set a 10-year goal for improvement. The goal? A 20% reduction in cardiovascular disease and stroke mortality and a 20% improvement in cardiovascular health in all Americans by 2020.1 While data isn’t available through the end of 2020 at this time, the death rates from cardiovascular disease have decreased since the Simple 7’s introduction,3 highlighting the potential effectiveness of the initiative. 

But, we’re not finished yet. In fact, a recent study suggests that adding sleep to the Simple 7 could improve the accuracy of cardiovascular disease risk prediction. We will be diving into the facts on why sleep is missing from this important list of risk factors in our next article. 


  1. Lloyd‐Jones DM, Hong Y, Labarthe D, Mozaffarian D, Appel LJ, Van Horn L, Greenlund K, Daniels S, Nichol G, Tomaselli GF, Arnett DK, Fonarow GC, Ho PM, Lauer MS, Masoudi FA, Robertson RM, Roger V, Schwamm LH, Sorlie P, Yancy CW, Rosamond WD. Defining and setting national goals for cardiovascular health promotion and disease reduction: the American Heart Association’s strategic Impact Goal through 2020 and beyond. Circulation. 2010; 121:586–613.
POST2 REVISEDsimple 7 1080X1080

10 years ago, the American Heart Association rolled out an initiative called Life’s Simple 7, aimed at raising awareness of multiple factors that can contribute to cardiovascular disease.1  These seven factors; blood pressure, cholesterol, blood sugar, smoking, weight, diet, and exercise can have a profound impact on cardiovascular health. In one study involving 7,622 participants, those who scored in the ‘ideal’ category for at least five of Life’s Simple 7 reduced their risk of heart-releated death by 78% compared to participants who did not meet those metrics.2

Life’s Simple 7 has come a long way in raising risk factor awareness in the minds of clinicians and patients. However, as time has passed and additional research has been conducted, we’ve become aware of one additional cardiovascular risk factor that has been left out of heart health discussions for too long. Sleep.

“Sleep, like diet and physical activity, is a health behavior we engage in every day,” says Nour Makarem, an associate research scientist at Columbia University Irving Medical Center in New York.3 “Increasingly, it is linked to not only the risk of heart disease but also to the risk factors that lead to cardiovascular disease”. 3

In 2020, Dr. Nour Makarem’s team evaluated 1,920 patients who participated in the MESA Sleep study. 3 The team investigated a variety of sleep characteristics and their impact on cardiovascular health. 3 Dr. Makarem’s research found that poor sleep quality was strongly associated with cardiovascular disease

  • Patients with obstructed sleep apnea had a 200% greater chance of poor heart health. 
  • Variations in sleep duration were associated with a 24% greater risk of poor heart health
  • Variations in sleep timing were associated with a 31% greater risk of poor heart health

The findings of this research highlight the important role that sleep can play in cardiovascular outcomes.3 

Despite this importance,” says Dr. Makarem,”unlike diet and exercise, sleep has received less attention and is not currently included in guidelines for cardiovascular disease prevention or as a measure of cardiovascular health.”3

With this in mind, we propose adding sleep to Life’s Simple 7 and making it Life’s Essential 8.

With 50 to 70 million Americans suffering from sleep disorders including sleep apnea,4 raising awareness of the link between sleep and cardiovascular health (and more importantly, screening for sleep disorders in the cardiology office) could significantly help improve cardiovascular outcomes.

American Heart Health month is the perfect month to begin stretching the Life’s Simple 7 tool to fit the true realities of heart disease risk factors. Switch the conversation from “Life’s Simple 7,” to “Life’s Essential 8,” and be inclusive of all risk factors that could potentially impact your patients’ cardiovascular well-being. 


  1. Lifes Simple 7. Accessed February 1, 2021. 
  2. Ford ES, Greenlurd KJ, Hong Y. Ideal Cardiovascular Health and Mortality From All Causes and Diseases of the Circulatory System Among Adults in the United States. Circulation. 2012;125(8). doi:CIRCULATIONAHA.111.049122 
  4. National Center for Chronic Disease Prevention and Health PromotionDivision of Population Health Accesseed February 10, 2020.
obstructive sleep apnea infographic

This is the time of year for new year’s resolutions. People take this time to improve their health by joining a gym, cutting out processed foods, or just plainly visiting their physician more often. One new year’s resolution that could lead to better sleep and better health for your cardiac patients is sleep apnea evaluation. This sleep disorder is common among patients with cardiovascular disease and contributes to increased morbidity and mortality. Cardiac patients often suffer from sleep apnea, but unfortunately too commonly it remains undiagnosed.     

Pathophysiology of Sleep Apnea  

There are two types of sleep apnea: 

  • Obstructive sleep apnea: airflow obstruction due to nocturnal relaxation of pharyngeal muscles.  
  • Central sleep apnea: nocturnal neurologic cessation of all breathing effort. 

Obstructive sleep apnea 

Obstructive sleep apnea (OSA), caused by physiologic aspects of patients, is more common among obese and patients with coronary disease. Despite the disorder’s prevalence, it is often missed during exams, and often goes undiagnosed.   

OSA episodes have many detrimental consequences, including lower oxygen levels, due to obstructed airways. Obstructed airways also cause exerted abdominal effort, which causes changes in intrathoracic pressure and leads to oxidative stress. OSA also leads to constriction as well as increased pressure of pulmonary veins.   

This causes the cardiac load to increase, which is very damaging to patients with a coronary disease whose hearts are already working overtime dramatically. OSA episodes cause a swing in intrathoracic pressure, which results in a decrease in cardiac output and is worse during REM sleep. Decreased cardiac output can ultimately lead to cardiogenic shock. 

Central sleep apnea 

Central sleep apnea (CSA) as opposed to obstructive sleep apnea, does not include thoracoabdominal effort. While physiologic in some cases, CSA is more often caused by sensitive chemo responses due to alterations in carbon dioxide levels. These alterations can be a result of arousal from sleep. In CSA episodes, Hunter-Cheyne-Stokes respiration can occur, which is a cyclical crescendo-decrescendo respiratory effort. This type of respiration is worse during NREM sleep.   

Sleep apnea is more prevalent than one might think, affecting 30-60% of patients with underlying coronary disease and cardiovascular risk conditions such as diabetes, hypertension, and heart failure. Patients with underlying conditions such as coronary disease are more likely to 

develop sleep apnea, but may not be aware of it, which is why it is crucial to suggest that patients get tested.  

Sleep Apnea and Cardiac Health 

Both forms of sleep apnea are common in patients with underlying cardiovascular conditions. 

Patients with heart failure have been shown to have fluid in the neck and alveoli of the lungs.  This shift of fluid causes pharyngeal edema, nearly causing OSA. Episodes of OSA impair diastolic function and cause atrial and aortic enlargement. REM-related OSA, in particular, is associated with an increased risk for cardiovascular complications.   

Patients with heart failure may also develop pulmonary congestion, which could cause CSA. Sleep apnea causes overworking of the heart and could potentially cause cardiovascular problems, if not worsen those already present. Sleep apnea tests should be suggested to patients with underlying conditions to reduce the risk of further heart damage. 

Effects of Sleep Apnea  

Sleep apnea effects include, but are not limited to, lower oxygen levels, increased cardiac output, and increased blood pressure. All of these symptoms are harmful, especially to patients with coronary disease. The effects of obstructive sleep apnea in cardiac patients can be ranked as immediate, intermediate, and chronic. Direct effects include lower oxygen and carbon dioxide levels, intrathoracic pressure swings, and fluctuations in the autonomic nervous system.   

Intermediate effects include systemic inflammation, oxidative stress, vascular dysfunction, and upregulation of prothrombotic pathways. Chronic effects of sleep apnea include cardiac electrical and structural remodeling. Patients with sleep apnea typically have fatigue, headaches, memory impairment, and tend to snore at night.   

A simple questionnaire for cardiac patients can determine if sleep apnea tests are needed and can serve as a future reference if these symptoms develop later on. Educating patients on the causes, symptoms, and effects of sleep apnea can help decrease this disorder’s prevalence. 

Getting Tested 

Although sleep apnea is associated with many cardiovascular complications, it can often go undiagnosed.

That’s where WatchPAT® ONE can help. Patients can use this test in the comfort of their own beds (especially important in light of the COVID-19 pandemic) and in just a few simple steps, complete their sleep study. Once the test is complete, physicians can review the automatic results and discuss them with the patient.   

With no wait time for the test or the results, no risk of exposure, and no need to mail in any part of the device, WatchPAT® ONE provides a simple solution for your cardiac patients. 

As cardiac patients are vulnerable to sleep apnea, among other conditions, take the opportunity to recommend sleep apnea tests. Diagnosing sleep apnea is the first step to keeping a patient’s health under control and reducing the risk of further complications. A proper diagnosis and taking the time to educate patients is what will get them on the right path toward appropriate treatment and better health.

While it has long been understood that sleep apnea often underlies heart issues, the rate of the condition is still under-diagnosed in these patients, leaving their condition and its possible complications to worsen unchecked. Yet, the reason for the difficulty in reaching a sleep apnea diagnosis, especially in patients living with atrial fibrillation, has been a matter of debate. Now however, two separate peer-reviewed studies have revealed a common issue behind the diagnostic failure – the fact that the questionnaires currently in use are not identifying the sleep apnea patient in proper way.

Here we will take an in-depth look at each study in order to highlight the conclusions reached by the research teams.

Sleep apnea in ablation candidates with paroxysmal atrial fibrillation

The first study, reported in IJC Heart & Vasculature, set out to determine the prevalence, characteristics, and risk factors as well as type of sleep apnea most common in ablation candidates with paroxysmal atrial fibrillation.

The researchers recruited 579 patients with paroxysmal AF and utilized polygraphy for two nights at home to diagnose sleep apnea. These results were also compared against questionnaire results including, the Epworth Sleepiness Scale (ESS), STOP-Bang Questionnaire, and Berlin Questionnaire (BQ), which assessed the degree of sleep apnea symptoms.

The team found that approximately 82.7 percent of patients had an apnea-hypopnea index (AHI) ≥ 5, with 42.1 percent of those studied having an AHI ≥ 15. The researchers also determined that the predominant type of sleep apnea affecting these patients was obstructive and that AHI increased with:

  • Age
  • BMI
  • Waist and neck circumference
  • Body and visceral fat

Importantly, the researchers also found no association between ESS and AHI and stated in their conclusions that “The high prevalence of SA detected in this study may indicate that SA is under-recognized in patients with AF.”

They also reported that none of the screening questionnaires predicted SA reliably.

The prevalence of undiagnosed sleep apnea in patients with symptomatic atrial fibrillation

The second study we will discuss, briefly titled, “Prevalence of OSA in patients with AF”, set out to examine the prevalence of sleep apnea in atrial fibrillation patients referred for ablation.

This stated goal is due to the fact that while sleep apnea is known to be common if atrial fibrillation patients and is also associated with atrial remodeling as well as a high recurrence post-ablation, the prevalence of atrial fibrillation patients with undiagnosed sleep apnea had not been well established.

The research team recruited 188 patients scheduled to undergo ablation and who had no prior diagnosis of sleep apnea. All participants were required to complete the STOP-Bang sleep apnea screening questionnaire and undergo home sleep apnea testing.

The results of the home sleep apnea testing were positive in 82.4 percent of participants without a prior diagnosis of sleep apnea as follows:

  • Mild- 43.8 percent
  • Moderate- 32.9 percent
  • Severe- 23.2 percent

For all positive participants a predominantly obstructive component was observed.

The researchers also found that a positive STOP-Bang questionnaire was not predictive for sleep apnea and that symptoms of the condition, including snoring, daytime sleepiness, and observed apneic episode were reported at a similar frequency in patients positive and negative for sleep apnea.

The conclusion of the study was that while undiagnosed sleep apnea is exceedingly prevalent in patients with atrial fibrillation who are referred for ablation, the use of screening questionnaires or symptom evaluation for diagnosis has limited predictive value.

The authors also stated that, “A universal SA screening strategy may be considered in all patients with symptomatic AF.”

Home sleep apnea testing enhances diagnosis and care

The results of these studies mean that physicians treating atrial fibrillation patients can no longer afford to rely upon screening questionnaires for sleep apnea diagnosis, since these tools are failing to pinpoint the condition accurately, which ultimately translates to a failure to provide appropriate care.

Instead, home sleep apnea testing is necessary on a broad scale for patients with atrial fibrillation so that they can receive the necessary treatment with continuous positive airway pressure ventilators to improve atrial fibrillation control. 

Cardio Sleep Review (CSR) talks with Daniel Bensimhon, MD, Medical Director of The Advanced Heart and Mechanical Circulatory Support Program at Moses Cone Memorial Hospital in Greensboro, NC. Dr. Bensimhon is an Advanced Heart Failure cardiologist who treats patients with all levels of heart failure—from very mild (Class II) to patients who need full mechanical support and referral for cardiac transplantation (Class IV).

Dr Bensimhon
Dr Bensimhon


There are interventional cardiologists, electrophysiologists, imaging specialists, among other specialties in a cardiology department. Why the need for a heart failure specialist?

Dr. Bensimhon

Cardiology is becoming more and more subspecialized. We’re seeing more technologies and new devices in all fields of cardiology, especially in electrophysiology and interventional cardiology to help support people in cardiac distress. We’re finding that as people are living longer, surviving their heart attacks and living with heart failure, we need more and more treatment options in heart failure as well.  The care of these patients is becoming more sophisticated and more complicated. There are new pharmaceutical agents and new devices coming to market. So, providing care for this potentially very sick patient population has warranted its own subspecialty of clinicians trained to care for patients with advanced heart failure and these issues that go along with it. 


How do you collaborate and work with the other specialists within cardiology?

Dr. Bensimhon

There are still many smaller practices in the country where they don’t have the ability to have multiple specialists.  We have over 40 cardiologists in our group who all work well together. Although we are in a large community center, we function much like an academic program. Many of the complicated patients require services from general cardiology, but we still need imaging, interventional, and electrophysiology support as well. We work hand-in-hand. They rely on us to take care of the sickest heart failure and shock patients and we rely on them for interventional procedures and devices and to refer their appropriate patients to us in a timely fashion so that we can offer therapies before it’s too late.


Could you describe the patient population that you treat in the clinic?

Dr. Bensimhon

We have about 3000 patients in our outpatient Heart Failure clinic. About two-thirds of them have systolic heart failure or HFrEF where their heart muscle is actually weak. And the other third has diastolic heart failure or HFpEF where their heart function is actually preserved, but they have a stiff heart.

Many of these patients are very limited.  They have symptoms with minimal activity. They struggle with additional fluid overload and it’s quite intense to manage not only their volume status but to make sure that we’re treating their comorbidities. We want to make sure we are addressing everything that we feel affects their heart failure and functional capacity. We’re getting them on guideline-directed medical therapy, having devices implanted, referring for rehab, placing heart monitors, and ordering sleep studies.

If those strategies are not enough to optimize a patient, we then consider our advanced therapy options. There’s a lot of data now that says these patients are difficult to treat, that the majority of these patients aren’t on the guideline-directed medical therapies, and that they are under-treated. Our focus is to be very aggressive and make sure these patients are treated as aggressively as possible before we turn to an LVAD or transplant.


From your perspective, what’s the connection between sleep apnea and heart failure?

I think we’ve realized for a long time that there is a link between sleep apnea and worse cardiovascular outcomes in our patients. That said, not all the data has been consistent. There has been a direct link between untreated sleep apnea and atrial fibrillation and hypertension —both of which are huge risk factors for congestive heart failure. Unless you get their sleep apnea under control, you are not going to get those risk factors under control. Whether or not there is a direct link between sleep apnea and worsening heart failure outcomes or it is mediated by these risk factors remains unclear. In our clinical experience, certainly, it seems that heart failure patients with the worst sleep apnea are more symptomatic and have been more difficult to manage.

More recently, I think people are realizing that many of the abnormalities in ventilation that we see in sleep apnea, also occur in heart failure – and we see this frequently in our cardiometabolic exercise lab. Heart failure patients have a much higher incidence of central sleep apnea where the ventilation processes in the brain don’t work as well as they should, and they can have very abnormal ventilatory patterns both during sleep and during activity.

There is a tighter and tighter link between undetected or uncontrolled sleep apnea and heart failure. One line that we’re still trying to connect is, is there a direct connection between the treatment of sleep apnea and improved heart failure outcomes. There has been some data on both sides of the fence saying that yes there’s a huge benefit and on the other side, maybe not.  Maybe there could even be harmful. We need more studies, more data to confirm what instinctively we know.

As I mentioned above, in our clinic, we see that with our patients who have sleep apnea and are under-treated or not treated, we have a much harder time controlling their risk factors. We have a much harder time controlling their hypertension, a much harder time controlling their atrial fibrillation; and most importantly, we have a really hard time controlling their symptoms. They come in and say that they’re fatigued, and we can’t tell if its heart failure or sleep apnea. What is it? Why are they so fatigued and why are they so limited? So, our goal is to address all their risk factors and to improve their sleep apnea symptoms to really try and get at what effect is it having on their heart failure.

Personally, I think that there’s a very strong link between the treatment of sleep apnea and improvement in heart failure symptoms and potential outcomes. But the data we have so far has been limited and doesn’t completely support these observations. I do not think we know the whole story yet. We still need more studies, more data. 


What would be the best scenario for how you would describe sleep apnea management in the clinic?

It’s different in every situation.  Cardiology clinics come in many different forms. For us, in our Heart Failure clinic, it’s important for us to own the process. Given what’s on the line for these patients with advanced symptoms, we want to own the patient. If we think there’s something important that’s going to improve their heart failure, whether it be managing their fluid status or getting them an ICD,  we’re going to manage that process. We’re going to start the therapy. We’re going to prescribe and implement that therapy. We’re going to follow up with them.  With sleep apnea, we really haven’t had the ability to do that. What typically happens is that we say, “you need a sleep study.” We write the order and then we trust that the process works.

We need to own that process.  We need to be able to get the patients to comply with testing and get them tested quickly. We need to see the results and know how bad the problem is. We then need to decide how hard we’re going to push to get our patients on therapy quickly. Finally, as with any therapy we prescribe, we want to be able to track compliance and outcomes. Are they using their CPAP? How often? How long? Is their AHI improving?  

In our clinic, we are fortunate to have two cardiologists who are also well-trained sleep doctors. Nevertheless, as these are our patients, we want to own the process in conjunction with our sleep doctors and work collaboratively with them to make sure patients are getting treated aggressively in a timely fashion. If our patients aren’t following up with their sleep doctor, we want to know about it so we can get them back to their sleep doctor and work on this.

Our philosophy can be summed up by one word—ownership.  Ownership of our patients and their outcomes every step of the way.


Prior to using the WatchPat TurnKey program,  how were you diagnosing, managing, and treating cardiac patients with sleep apnea?

As I said above, we’re fortunate enough in our practice to have two cardiologists who are also trained in sleep medicine. In the past, we would typically refer our patients with suspect sleep apnea to them for a sleep evaluation and potential sleep study. Many smaller cardiology practices are still referring patients to neurology or pulmonology or to internal medicine doctors who are also trained in sleep apnea. T

The reason we started looking at the WatchPat device is that prior to using it there were many opportunities for a breakdown. We would see a patient in the clinic,  and say “hmmm, I think he or she may have sleep apnea” and then there’s a process that has to happen between the time of your suspicion and the time of effective therapy. There are several steps in that process.

The first step is to get the patient to the sleep doctor to see if they agree with the need for a sleep study or not. This involved scheduling the patient for an appointment at another office and hoping they would keep their appointment.

Step two. Once they were seen by our sleep doctor, the next step was getting them to agree to go to the sleep lab for a sleep study. Telling a patient who is relatively non-compliant and who might not get the link between sleep and their heart failure isn’t often an easy sell. Basically, you’re saying, “you have to go to the hospital or somewhere and sleep in a strange bed for a night or two, and they’re going to put this mask on you…It didn’t always go over well.”

Step three.  Once you finally get them to agree to a sleep study, there’s typically a two or three-week waiting period before they get an appointment in the sleep lab – which they may or may not show up for – and then you have to wait for the results to be analyzed and get a report back; which can also take a few days.

Step four. The patient had to follow-up with the sleep physician to determine the best treatment and implement therapy. If they’re diagnosed with sleep apnea, they’ll probably be prescribed a C-PAP mask. Finding the right mask and fit can be problematic. The patient may not like the first mask and just give up without ever working through the options.  They drop out of sight and you have no idea what happened. Then they show up in the heart failure clinic in 4 months and you ask them how their sleep study went and over half the time they either never had their sleep study or they had it and didn’t get the results or couldn’t tolerate the mask and we never knew anything about it.

To be more successful in getting patients on therapy we set out to own the process and break down the barriers at each step along the way.  Things like,  “How can we make sure that the patient agrees to and gets scheduled for a sleep study before they leave our clinic? Can we send a device to their home and make the test simpler for them? How can we make sure that we get the results quickly and follow up on those results quickly?  How do we connect the loop with the DME and make sure that once the study is positive, we have a DME that’s engaged and willing to follow them?  And then once therapy is prescribed, how do we make sure they’re complying with their therapy and how do we monitor that? And most importantly, how do we get kept in the loop along the way?”

Those are the reasons for us using the WatchPAT Turnkey.  The desire to simplify the process and own the process– so it’s not able to break down at so many different touchpoints.


How has using WatchPAT affected your practice and patient outcomes?

We’re early on into the process—probably about 40 studies in. We operate in a larger practice and we want to have buy-in with our sleep doctors. We want to make sure that what we’re doing is not only good for our patients but also works for our practice flow.

Currently, we see the patient in the clinic, and we order the device right then and there. The order goes out, and in a day or two, the device shows up at the patient’s house. The patient’s ability to-do their sleep study and we’re seeing the results very quickly. In fact, our pull-through rate has probably gone from 50 to 90 percent for prescribing and compliant use of the at-home sleep apnea test. Now we are focusing on working through the DME process to make sure that more patients are getting the therapy that works for them and setting up the WatchPAT Cloud system so we can follow their progress in real-time.


Were you able to use the WatchPAT system during Covid-19 for any of your patients?

That was a major impetus. Typical sleep studies are an aerosolized procedure much like PFTs and exercise stress tests. So these were all completely canceled at our center for several months due to the high-risk f viral transmission and are still only done only on a limited basis.

The WatchPAT offers us a way to not only continue testing but to do so in a much lower risk setting. The WatchPAT can be done at home, is completely disposable, and does not utilize an airway component. Thus, we can reassure patients that not only are they getting the test they need but we are doing it in the safest way possible. At our hospital, we call this iCARE values and it means putting the patient first and saying, “we’re concerned about you.” So now we cannot only offer our patients easy access to testing, but we can offer testing in the convenience and safety of their own homes. Patients have responded dramatically well to this approach and we are actually doing more testing in our clinic now then we were doing before the COVID pandemic hit. It has been a true win-win so far.

By Gilad Glick | August 16, 2017

February was Heart month, and the national Healthy Sleep Project launched the “Sleep Apnea Hurts Hearts” campaign in collaboration with the American Academy of Sleep Medicine (AASM), the Centers for Disease Control and Prevention (CDC) and the Sleep Research Society (SRS). The campaign intended to raise awareness and urge individuals with symptoms of Sleep Apnea to talk to a doctor about their risk.

Cardiovascular comorbidities of Sleep Apnea have been known for a long time. Sleep apnea affects about 50% of heart patients on average (higher for certain conditions)1. Sleep Apnea has been linked to drug-resistant hypertension, Coronary Artery Disease, Heart Failure, Diabetes, Atrial Fibrillation and other Arrhythmias, Stroke and even depression. However, the CVD outcomes following proper Sleep Apnea treatment have only been studied in the past 5-10 years. And, the initial results are significant.

Yet, systematic screening and integration of Sleep Apnea management into the continuum of cardiac care is just at its infancy.

However, recently we have seen a clear momentum from the cardiac establishment endorsing this need. In September 2016, The American Heart Association (AHA) released a scientific statement on sleep duration and quality, which stated that moderate and severe Sleep Apnea were associated with a substantially higher risk of cardiovascular disease2. The authors of the AHA statement recommended that a public health campaign addressing sleep behavior should be launched to promote ideal cardiac health.

At the same time, the European Society of Cardiology (ESC) published revised guidelines for the management of Atrial Fibrillation including a clear call that “Interrogation for clinical signs of Obstructive Sleep Apnea should be considered in all AF patients. Obstructive sleep apnea treatment should be optimized to reduce AF recurrences and improve AF treatment results”.3

Right after that, the ACC came out during their annual meeting in March 2017 with a special editorial Sleep Apnea: Types, Mechanisms, and Clinical Cardiovascular Consequences calling all Cardiologists to consider Sleep Apnea as modifiable cardiovascular risk factor4.

Our vision with Cardio Sleep Solutions

Our vision at Itamar Medical is to be the world leader in providing complete Sleep solutions to all Cardiologists and their heart patients. We are passionate about the integration of Sleep medicine in cardiology care pathway by providing simple, timely and tailored solutions, that actually work.

As more and more cardiologists realize the importance of sleep to their success, and look for ways to improve outcomes, patient experience and quality of care, I invite you to join us and test our Cardio-Sleep Solutions to improve not only your patients’ heart health, but also every aspect of their lives and overall wellbeing.

1 Seet & Chung, Anesthesiology Clinical 2010
2 St.-Onge et al, Sleep Duration and Quality: Impact on Lifestyle Behaviors and Cardiometabolic Health: A Scientific Statement From the American Heart Association Circulation Sept 2016
3 Benussi et al, 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS, European Heart Journal (2016) 37, 2893–2962
4 Javaheri et al, Sleep Apnea: Types, Mechanisms, and Clinical Cardiovascular Consequences J Am Coll Cardiol. 2017;69(7):841-858.

By Gilad Glick | September 6, 2017

Why has sleep breathing management not integrated into cardiology care pathway?

In my previous article, I briefly mentioned the increased awareness and the broad acceptance of the role of Sleep Apnea in Cardiac disease and the main studies and scientific statements published by the ESC, AHA and ACC which were the driver behind the American Sleep Academy  “Sleep Apnea Hurts Hearts” campaign.

The question remaining is:

If the link between Sleep Apnea and several main cardiovascular diseases such as Atrial Fibrillation and Hypertension has been broadly accepted – why DO most heart patients remain undiagnosed and majority of cardiologist are not integrating this factor into their care pathway?

There are two main barriers that we hear about from practitioners:

The first obstacle is awareness of cardiologists and their patients about how prevalent Sleep Apnea is among cardiology patients and the fact that most will not be visually detected.  Most cardiologists “eyeball” patients to assess obvious signs of sleep apnea such as a thick neck, visually high BMI, chronically blocked nose etc.

This results in significant underdiagnosis of sleep apnea as demonstrated in a recent study conducted in Montefiore medical center (New York) by Dr. Wharton and Dr. Zaremski.  Their conclusion was that systematic and broad screening is recommended in cardiology clinics, with  84% of their patients screened positive for sleep apnea, while BMI was a poor predictor of screening results.

The second obstacle lies in the dynamics of referring a patient to a sleep medicine physician: to start with, cardiology patients are pre-occupied with their heart condition, and do not understand the link between their Sleep Apnea and their heart. If not given a motivational explanation by the cardiologist or pressed hard to show up at the sleep doctor – most will not make this extra effort this requires.

Furthermore, when patients finally overcome this obstacle and wish to take a sleep study, they encounter the lack of sufficient sleep certified physicians, resulting in inconvenient waiting times, sometimes reaching months combined with geographical accessibility limitations driven by the tendency to diagnose simple OSA with full in-lab polysomnography (PSG) as first line procedure which has a host of barriers imbedded in it.

For example, more and more medical insurers will require Home Sleep Apnea Test (HSAT) before authorizing PSG. Sleep physicians, preferring PSG – require the patient to undergo 2 procedures or debate the insurance. Not an insignificant portion of the patients refuse to undergo in-lab PSG because they are worried about being hospitalized or fear the financial impact of the co-pay.  Sleeping at a sleep lab is also not an experience people look forward to.

Harnessing the simplicity of home sleep tests

As a result, the integration between cardiology and sleep needs to be done differently.  Home sleep tests, which revolutionized sleep medicine and made sleep studies available to all patients, whether they lived far, had a disability or simply liked sleeping in their own beds – has the promise to enable the cardiology patient population to easily manage their sleep. By either moving the point of dispatch to Cardiology or even to direct shipment – just like Amazon did with retail.

How do we solve these challenges?

Recently Itamar Medical launched the Total Sleep Solution program that has all the components necessary to successfully integrate Sleep medicine into Cardiology patient care. It has:

(A) Cardiology oriented screening tools – combined with patient education materials to achieve efficient accessibility for all patients while maintaining a seamless and pleasant patient experience.

(B) Unique Home Sleep Testing – Enabling Technology with the WatchPAT home sleep test which offered unparalleled simple user experience, requiring only a finger sensor and a watch instead of all the cumbersome home sleep tests available. It’s FDA cleared, listed as technically adequate in the AASM guidelines for HSATs[1] and fully reimbursed*

(C) Remote sleep expert interpretation – Cloud based technology that enables immediate transmission of the test report to a sleep specialist for interpretation and diagnosis, because we at Itamar understand cardiologists are not interested in practicing sleep or pulmonary medicine and

(D) Connection to sleep apnea management service providers of high quality that understand the standards Cardiologists are expecting and help ensure patient compliance and adherence.

To learn more about our comprehensive customizable solutions, you may always contact your local Itamar Sales Representative or leave your details here:

[1] Kapur VK, et al. 2017 “Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea: an American Academy of Sleep Medicine clinical practice guideline.”J Clin Sleep Med. 13(3):479–504.

*Please verify with your insurance mix as local policies varies

By Gilad Glick

To some it may come as a surprise that SDB (Sleep Disordered Breathing) or Sleep Apnea is common among AFIB patients, and that it has been found an independent major risk factor, significantly affecting outcomes.

However, leading electrophysiologists and cardiologists have already been increasingly aware of the link between Atrial Fibrillation and Sleep Apnea.  Such clinicians seek to actively diagnose OSA and integrate effective screening tools to identify Sleep Apnea risk among their patients as part of their patient care pathway. In addition, the ESC and ACC have updated their AFib guidelines to include sleep apnea screening and treatment in consideration of accumulating evidence linking the two

Here’s a brief overview of the AFIB practice guidelines and evidence related to the link between sleep apnea and AFIB.

Clinical Practice Guidelines  

According to the 2016 ESC guidelines for the management of atrial fibrillation interrogation for clinical signs of obstructive sleep apnea (OSA) in all AFib patients is a Class IIa, level B recommendation. Further, once OSA is diagnosed, treatment should be optimized to improve AF treatment results in appropriate patients (Class IIa, level B).1

These guidelines have recently been cited by the ACC.

The Heart Rhythm Society also published a patient brochure to educate AFib patients about Sleep Apnea symptoms and the importance of getting tested for sleep apnea and treating it to improve their overall health. You can find it here2.

The link between Atrial Fibrillation and Sleep Apnea

Obstructive Sleep Apnea is a known risk factor associated with both onset and recurrence of AFib after therapy. Sleep Apnea is now established as an independent predictor of AFib with a HR of 2.18.8

How common is Sleep Apnea among AFib patients?

In the general population, OSA (Obstructive Sleep Apnea) affects approximately 24% of men and 9% of women, between 30 and 60 years of age. The prevalence of Sleep Apnea rises with age. Up to 80% remain undiagnosed.2,3

Among AFib patients, the comorbidity of Sleep Apnea is estimated at about 49%.4,5 A recent study in Sweden showed a prevalence of over 80 percent of sleep apnea among patients treated for atrial fibrillation.

Mehra and colleagues showed, with a large, prospective, community-based cohort, that individuals with Sleep apnea had 4 times the odds to develop AFib as those without SDB (OR 4.02, 95% CI 1.03- 15.74) after adjustment for age, sex, BMI and prevalent coronary heart disease.6

How does Sleep Apnea and its management affect AFib outcomes?

A major challenge for electrophysiologists nowadays is a persistently high 1-year AFib recurrence despite treatment by cardioversion, catheter ablation or drugs. Often a repeat ablation is necessary to treat AFib efficiently, and AFib may still recur despite these additional interventions. Electrophysiologists were concerned about a group of patients who seemed refractory to maintenance of sinus rhythm despite aggressive therapy.

In recent years, multiple published studies linked untreated sleep apnea with substantial increases in the rate of AFIB recurrence – practically telling us that the common 20% – 40% recurrence rate has two groups:  those with Sleep Apnea, about half the patients, with a much higher rate of AFib recurrence and the other half, without Sleep Apnea, with lower rate.

Moreover, when patients with confirmed OSA complied properly with CPAP Sleep Apnea treatment, ablation success rates improved to match those among non-apnea sufferers in all AFib types.

Sleep Apnea Treatment – what is the effect on AFib outcomes?

The first to show that treatment of Sleep Apnea correlated with a lower incidence of atrial fibrillation recurrence was the team led by Dr. Virend Somers4.

As far back as 2010, a group led by Dr. Andrea Natale, showed that Sleep Apnea was an independent predictor for PVAI failure, and that treatment with CPAP improved PVAI success rates. Patients not treated with CPAP in addition to having higher prevalence of non-PV triggers were 8 times more likely to fail ablation.7

A broader landmark study was published by Dr. Fein, Dr. Anter and colleagues. These authors found that AFib-free survival rate among patients with CPAP-treated OSA was similar to a group of patients without OSA (71.9% vs. 36.7%; p = 0.01). AFib recurrence following PVI in CPAP-nonuser patients was significantly higher (HR: 2.4, p < 0.02) and similar to that of OSA patients managed medically without ablation (HR: 2.1, p = 0.68).  Summary of the study conclusions is below.8

The authors concluded that CPAP is an important therapy in OSA patients undergoing RF Ablation that improves arrhythmia free survival. RF Ablation offers limited value to OSA patients not treated with CPAP.8

A recent study from Duke University found that patients who underwent focal impulse and rotor modulation (FIRM) ablation and also suffered from OSA, exhibited increased rotor prevalence, driven predominantly by an increase in RA rotors. CPAP therapy was associated with fewer RA rotors.10

Finally, a meta-analysis conducted by Dr. Shukla, Dr. Chinitz and colleagues from the Charney Division of Cardiology, New York University Langone Medical Center in NYC,  found that the association between CPAP and reduced AF recurrence remained the same whether treated medically or with catheter ablation.9

CPAP use in patients with OSA was associated with a reduced relative risk of AF recurrence in comparison to non-users – with a 42% relative risk reduction and a very highly significant statistical data. Authors noted that the effect remained consistent and similar across patient populations irrespective of whether they undergo PVI.9

Clinical practice: Implementing AFib guidelines related to Sleep

Cardiologists are becoming increasingly aware of the possibility of the benefits of home sleep testing and cloud technology to connect with sleep specialists and pulmonologists and conduct wide screening for undiagnosed sleep breathing disorders, refer for treatment and follow up on therapy and CVD outcomes.

Given the strength of evidence, it’s no surprise that electrophysiologists were the first to take practical steps in integrating sleep medicine in cardiology care.

Since we started offering the WatchPAT home sleep test to cardiology departments around the world, we hear from physicians that they no longer convince their patients to take the test. The patients are eager to get tested at home as the process is so simple and cardiologists explain how essential it is to improve outcomes and AFib recurrence. The WatchPAT home sleep test is as easy for patients to use as a home holter monitor and clinicians can view the report via the cloud and share with pulmonologists to obtain interpretation.

And because cardiologists were anxious to verify that patients comply with treatment and linked non-usage to recurrence of AFib, we started connecting them with leading service and CPAP providers. We now offer customized solutions to all types of institutions or clinics, depending on size, workflow and physician needs.

To learn more about sleep and arrhythmias – we recommend this video series of the scientific symposium we sponsored at HRS in 2016.

I invite you to join learn more about Cardio Sleep solutions here.


1 2016 ESC Guidelines for the Management of Atrial Fibrillation Developed in Collaboration With EACTS. Eur Heart J 2016; Aug 27:[Epub ahead of print]
3 Young et al. The Occurrence of Sleep-Disordered Breathing among Middle-Aged Adults. N Engl J Med 1993; 328:1230-1235
4 Gami AS, Pressman G, Caples SM, et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation 2004; 110:364–7.  [PubMed]
5 Seet & Chung, Anestsiology Clin 2010
6 Mehra R, Sleep apnea ABCs: airway, breathing, circulation, Cleve Clin J Med 2014;81:479–89 | Pubmed
7 Dimpi Patel el al “Safety and Efficacy of Pulmonary Vein Antral Isolation in Patients With Obstructive Sleep Apnea” Circulation Arrhy and Electro, 2010
8 Fein AS, Anter E., et al. Treatment of obstructive sleep apnea reduces the risk of atrial fibrillation recurrence after catheter ablation. J Am Coll Cardiol. 2013; 62:300-305. | Pubmed
9 Shukla et al. CPAP Use on Recurrence of AF in Patients with OSA JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 1, NO. 1-2, 2015
10 Friedman et al, Obstructive sleep apnea is associated with increased rotor burden in patients undergoing focal impulse and rotor modification guided atrial fibrillation ablation,  Europace, eux248,

By – Gilad Glick

According to latest CDC data, 1 in 3 American adults suffers from hypertension[1], and only about 54% have their condition under control[2]. This is surprising, given the extensive research on Hypertension as a cardiovascular risk factor and the wide variety of hypertensive drugs available. Patients also have numerous home BP measurement devices they can use. Despite all this, cardiologists and primary care providers still struggle with drug-resistant hypertension or simply badly controlled blood pressure.

Recently the AHA launched a major initiative called TargetBP committed to reducing the number of Americans with uncontrolled blood pressure. TargetBP focuses on 3 key areas with M.A.P framework: M-Measurement – accurate measurement every time; A- Action taken rapidly to address high readings; and P – Partnering with patients, families and communities to promote self-management. The program uses latest science in blood pressure control and has already shown promising results.

Starting at home

There are simple actions you can take today to improve the way hypertension is managed and how patients self-manage their condition and they both can be done at home: (1) Get blood pressure measured at home and (2) control for Sleep Apnea

Help your patients accurately measure their Blood Pressure at home

The American Heart Association recommends home monitoring for all hypertensive patients to help healthcare providers determine whether treatments are effective. And accurate measurement is at the heart of TargetBP.

The advantages of blood pressure home monitoring are known. Self-tracking of blood pressure helps empower patients to take ownership of their treatment. Clinically, a single reading at the doctor’s office is not enough, as blood pressure fluctuates and one measurement is not enough to ascertain patient’s response to medication. “White-coat” syndrome leading to higher readings at the doctor’s office is another reason to add home monitoring, where the patient is more relaxed.

Recently, though, a study in the American Journal of Hypertension showed that some home monitors can be quite inaccurate.[3]

This is the reason why many cardiologists now encourage patients to bring their automated blood pressure devices to their clinic visits once or even twice to measure their accuracy against the clinic-standard manual measurement. While they do this, patients learn how to accurately use the device.

TargetBP prepared a set of educational materials to help clinicians communicate with their patients and teach them about proper BP measurement and management:

7 simple tips to get an accurate blood pressure reading

Other TargetBP resources for patients can be found here.

Screen your patients for Sleep Apnea

And for patients at risk – refer to a home sleep test

Sleep Apnea is a major comorbidity to hypertension. In fact, sleep apnea was found in 83% of adults with drug-resistant hypertension.[4]

A meta-analysis published in the Journal of Hypertension in 2014 suggests that untreated sleep apnea may be a major factor in why medications appear to be less effective in reducing high blood pressure in some people. Further, the study shows that CPAP therapy may be the key to helping those with difficult to treat hypertension get their blood pressure under control.[5]

Already in 2008, Prof. VK Somers and colleagues published the AHA/ACCF scientific statement, Sleep Apnea and Cardiovascular disease. This statement was published by the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing, in collaboration with NIH.[6]

In this statement, authors review the evidence related to Sleep Apnea and CVD and proposed to treat OSA as an independent risk factor for the development of essential hypertension, since it can precede and predict the onset of hypertension (as demonstrated in the Wisconsin Sleep Cohort Study, which noted a consistent OSA-BP dose-response relationship, even after controlling for age, sex, BMI, and antihypertensive medications).6

Authors also noted that the weight of evidence has led the most recent Joint National Committee on the Detection and Management of Hypertension to identify OSA as an important identifiable cause of hypertension. 6

Also in 2008, AHA’s scientific statement: Resistant Hypertension: Diagnosis, Evaluation, and Treatment, listed Obstructive sleep apnea as a common secondary cause of resistant hypertension. It also recommended to screen for obstructive sleep apnea as a first step in screening for secondary causes of resistant hypertension. “Obstructive sleep apnea should be treated if present” according to statement. Treatment by CPAP is recommended, with the largest benefit in patients with severe sleep apnea and in patients already receiving antihypertensive treatment.[7]

You can easily identify patients at risk for sleep apnea with basic STOP-BANG questionnaire and can prescribe a home sleep test or an in-lab study when necessary. It’s also very easy to use our HIPAA-compliant Cloud-PAT platform to share the report with a sleep specialist or pulmonologist and get the interpretation.

Our simple screening methods can be easily integrated into any cardiac care pathway. Watch Prof. David Vorchheimer talk about his experience in successfully implementing CardioSleepSolutions in the cardiology clinics he manages.

We have tailored our solutions to suit all cardiologists and clinics of all sizes.

Contact us to arrange a discussion with one of our users or reps.

And just as a patient easily measures blood pressure at home, our WatchPAT home sleep test is one of the easiest most convenient sleep apnea tests on the market, while providing excellent clinically-validated data.


[1] Merai R, Siegel C, Rakotz M, Basch P, Wright J, Wong B; DHSc., Thorpe P. CDC Grand Rounds: A Public Health Approach to Detect and Control Hypertension. MMWR Morb Mortal Wkly Rep. 2016 Nov18;65(45):1261-1264

[2]  Yoon SS, Fryar CD, Carroll MD. Hypertension Prevalence and Control Among Adults: United States, 2011-2014. NCHS data brief, no 220. Hyattsville, MD: National Center for Health Statistics; 2015.

[3] Ringrose J et al; An Assessment of the Accuracy of Home Blood Pressure Monitors When Used in Device Owners, American Journal of Hypertension, Volume 30, Issue 7, 1 July 2017, Pages 683–689

[4] Logan AG et al, High prevalence of unrecognized sleep apnoea in drug-resistant .J Hypertension. 2001 Dec;19(12):2271-7.

[5] Iftikhar I et al, Effects of continuous positive airway pressure on blood pressure in patients with resistant hypertension and obstructive sleep apnea: a meta-analysis, Journal of Hypertension: December 2014 – Volume 32 – Issue 12 – p 2341–2350

[6] Somers VK et al. Sleep apnea and cardiovascular disease: an American Heart Association/American College of Cardiology Foundation scientific statement from the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing. Circulation. 2008;118:1080–1111.

[7] Calhoun et al, Resistant Hypertension: Diagnosis, Evaluation, and Treatment A Scientific Statement From the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Hypertension. 2008;51:1403-1419

By Gilad Glick

  • Mechanical Stretch due to negative Intra-Thoracic Pressure

Obstructive Sleep Apnea is defined as a physiological event that happens when upper airway is partially or completely blocked during sleep. Mostly, as a result of collapsed soft tissue in the throat while lying on your back. This makes your diaphragm and chest muscles work harder to open the obstructed airway and pull air into the lungs. As the obstruction persists, significant negative pressure is developed in the inner space of the thorax. Breathing usually resumes when the sympathetic nerve system is activated, regaining control over the throat muscles and reopening the airways –  ending up with a loud gasp, snort, or body jerk. You may not sleep well, but you probably won’t be aware that this is happening.

Since the heart is “sitting” on the diaphragm on the lower end and attached to the aorta and pulmonary veins in the upper part, this negative intra-thoracic pressure is causing the heart muscle to stretch mechanically, potentially causing micro scarring of the left atrial tissue which in turn promotes arrhythmogenic characteristics (in particular Atrial Fibrillation).

Given that a moderate to severe sleep apnea patients experience Sleep Apnea events between 15 and 60 times an hour, or hundreds of times a night – the accumulated damage can be significant.

  • Frequent interruptions to the sympathetic nerve system

As described above, most sleep apnea events end with a surge of the sympathetic branch of the autonomic nerve system. It is also known that the heart electrical system is tightly connected and to some degree regulated by this exact same system.  Therefore, it is assumed that the load sleep apnea is imposing on the system has a profound impact on the promotion of irregular electrical activation patterns or arrhythmias.

  • Drop in blood oxygen saturation leads to Oxidative Stress

There are serious negative consequences of repetitive oxygen desaturations, also known as Intermittent hypoxia, occurring during Sleep Apnea and affecting the entire cardiovascular system.

“The two most significant are the formation of reactive oxygen species (ROS) and inducing oxidative stress (OS). ROS can damage biomolecules, alter cellular functions and function as signaling molecules in physiological as well as in pathophysiological conditions. Consequently, they promote inflammation, endothelial dysfunction and cardiovascular morbidity. Oxidative stress is also a crucial component in obesity, sympathetic activation and metabolic disorders such as hypertension, dyslipidemia and type 2 diabetes/insulin resistance, which aggregate with OSAHS.[1]

Another correlation was found between the Apnea/Hypopnea Index (AHI) severity, and Lipid peroxidation, protein oxidation [2], and impaired endothelial function which is a pivotal factor in vascular pathogenesis, which is known to be adversely affected due to the promotion of oxidative stress and inflammation, resulting in educed Nitric Oxide, (NO) availability and thus diminishing its vital vascular repair capacity [3][4].

To learn more about how EPs and cardiologists address sleep apnea in their cardiac care pathway to improve outcomes, quality of life and reduce AFib recurrence – read the article “How Electrophysiologists Reduce AFib Recurrence by Addressing Sleep Apnea”

To learn more about how our Cardio-Sleep customized solutions can help you address Sleep Apnea as part of your cardiac care workflow, while maintaining a positive patient experience and minimal workload on your staff – contact us here.

[1] Lavi et al, Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link.  Eur Respir J 2009; 33: 1467–1484

[2]  Hopps et al, Lipid peroxidation and protein oxidation are related to the severity of OSAS. European Review for Medical and Pharmacological Sciences 2014; 18: 3773-3778

[3] Oxidative Stress, and Repair Capacity of the Vascular Endothelium in Obstructive Sleep Apnea

Jelic S, Padeletti M, Kawut SM, Christopher Higgins C, Canfield SM, Onat D, Paolo C. Colombo PC,  Basner RC, Factor P,  and LeJemtel  TH. Circulation. 2008 April 29; 117(17): 2270–2278.

[4] Scherbakov et al, Sleep-Disordered Breathing in Acute Ischemic Stroke: A Mechanistic Link to Peripheral Endothelial Dysfunction. J Am Heart Assoc. 2017 Sep 11;6(9).