CARDIO SLEEP BLOG

By Efrat Magidov

Bradycardia is defined by the American Heart Association as a heart rate of less than 60 beats per minute (BPM) but adds that what’s “too slow” depends on various factors such as age, physical fitness and physiological condition. During sleep for example, the parasympathetic tone predominates (as NREM sleep occupies 80% of total sleep time), resulting in commonly occurring bradyarrythmias, sinus pauses greater than 2 seconds, and atrioventricular (AV) conduction delays. However, some cases of nocturnal bradyarrythmias are not normal, and reflect acute bradycardia that is prevalent also in wakefulness and can lead to various hazardous complications. Obstructive Sleep Apnea (OSA) was found to be a promoting factor for such incidences.

Numerous studies have demonstrated increased prevalence of bradyarrytmias in OSA patients; In the classic study by Guilleminault et al1 who looked at 400 patients with OSA, 48% had significant nocturnal arrhythmia with 18% bradyarrhythmia, 11% sinus arrest, and 8% AV blocks. These percentiles were surprisingly high, considering that the known prevalence of nocturnal bradyarrythmias in the general population was around 3%2. There were no important differences in age, body weight, apnea-hypopnea index (AHI), or minimum oxygen saturation between those with and without arrhythmias. In a more recent Japanese study by Abe et al3, 1350 OSA patients and 44 control subjects were screened, and significant increase in incidence of sinus bradycardias (12.5% with OSA vs. 2.3% control, p=0.036) and sinus pause (8.7% with OSA vs. 2.3% control, p<0.001) was noted. Importantly, using long-term monitoring by implanted pacemakers reveals an even higher bradyarrythmias percentages (up to 34%4), suggesting that OSA increase the risk for bradycardia even more dramatically.

Not only that OSA increases the prevalence of brayarrythmias, some studies have found that OSA severity is correlated to the extent of bradyarrytmias, with up to 3 times higher incidence of bradycardic arrhythmias in severe OSA patients (compared to milder OSA)5. Such correlation implies that there’s a causal relation between the two, in which OSA promotes bradycardia.
The mechanism by which OSA can reduce the heart rate is demonstrated in the presented figure: during OSA, structural changes occur in the airway to obstruct airflow (Resp), and the resulting apnea activates hypoxic reflexes (SaO2 %), which in turn lead to profound elevation in sympathetic nerve activity (SNA) and subsequently elevation of atrial blood pressure (ABP) and decrease of the heart rhythm  (ECG). Various studies confirmed that the elevation in vagal tone is the key contributor to the bradyarrythmias, whereas other factors such as sinus node anatomy or artioventrucular conduction are largely intact in OSA patients6. The finding that intravenous atropine administration eliminates the marked sinus arrhythmia and bradyarrhythmias observed in such patients6 supports this hypothesis. Moreover, mimicking OSA in wakefulness with the Mueller maneuver results in induced bradycardia7, further confirming that the combination between prolonged negative intrathoracic pressures and the resulting hypoxemia is the necessary underlying “mix” i n this unique pathophysiology.

The crossover between Bradyarrythmias and OSA is also apparent by the beneficial implications of OSA treatment on bradycardia severity. Specifically, Positive airway pressure (PAP) therapy has been shown to be highly effective in abolition and reduction of bradyarrhythmias. In the Abe study for example, sinus bradycardia (p<0.001) and sinus pauses (P=0.004) were dramatically reduced by CPAP therapy3. Thus, the current recommendation for physicians for patients with bradyarrhythmias who are at risk for OSA, is to perform overnight polysmonography prior to pacemaker implantation, especially in younger individuals without underlying cardiac disease. Permanent pacemakers should be considered if significant bradyarrhythmia or pauses persist after adequate treatment trial with PAP therapy.

WatchPAT, Home Sleep Apnea Test device, is an easy to use, effective and accurate tool for polysomnography and OSA diagnosis. You may learn more about WatchPAT and our comprehensive “Total Sleep Solution” for Cardiology practices in www.cardiosleepsolutions.com

  1. Guilleminault, C., Connolly, S. J., & Winkle, R. A. (1983). Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. American journal of cardiology52(5), 490-494.
  2. Fleg, J. L. & Kennedy, H. L. (1982). Cardiac arrhythmias in a healthy elderly population: detection by 24-hour ambulatory electrocardiography. Chest, 81, 302–307.
  3. Abe, H., Takahashi, M., Yaegashi, H., Eda, S., Tsunemoto, H., Kamikozawa, M., … & Ikeda, U. (2010). Efficacy of continuous positive airway pressure on arrhythmias in obstructive sleep apnea patients. Heart and vessels25(1), 63-69.
  4. Simantirakis, E. N., Schiza, S. I., Marketou, M. E., Chrysostomakis, S. I., Chlouverakis, G. I., Klapsinos, N. C., … & Vardas, P. E. (2004). Severe bradyarrhythmias in patients with sleep apnoea: the effect of continuous positive airway pressure treatment: a long-term evaluation using an insertable loop recorder. European heart journal25(12), 1070-1076.
  5. Rossi, V. A., Stradling, J. R., & Kohler, M. (2013). Effects of obstructive sleep apnoea on heart rhythm. European Respiratory Journal41(6), 1439-1451.
  6. Cutler, M. J., Hamdan, A. L., Hamdan, M. H., Ramaswamy, K., & Smith, M. L. (2002). Sleep apnea: from the nose to the heart. The Journal of the American Board of Family Practice15(2), 128-141.
  7. Huettner, M., Koehler, U., Nell, C., Kesper, K., Hildebrandt, O., & Grimm, W. (2015). Heart rate response to simulated obstructive apnea while awake predicts bradycardia during spontaneous obstructive sleep apnea. International journal of cardiology186, 216-218.

By Efrat Magidov

Abdominal aortic aneurysm (AAA) is a potentially life-threatening condition that may be exacerbated by Obstructive Sleep Apnea (OSA) which has been verified as an independent causal factor in the pathogenesis of hypertension and vascular dysfunction. More specifically, several pathomechanisms have been suggested to account for the potential adverse effect of OSA on AAA:

  1. The intrathoracic pressure changes leading to shear stress on artery walls;
  2. Intermittent hypoxia leading to oxidative stress, sympathetic stimulation, and possibly atherosclerosis;
  3. Arousal-induced sympathetic activation inducing subsequent repetitive blood pressure surges and chronic hypertension.

The attempts to link obstructive sleep apnea (OSA) to AAA are based on early studies of patients with Marfan’s syndrome. In the early 90s, it was first suspected that OSA may have deleterious effects on the aorta in Marfan’s syndrome patients. Later researchers demonstrated higher prevalence of OSA in those patients and described a correlation between OSA severity (as measured by the apnea-hypopnea index (AHI)) and aortic root diameter (r=0.5, p<0.001). In a follow-up longitudinal study of 44 Marfan’s syndrome patients, only subjects with OSA developed an aortic event (after a median follow-up time of 29 months). Although the relative risk of OSA was not successfully assessed due to the small sample size, this remains the only longitudinal study which investigated the effect of OSA on the aorta by means of events (rather than disease parameters).1

Several cross-sectional studies on the general population found a positive association between the aortic root diameter and OSA severity.
Interestingly, simulating OSA in healthy volunteers with the use of Muller’s maneuver induced considerable changes in both blood pressure and proximal aortic diameter and area, probably due to increased aortic dilatory pressures. Observational studies have consistently reported that OSA is highly prevalent among patients with AAA. In one such study by Mason and colleagues, 127 patients (11 women, mean age 67.9±6) with an abdominal aortic measurement greater than or equal to 30 mm were examined. Home sleep monitoring was used to assess OSA presence in terms of ODI (>4%) and AHI. Approximately 40% of the patients were found to have an ODI greater than 10 per hour, representing a 5-fold greater incidence than in a comparable normal population. Similarly, 29% of the patients had AHI greater than 15, almost 2 times higher than the normal prevalence values.
These results correspond to other studies demonstrating up to 60% OSA presence in AAA patients which is significantly higher than the estimated prevalence of 17% in the general population. Importantly, subjective reports did not reveal a correlative sleepiness, suggesting that daytime sleepiness is not suitable for detecting OSA in AAA patients.

The researchers went on to examine whether OSA can explain occurrences of AAA expansion. They compared the AAA diameter of two duplex scans; one from the recruitment phase and another before the sleep study (median follow-up time was 18 months). Severe OSA, represented by ODI and AHI greater than 30, was found to be significantly associated with a high AAA expansion rate (ODI- 2.9 mm per year, p=0.009; AHI- 2.2 mm per year, p=0.043 – Figure 1). These results were derived after adjustment to cardiovascular risk factors and medication use, and therefore represent OSA relative risk. The presence of correlation only at severe OSA suggests a threshold effect rather than a simple linear dose–response relationship between OSA severity and AAA expansion rate.2

Through these studies, it is becoming clear that successful diagnosis of OSA in AAA patients can be an important factor in managing the risk of lethal aortic complications. Future studies will hopefully examine the potential beneficial effects of OSA-treatment on AAA. WatchPAT, a home sleep apnea test device, is a simple, accurate and reliable tool for OSA diagnosis. You may learn more about WatchPAT and our comprehensive “Total Sleep Solutions” for Cardiology practices at www.cardiosleepsolutions.com

sources:

  1. Gaisl, T., Bratton, D. J., & Kohler, M. (2015). The impact of obstructive sleep apnoea on the aorta. European Respiratory Journal46(2), 532-544.
  2. Mason, R. H., Ruegg, G., Perkins, J., Hardinge, M., Amann-Vesti, B., Senn, O., … & Kohler, M. (2011). Obstructive sleep apnea in patients with abdominal aortic aneurysms: highly prevalent and associated with aneurysm expansion. American journal of respiratory and critical care medicine183(5), 668-674.