Mr. WA is a 74-year-old morbidly obese Caucasian male with a calculated body mass index (BMI) of 45. His past medical history is significant only for hypertension and obesity. He was first diagnosed with atrial fibrillation in March of 2012 (Fig 1 and 2) after presenting to his PCP's office with palpitations. He underwent direct current cardioversion after a TEE showed absence of left atrial appendage thrombus. His left ventricular ejection fraction was noted to be normal at that time. He was subsequently discharged to home with a remote cardiac monitoring device. Ten days post discharge his rhythm again reverted to atrial fibrillation and multiple PVC's along with episodes of nonsustained ventricular tachycardia were noted (Fig.3). Interestingly, remote monitoring also demonstrated significant slowing of the ventricular rate associated with multiple 4 second long pauses during the night (Fig. 4). He was again admitted with the aim of repeating cardioversion and initiating antiarrhythmic therapy. However, he developed a wide complex tachycardia presumed to be ventricular tachycardia (Fig 5) and suffered a cardiac arrest. After successful resuscitation and initiation of antiarrhythmic therapy an ICD was implanted.
Figure 1: Baseline EKG showing normal sinus rhythm
Figure 2: EKG showing the development of atrial fibrillation with occasional PVC's
Figure 3: Remote monitoring showing a run of WCT
Figure 4: Remote monitoring showing a 4.1 second pause during sleep
Figure 5: Wide complex tachycardia leading to cardiac arrest
Because of the association of obstructive sleep apnea with cardiac dysrhythmias, his elevated BMI and admitted daytime sleepiness, polysomnography was performed. This confirmed the presence of poor sleep architecture, nocturnal hypoxemia and severe OSA. He was prescribed bi-level PAP therapy initiated at IPAP 12, EPAP 8 and 2L of oxygen. Since initiating this therapy his monitoring ICD has not recorded any ventricular arrhythmias. His atrial fibrillation and frequent PVC's have not recurred.
Ventricular arrhythmias and sudden cardiac death associated with obstructive sleep apnea usually occur at what time?
The correct answer is: C. 12 midnight to 6 am
Discussion: Obstructive sleep apnea (OSA) affects approximately 15 million adults and is a known independent risk factor for the development of hypertension (HTN), atrial fibrillation (AF), stroke, and coronary artery disease (CAD). Cardiac arrhythmias are more frequent in persons with OSA but controversy exists regarding its role as the primary etiologic factor, since patients with OSA frequently have other confounding factors. However, results from the Sleep Heart Health Study; which compared the prevalence of arrhythmias between subjects with (n=228) and without (n=338) sleep-disordered breathing, show a four fold increase in the odds of AF (OR, 4.02; 95% CI, 1.03-15.74), three times the odds of non-sustained VT (OR, 3.40, (95% CI, 1.03-11.20), and almost twice the odds of complex ventricular premature beats (OR 1.74, 95% CI, 1.11-2.74), even after adjusting for age, sex and BMI. The odds of an arrhythmic event occurring after an apneic or hypopneic episode increase almost 18 fold (OR, 17.5, 95% CI, 5.3-58.4).
In patients without OSA, ventricular arrhythmias are usually suppressed during sleep with a concomitant decrease in the incidence of myocardial infarction and sudden cardiac death (SCD). In contrast, Gami et al. noted a nocturnal peak in the occurrence of SCD in patients with sleep-disordered breathing. This peak usually occurs between 12 am to 6 am and is thought to be a result of a combination of acute hemodynamic and autonomic changes that occur with sleep apnea. Doherty et al. compared cardiovascular mortality in 107 patients with OSA who were stratified by CPAP use. After a follow up of approximately seven years there was no SCD in the group that was compliant with CPAP therapy, compared to 7% in the noncompliant group.
Although there is a paucity of clinical randomized controlled trials to support the efficacy of CPAP for the prevention and treatment of arrhythmias, patients with observed nocturnal arrhythmias and those in whom arrhythmias are refractory despite standard therapy, should be considered for evaluation for possible OSA.
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