4 A prospective study of hypertrophic cardiomyopathy and sleep disordered breathing

Background Hypertrophic cardiomyopathy (HCM) represents the most common inherited cardiomyopathy characterized by otherwise unexplained left ventricular hypertrophy. Sleep disordered breathing (SDB) (including both central and obstructive sleep apnea) is considered to be an important and potentially reversible cause of cardiovascular disease progression. This prospective trial aims to define the prevalence of SDB within patients diagnosed with HCM using gold standard polysomnography (PSG). Previous studies have suggested a prevalence of SDB in the general population of 25.5%. Methods Previous trials have been retrospective studies and have used overnight oximetry analysis to find the prevalence of SDB in HCM using portable, at-home monitors, however overnight oximetry is unable to accurately delineate between central and obstructive sleep apnea – both of which vary significantly in terms of prognosis and management - and is not as sensitive nor specific in diagnosing or classifying SDB as polysomnography assessment. An ongoing prospective analysis of 85 patients diagnosed with HCM was performed at Mayo Clinic using PSG. Apnea is defined as the absence of inspiratory airflow for at least 10 seconds. Hypopnea is defined as a decrease in airflow lasting 10 seconds or longer associated with a desaturation >4%. Apnea Hypopnea Index (AHI) – the number of events per hour was assessed using PSG. SDB is defined as an AHI>5/hour of sleep. Results Of 85 HCM patients examined using PSG, 49 were found to have an AHI>5/hour. Average AHI was 20.0, Standard Deviation 23.3, Interquartile range 3.3-28.2. 15 patients had central sleep apnea defined as the absence of inspiratory effort for at least 10 seconds. 17 patients had obstructive apneas. 18 patients had severe SDB (AHI>30/hour). Conclusion Given the paucity of available treatments for HCM and noting that treatment of SDB in heart failure with CPAP has been shown to attenuate diastolic dysfunction, this represents a potentially novel avenue of treatment for patients diagnosed with HCM. OSA is known to increase risk factors that contribute to morbidity and mortality in HCM including arrhythmias, myocardial infarction and sudden cardiac death. Previous studies have suggested a higher prevalence of non-sustained ventricular tachycardia in HCM patients diagnosed with OSA likely explained by excessive sympathetic activation. Systemic blood pressure and sympathetic activity have also previously been seen to improve with CPAP therapy and there is evidence to suggest CPAP therapy may reverse or slow progression of left ventricular hypertrophy in HCM patients with SDB. Our study suggests a significantly higher prevalence of SDB in HCM patients when compared to the general population and whether treatment of SDB in HCM improves outcomes requires further investigation which our prospective study aims to answer. Conflict of Interest None