Although coronary anomalies are recognized as the second leading cause of sudden death amongst young and seemingly healthy persons, they constitute a diverse group of uncommon and poorly understood cardiac disorders. Despite widely known implications of sudden cardiac death occurring from malignant forms of coronary anomalies within the medical community as well as among the general public, the pathophysiologic mechanisms that characterize the clinical presentations, long-term clinical repercussions and prognoses coronary anomalies are not well-defi ned. Imaging remains a cornerstone in the diagnosis and prognostication of these disorders. However, the optimal screening tool for these conditions remains elusive. Larger, longer-term data are needed to understand these entities with further clarity.
Background: Prevalence of obstructive sleep apnea (OSA) in hypertrophic cardiomyopathy (HCM) is estimated between 32% and 71%. Individuals with HCM and OSA have increased blood pressure, BMI, , ascending aorta size, left atrial size, left ventricular end diastolic diameter, E/e’ ratio, atrial fibrillation rates and NYHA functional class. It has been suggested that treatment of OSA can decrease the need for septal reduction. However, studies have found no effect of OSA on septal thickness or outflow gradient. It is not known how OSA affects exercise performance or cardiac remodeling assessed by MR. Genetic propensity toward OSA in HCM has not been reported. We propose that OSA predicts decrease exercise tolerance and that cardiac remodeling could be identified using MR. We sought to report on HCM genotype in OSA as well as compare our clinical and echo data with other investigators. Methods: Subjects were identified through our institution’s HCM database. They were surveyed using the STOP-BANG (SB) questionnaire, a validated questionnaire to identify individuals at high risk for OSA. We stratified patients into high risk (HR) and low risk (LR) groups, based on a cut point of greater than or equal to 3 on SB. Demographics and clinical characteristics were extracted from our database. Prevalence and means were compared between the two groups, using Chi-square and t-tests. Differences between the groups were adjusted for age, sex, and BMI using linear mixed models for continuous measures and logistic regression for dichotomous measures. Results: There were 206 respondents, of those 160 (78%) scored high risk for OSA, 60 of which had a history of polysomnogram (PSG) confirming OSA. Having a HR vs. LR SB was associated with a significantly greater likelihood of stroke, CHF hospitalization, NYHA functional class >2, reduced peak VO2, reduced anaerobic threshold and increased LA diameter. Adjusted comparisons for age, gender, and BMI showed that had significantly higher PAWP and LV mass index. Of those with a prior diagnosis of OSA we compared therapy compliant and non-compliant individuals and found they differed on LV mass index (HR=98.7 g/m2 vs. LR=62.0 g/m2, p=0.01). Conclusions: OSA occurs frequently in HCM and is associated with decreased exercise tolerance, worse hemodynamics, poor outcome as well as increased LV mass, which may be attenuated by therapy. OSA is an important and modifiable risk factor in HCM. Prospective evaluation utilizing PSG based diagnosis and positive pressure therapy is warranted.
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