Coronary Flow Reserve Impairment in Apical vs Asymmetrical Septal Hypertrophic Cardiomyopathy
Open Access
- 3 February 2013
- journal article
- research article
- Published by Wiley in Clinical Cardiology
- Vol. 36 (4) , 207-216
Abstract
Background Mechanisms underlying a reduction in coronary flow reserve (CFR) in hypertrophic cardiomyopathy (HCM), especially apical HCM (ApHCM), are elusive. This study set out to evaluate mechanisms underlying a reduction in CFR in 2 HCM subtypes. Hypothesis Mechanisms for CFR reduction in HCM are different between the 2 subtypes of HCM. Methods Thirty-one patients with asymmetrical septal hypertrophy (ASH), 43 with ApHCM, and 27 healthy volunteers were recruited. Mean diastolic coronary flow velocity (CFmv) was monitored before and after adenosine infusion by transthoracic echocardiography in the mid-to-distal left anterior descending coronary artery. Coronary flow reserve was defined as the ratio between CFmv before and after adenosine infusion. Left ventricular mass index and stress myocardial perfusion were assessed by cardiac magnetic resonance imaging. Results Although basal CFmv was higher in ASH patients than in healthy controls (P < 0.05), it was similar in ApHCM patients and controls (P = 0.85). Poststress CFmv was significantly lower in both HCM subtypes than in controls (P < 0.05). Consequently, CFR was higher in controls than in ASH or ApHCM patients (P < 0.05). When HCM patients were stratified into 2 groups based on the presence of CFR impairment, no difference was observed between these 2 groups in terms of left ventricular mass index by cardiac magnetic resonance imaging. Multivariate logistic regression analysis identified basal CFmv as the only independent variable associated with CFR reduction in HCM (r2 = 0.49, P < 0.001). Conclusions Whereas the inability to augment coronary flow to its maximal level during stress was found to underlie CFR impairment in both HCM subtypes, the recruitment of vasodilatory capacity at baseline was more prominent in ASH than in ApHCM patients. This study was presented in the Annual Scientific Meeting of the American Society of Echocardiography, June 30–July 3, 2012, National Harbor, Maryland. This research was supported by Handok Research Fund 2012 and by the Leading Foreign Research Institute Recruitment Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (0640-20100001). The authors have no other funding, financial relationships, or conflicts of interest to disclose.Keywords
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