title: Coronary flow reserve impairment in apical vs asymmetrical septal hypertrophic cardiomyopathy.
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.
  
  
  OBJECTIVE
  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.
authors: Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
authors: Hyo-Suk
authors: HS
authors: Ahn
authors: Hyung-Kwan
authors: HK
authors: Kim
authors: Eun-Ah
authors: EA
authors: Park
authors: Whal
authors: W
authors: Lee
authors: Yong-Jin
authors: YJ
authors: Kim
authors: Goo-Yeong
authors: GY
authors: Cho
authors: Jae-Hyung
authors: JH
authors: Park
authors: Dae-Won
authors: DW
authors: Sohn
mesh_terms: D000241:Adenosine; D001783:Blood Flow Velocity / Q000502:physiology*; D002312:Cardiomyopathy, Hypertrophic / Q000473:pathology / Q000503:physiopathology*; D016022:Case-Control Studies; D003326:Coronary Circulation / Q000502:physiology*; D003971:Diastole / Q000502:physiology; D004452:Echocardiography; D015150:Echocardiography, Doppler; D005260:Female; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D055414:Myocardial Perfusion Imaging; D014665:Vasodilator Agents
chemical_list: D014665:Vasodilator Agents; D000241:Adenosine
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