title: Impaired coronary circulation in patients with apical hypertrophic cardiomyopathy: noninvasive analysis by transthoracic Doppler echocardiography.
abstract: OBJECTIVE
  We designed this study to examine the characteristics of coronary circulation in patients with apical hypertrophic cardiomyopathy (ApHCM) using noninvasive transthoracic Doppler echocardiography (TTDE).
  
  
  BACKGROUND
  Recent advances in TTDE have allowed noninvasive assessment of coronary circulation by the measurement of coronary flow velocity (CFV) patterns and coronary flow velocity reserve (CFVR). However, there have been no previous studies evaluating coronary circulation in ApHCM.
  
  
  METHODS
  We analyzed CFV and CFVR in the left anterior descending coronary artery (LAD), and apical wall thickness in the left ventricle, in 10 ApHCM subjects and 10 control subjects. Mean diastolic velocity (MDV) and time from the beginning of diastole to peak velocity (TPV), and CFVR, defined as a ratio of drug-induced hyperemic to basal MDV, were measured.
  
  
  RESULTS
  At baseline, MDV was higher, and TPV was longer, in ApHCM subjects than in control subjects (29 +/- 5.7 versus 19 +/- 6.5 cm/sec; p < 0.01 and 5.2 +/- 1.0 versus 3.5 +/- 0.6 msec; p < 0.005, respectively). CFVR in ApHCM subjects was significantly lower than in control subjects (1.9 +/- 0.4 versus 3.1 +/- 0.8; p < 0.005). CFVR and basal MDV in ApHCM subjects showed significant correlations with apical/posterior wall thickness ratio [CFVR; r =-0.84, p < 0.01 and MDV; r = 0.74, p < 0.05, respectively].
  
  
  CONCLUSIONS
  Noninvasive coronary flow assessment by TTDE revealed an impaired coronary circulation with reduced CFVR, high MDV at baseline and prolonged TPV. These results suggest that these characteristics of coronary circulation may provide an additional index for the assessment of ApHCM.
authors.affiliation: Department of Internal Medicine and Cardiology, Osaka City University Medical School, Osaka, Japan.
authors.forename: Ken
authors.initials: K
authors.lastname: Yoshida
authors.forename: Takeshi
authors.initials: T
authors.lastname: Hozumi
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Takemoto
authors.forename: Kenichi
authors.initials: K
authors.lastname: Sugioka
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Watanabe
authors.forename: Takashi
authors.initials: T
authors.lastname: Muro
authors.forename: Minoru
authors.initials: M
authors.lastname: Yoshiyama
authors.forename: Kazuhide
authors.initials: K
authors.lastname: Takeuchi
authors.forename: Junichi
authors.initials: J
authors.lastname: Yoshikawa
mesh_terms: D000255:Adenosine Triphosphate; D001783:Blood Flow Velocity / Q000502:physiology; D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003326:Coronary Circulation / Q000502:physiology*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000503:physiopathology; D004452:Echocardiography; D015150:Echocardiography, Doppler; D018618:Echocardiography, Doppler, Color; D025401:Echocardiography, Stress; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D006940:Hyperemia / Q000000981:diagnostic imaging / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology
chemical_list: D000255:Adenosine Triphosphate