Diastolic spectrum of left-ventricular hypertrophy: The impact of etiology and coronary artery disease on Doppler transmitral velocity

Faculty Medicine Year: 1996
Type of Publication: Article Pages: 436-442
Authors: DOI: 10.1159/000177133
Journal: CARDIOLOGY KARGER Volume: 87
Research Area: Cardiovascular System \& Cardiology ISSN ISI:A1996VJ36200012
Keywords : relaxation abnormality, compliance abnormality, hypertrophic cardiomyopathy, pressure overload hypertrophy    
Abstract:
Diastolic Filling of hypertrophied left ventricles has frequently been observed by Doppler methods. We hypothesized that filling characteristics in hypertrophy vary with etiology and concurrent ischemia. For patients with hypertrophy, the left-ventricular ejection fraction was >0.47 +/- 0.16, end-diastolic pressure was > 15 +/- 2 mm Hg, end-diastolic volume index was <96 +/- 12 ml/m(2) and left-ventricular mass index was 127 +/- 7 g/m(2). Peak E (early) and peak A (late) diastolic velocities and E-wave deceleration time, respectively, were as follows (significant unless otherwise indicated): normal subjects (NS), 79 +/- 9 and 82 +/- 19 cm/s, and 151 +/- 7 ms; cardiomyopathic hypertrophy, 63 +/- 16, 83 +/- 15 (NS) and 193 +/- 63, aortic stenosis without coronary disease, 110 +/- 10, 128 +/- 12 and 158 +/- 22 (NS); aortic stenosis with coronary disease, 57 +/- 12, 86 +/- 26 (NS) and 187 +/- 39; hypertension without coronary disease, 107 +/- 9, 128 +/- 9 and 143 +/- 22 (NS); hypertension with coronary disease, 58 +/- 12, 84 +/- 26 (NS) and 189 +/- 29. Conclusions: Hypertrophied left ventricles filled with two diastolic Doppler patterns: a relaxation abnormality with low peak E and delayed deceleration in hypertrophic cardiomyopathy, and a compliance abnormality with tall peak E and normal deceleration in pressure overload hypertrophy. When coronary artery disease occurred with pressure overload hypertrophy, impaired relaxation was the dominant pattern. Therefore, in addition to the known physiologic influences on diastolic filling, the etiology and presence of coronary artery disease modulate the configuration of transmitral velocities into hypertrophied ventricles.
   
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