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Circulation. 1998;97:1342-1347

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(Circulation. 1998;97:1342-1347.)
© 1998 American Heart Association, Inc.


Clinical Investigation and Reports

Effects of Cardiac Versus Circulatory Angiotensin-Converting Enzyme Inhibition on Left Ventricular Diastolic Function and Coronary Blood Flow in Hypertrophic Obstructive Cardiomyopathy

Michael Kyriakidis, MD, FESC; Filippos Triposkiadis, MD, FESC; John Dernellis, MD; Aristides E. Androulakis, MD; Panagiotis Mellas, MD; Glafkos A. Kelepeshis, MD; ; John E. Gialafos, MD, FESC

From the Department of Cardiology, Laiko Hospital of Athens (M.K., F.T., P.M., G.A.K.); Department of Cardiology, Hippokration Hospital (J.D., A.E.A.), University of Athens; and State Cardiac Department, Hippokration Hospital (J.E.G.), Athens, Greece.

Correspondence to Michael Kyriakidis, MD, Department of Cardiology, Laiko Hospital of Athens, 17 Agiou Thoma St, Goudi 115 27, Athens, Greece.

Background—Left ventricular (LV) diastolic function and coronary flow are impaired in hypertrophic obstructive cardiomyopathy (HOCM). This study was designed to evaluate the impact of cardiac and circulatory ACE inhibition on such derangements.

Methods and Results—Twenty patients with HOCM underwent cardiac ACE inhibition with intracoronary (IC) enalaprilat (0.05 mg/min infused into the left anterior descending coronary artery for 15 minutes) followed by circulatory ACE inhibition with 25 mg sublingual (SL) captopril. Contrast ventriculography, pressure, and coronary flow measurements were performed at baseline, after IC enalaprilat infusion, and 45 minutes after SL captopril. Heart rate was not affected by the respective interventions (75±11 versus 76±13 versus 75±10 bpm; P=NS), whereas mean aortic pressure dropped slightly after IC enalaprilat and significantly after SL captopril (90±8 versus 85±10 versus 74±9 mm Hg; P<.05). Compared with baseline, IC enalaprilat resulted in a decrease in LV end-diastolic pressure (17.6±5.9 versus 14.4±4.9 mm Hg; P<.05), time constant of isovolumic LV pressure relaxation ({tau}G) (69±9 versus 52±10 ms; P<.05), and outflow gradient (45.2±6.9 versus 24.4±3.7 mm Hg; P<.05) and in an increase in coronary blood flow (107±10 versus 127±12 mL/min; P<.05) and coronary flow reserve (2.2±0.4 versus 2.6±0.3; P<.05). After SL captopril, {tau}G was prolonged (60±13 ms; P<.05 versus IC enalaprilat), and LV outflow gradient, coronary blood flow, and coronary flow reserve values returned to baseline (45.5±5.3 mm Hg, 107±12 mL/min, and 2.2±0.5, respectively; P=NS versus baseline).

Conclusions—Activation of the cardiac renin-angiotensin system contributes to LV diastolic dysfunction as well as to the decreased coronary blood flow and coronary flow reserve in HOCM. Cardiac ACE inhibition restores and circulatory ACE inhibition aggravates the above derangements.


Key Words: angiotensin • enzymes • hypertrophy • cardiomyopathy




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