Effects of cardiac versus circulatory angiotensin-converting enzyme inhibition on left ventricular diastolic function and coronary blood flow in hypertrophic obstructive cardiomyopathy.
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.


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 (tauG) (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, tauG 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.
Kyriakidis
M
M
Department of Cardiology, Laiko Hospital of Athens, Greece.
Triposkiadis
F
F
Dernellis
J
J
Androulakis
A E
AE
Mellas
P
P
Kelepeshis
G A
GA
Gialafos
J E
JE
D000328:Adult; D000704:Analysis of Variance; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000097:blood / Q000627:therapeutic use*; D002216:Captopril / Q000627:therapeutic use*; D002312:Cardiomyopathy, Hypertrophic / Q000188:drug therapy* / Q000503:physiopathology; D003326:Coronary Circulation / Q000187:drug effects*; D003971:Diastole / Q000187:drug effects; D004452:Echocardiography; D015773:Enalaprilat / Q000627:therapeutic use*; D005260:Female; D006321:Heart / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007263:Infusions, Parenteral; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy*
D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril; D015773:Enalaprilat