Circulation, Vol 62, 764-772, Copyright © 1980 by American Heart Association
MF Rousseau, C Veriter, JM Detry, L Brasseur and H Pouleur
It has been shown that the maximal rate of left ventricular (LV) relaxation
is impaired in patients with coronary artery disease (CAD) under basal
conditions. To test the hypothesis that this impaired LV relaxation could
be related to viable but metabolically abnormal myocardium, we studied the
time course of isovolumic LV pressure fall in 21 patients with CAD and in
13 control subjects under basal conditions. This study was repeated after
intracoronary injection of the calcium antagonist nifedipine (N) in 11
patients with CAD and in eight controls. Our data showed that isovolumic
pressure fall was biexponential in 20 of 21 CAD patients and in six of 13
controls. Moreover, the time constant of isovolumic pressure fall during
the first 40 msec after peak (negative) dP/dt (T1) was significantly
greater in CAD patients than in controls (62 +/- 3 vs 44 +/- 1 msec, p <
0.002); the time constant of pressure fall during the 40-80 msec after peak
(negative) dP/dt (T2) was similar in both groups ( 42 +/- 2 vs 39 +/- 2
msec, NS). Thirty seconds after injection of nifedipine, T1 and T2, were
significantly prolonged in patients with CAD (14 msec and 16 msec,
respectively, p < 0.005) and in controls 12 msec and 14 msec,
respectively, p < 0.05), and a negative inotropic effect was observed in
both groups (peak (positive) dP/dt - 16% in controls and -23% in CAD
patients, p < 0.01). At rest, impairment of isovolumic relaxation in CAD
patients is mainly limited to the first 40 msec after peak (negative)
dP/dt, suggesting a dyssynchronous wall motion. This impairment of LV
relaxation is better identified by T1 than by peak (negative) dP/dt in
individual patients, and cannot be improved by administration of a calcium
antagonist.
ARTICLES
Impaired early left ventricular relaxation in coronary artery disease: effects of intracornary nifedipine
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