Circulation, Vol 68, 1035-1043, Copyright © 1983 by American Heart Association
G Specchia, S de Servi, C Falcone, L Angoli, A Gavazzi, E Bramucci, A Mussini, M Ferrario, J Salerno and C Montemartini
To investigate the mechanism by which nifedipine improves exercise
tolerance in patients with coronary artery disease, we studied 14 patients
with stable exertional angina and left anterior descending artery disease
by measuring great cardiac vein flow (GCVF) and calculating anterior
regional coronary resistance (ARCR) during exercise before and after
sublingual administration of 20 mg of nifedipine. After nifedipine seven
patients (group I) had no increase in exercise capacity and showed a
similar magnitude of ST segment depression at peak exercise, while another
seven patients (group II) had prolonged exercise duration (p less than
.001) with less ST segment depression at peak exercise (p less than .01).
Such effects were achieved despite a significant increase in double
product, an indirect index of myocardial oxygen consumption. In group I
patients no significant change was induced by nifedipine in GCVF or in ARCR
either at rest or at peak exercise. In contrast, in group II patients
nifedipine significantly increased GCVF at rest (p less than .05) and at
peak exercise (p less than .001). Moreover, resting ARCR was decreased (p
less than .01) and remained significantly lower at peak exercise (p less
than .01) compared with the prenifedipine values. These data show that
nifedipine may increase GCVF and decrease ARCR at rest and at peak exercise
in patients with left anterior descending artery disease. Such increase in
myocardial oxygen supply seems the most likely mechanism by which
nifedipine may improve exercise capacity in patients with stable exertional
angina.
ARTICLES
Effects of nifedipine on coronary hemodynamic findings during exercise in patients with stable exertional angina
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