Circulation, Vol 70, 465-471, Copyright © 1984 by American Heart Association
KF Hossack, BG Brown, DK Stewart and HT Dodge
To determine mechanisms of benefit from diltiazem, 13 patients with
coronary disease performed sustained isometric handgrip exercise and
repeated the procedure during intravenous infusion of diltiazem (0.25 mg/kg
bolus followed by 0.003 mg/kg/min). Cardiovascular responses to handgrip,
diltiazem, their combination, and nitroglycerin were assessed by
hemodynamic and electrocardiographic measurements and by computer- assisted
measurements of normal and diseased segments of epicardial coronary
arteries. Handgrip produced increases in heart rate (12%; p less than
.001), pulmonary arterial pressure (19%; p less than .005), and pulmonary
wedge pressure (33%; p less than .005). Diltiazem produced significant
reductions in heart rate (7%; p less than .05) and aortic pressure (14%; p
less than .001). Pulmonary arterial pressure and pulmonary wedge pressure
were unchanged by diltiazem. Diltiazem did not prevent the increase in
heart rate or in aortic or wedge pressure associated with handgrip.
Diltiazem prolonged atrioventricular conduction from 0.18 +/- 0.03 to 0.20
+/- 0.03 sec (p less than .001). Compared with control values,
nitroglycerin reduced aortic pressure (14%; p less than .005), pulmonary
arterial pressure (38%; p less than .001), and pulmonary wedge pressure
(42%; p less than .005). Heart rate was unchanged. The constriction (20%)
in lumen area of normal coronary arterial segments during handgrip was
effectively prevented by infusion of diltiazem (1%; p less than .001).
Nitroglycerin produced a significantly greater increase (20%) in diameter
of normal coronary arterial segments than diltiazem (3%; p less than .001)
and tended to have a more favorable effect than diltiazem on stenosis
minimum area and flow resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Diltiazem-induced blockade of sympathetically mediated constriction of normal and diseased coronary arteries: lack of epicardial coronary dilatory effect in humans
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