Circulation, Vol 65, 1114-1118, Copyright © 1982 by American Heart Association
PA Majid and J De Jong
We studied the acute hemodynamic effects of nifedipine in 20 patients with
angiographically proved coronary artery disease. Eight patients were
studied during exercise-induced pain. There was an expected abnormal
increase in pulmonary wedge pressure (28 +/- 8 mm Hg, mean +/- SD)
accompanying chest pain (onset 179 seconds, duration 334 seconds) and
ST-segment depression (2.2 +/- 0.9 mm) on the ECG. Pacing stress was used
in six patients and increased left ventricular (LV) end- diastolic pressure
(from 16 +/- 6 to 26 +/- 6 mm Hg), volumes (end- diastolic 63 +/- 20 to 81
+/- 22 ml/m2, end-systolic 26 +/- 15 to 47 +/- 16 ml/m2) and impaired
ejection fraction (0.60 +/- 0.15 to 0.44 +/- 0.11) compared with control
values. In both groups, nifedipine, 20 mg sublingually, significantly
shortened duration of pain, reduced ST depression on the ECG (p less than
0.001) and reversed all hemodynamic abnormalities. In another group of six
patients with recent (less than 4 months) acute myocardial infarction and
moderately severe LV dysfunction at rest, nifedipine reduced LV
end-diastolic pressure from 21 +/- 6 to 12 +/- 5 mm Hg and volumes
(end-diastolic from 109 +/- 35 to 95 +/- 32 ml/m2, end-systolic from 41 +/-
15 to 31 +/- 7 ml/m2), while the ejection fraction improved significantly,
from 0.43 +/- 0.08 to 0.58 +/- 0.11. Thus, the antianginal effect of
nifedipine is associated with improved systolic emptying and reduced
diastolic filling of the heart. Nifedipine appears to have no discernible
adverse effects in patients with depressed LV function.
ARTICLES
Acute hemodynamic effects of nifedipine in patients with ischemic heart disease
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