Circulation, Vol 60, 497-503, Copyright © 1979 by American Heart Association
J Mehta and P Mehta
We studied 11 patients with congestive heart failure and 10 normal
volunteers for in vivo platelet aggregate formation activity. The patients
with heart failure had significantly (p less than 0.01) more circulating
platelet aggregates than the normal volunteers. During sodium nitroprusside
infusion, the number of circulating platelet aggregates declined to normal
levels and in vitro platelet aggregation responses to epinephrine and
adenosine diphosphate were also suppressed significantly (p less than
0.01). This was associated with a 30% decline in systemic vascular
resistance and a 28% increase in cardiac output. In other in vitro
experiments, sodium nitroprusside was found to have direct, dose-related
platelet aggregation inhibitory actions. This study suggests that an
increase in vascular resistance in certain heart failure patients may in
part be related to an increase in circulating platelet aggregates. Direct
inhibition of platelet aggregation by sodium nitroprusside may be a
mechanism of its beneficial effects in heart failure.
ARTICLES
Platelet function studies in heart disease. VI. Enhanced platelet aggregate formation activity in congestive heart failure: inhibition by sodium nitroprusside
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