Nonplatelet effects of aspirin during acute coronary occlusion: electrophysiologic and cation alterations in ischemic myocardium.

Abstract:

BACKGROUND:Mortality after acute myocardial ischemia has been reduced by aspirin (ASA) but mechanisms other than the antiplatelet effect have not been established. This article evaluates an antiarrhythmic action during sympathetic stimulation in the intact anesthetized dog with and without ischemia. METHODS AND RESULTS:The ventricular fibrillation threshold (VFT) was examined before and after epinephrine (E) in normals (group I). A VFT reduction during E was normalized after 1 week of ASA (P<.01). Regional myocardial ischemia for 1 hour resulted in similar hypoperfusion in controls of group II and after ASA. Action potential responses in isolated superfused ischemic tissue showed prolonged repolarization (APD90) in response to E, which was normalized after ASA (P<.01). To assess the antiarrhythmic role of the anion in group III, Na salicylate was given. During 1 hour of ischemia, the VF incidence was reduced and cation abnormalities diminished in ischemic myocardium compared with untreated ischemia. CONCLUSIONS:ASA antagonizes the reduction of the VFT induced by catecholamine in normals as well as the repolarization abnormality elicited by E during acute ischemia. The salicylate anion appears to be the active component in view of the efficacy in preventing VF during the early ischemic period.

authors

Shehadeh AA,Arena J,Moschos CB,Regan TJ

doi

10.1053/XV.2000.5492

keywords:

subject

Has Abstract

pub_date

2000-04-01 00:00:00

pages

113-20

issue

2

eissn

1074-2484

issn

1940-4034

pii

ajcpt0050113

journal_volume

5

pub_type

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