Even low-dose aspirin inhibits arachidonic acid-induced vasodilation in heart failure

Background: There is some evidence that aspirin may be harmful to patients with congestive heart failure treated with angiotensin-converting enzyme (A CE) inhibitors, but there has never been any direct examination of the vasc ular effects of aspirin in these patients. We sought to determine whether t here is an arachidonic acid-dependent vasodilator pathway in resistance art eries in humans, whether it is affected by congestive heart failure, and wh ether it is inhibited by low-dose aspirin. Methods: A locally active dose of arachidonic acid was infused into the non dominant brachial artery while forearm blood flow was measured by venous oc clusion plethysmography in 10 healthy subjects in a control group and 15 pa tients with congestive heart failure treated with ACE inhibitor. Patients w ith congestive heart failure R-ere studied after administration of 0 mg, 75 mg, and 300 mg aspirin for 14 days. Results: Arachidonic acid produced progressive and incremental vasodilation (up to 64%). There was no significant difference between patients and heal thy control subjects studied after administration of 0 mg aspirin. In patie nts, hoc-ever, administration of 75 mg and 300 mg aspirin inhibited mean va sodilation by 55% and 59%, respectively Conclusions: There is an arachidonic acid-dependent vasodilator pathway in humans, This pathway is not significantly affected by congestive hart failu re. It is significantly inhibited by even low-dose aspirin therapy These re sults imply that even the very lon-est dose of aspirin in common use for ca rdioprotection has potentially detrimental vasoconstrictor effects.