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Even low-dose aspirin inhibits arachidonic acid-induced vasodilation in heart failure
A P Davie1, M P Love, J J McMurray
1Medical Research Council Clinical Research Initiative in Heart Failure, University of Glasgow, Scotland.
Insights
Low-dose aspirin significantly inhibits the arachidonic acid vasodilator pathway in humans, potentially causing detrimental vasoconstrictor effects, even in patients with congestive heart failure on ACE inhibitors.
Area of Science:
- Vascular physiology
- Pharmacology
Background:
- Evidence suggests aspirin may harm congestive heart failure (CHF) patients on angiotensin-converting enzyme (ACE) inhibitors.
- The vascular effects of aspirin in CHF patients remain under-examined.
Purpose of the Study:
- To investigate the arachidonic acid-dependent vasodilator pathway in human resistance arteries.
- To determine if CHF affects this pathway.
- To assess aspirin's inhibitory effect on this pathway.
Main Methods:
- Infusion of arachidonic acid into the brachial artery and measurement of forearm blood flow.
- Study included 10 healthy subjects and 15 CHF patients on ACE inhibitors.
- CHF patients received 0 mg, 75 mg, or 300 mg of aspirin daily for 14 days.
Main Results:
- Arachidonic acid induced dose-dependent vasodilation (up to 64%) in healthy subjects.
- No significant difference in vasodilation between CHF patients (0 mg aspirin) and controls.
- Aspirin (75 mg and 300 mg) significantly inhibited vasodilation in CHF patients by 55% and 59%.
Conclusions:
- A functional arachidonic acid-dependent vasodilator pathway exists in humans.
- Congestive heart failure does not significantly alter this pathway.
- Low-dose aspirin therapy significantly inhibits this pathway, suggesting potential adverse vasoconstrictor effects.
Background:
There is some evidence that aspirin may be harmful to patients with congestive heart failure treated with angiotensin-converting enzyme (ACE) inhibitors, but there has never been any direct examination of the vascular effects of aspirin in these patients. We sought to determine whether there is an arachidonic acid-dependent vasodilator pathway in resistance arteries in humans, whether it is affected by congestive heart failure, and whether it is inhibited by low-dose aspirin.
Methods:
A locally active dose of arachidonic acid was infused into the nondominant brachial artery while forearm blood flow was measured by venous occlusion plethysmography in 10 healthy subjects in a control group and 15 patients with congestive heart failure treated with ACE inhibitor. Patients with congestive heart failure were 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 healthy control subjects studied after administration of 0 mg aspirin. In patients, however, administration of 75 mg and 300 mg aspirin inhibited mean vasodilation by 55% and 59%, respectively.
Conclusions:
There is an arachidonic acid-dependent vasodilator pathway in humans. This pathway is not significantly affected by congestive heart failure. It is significantly inhibited by even low-dose aspirin therapy. These results imply that even the very lowest dose of aspirin in common use for cardioprotection has potentially detrimental vasoconstrictor effects.