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Sir—During recent years the beneficial effect of continued use of aspirin after acute myocardial infarction in patients with congestive heart failure has been questioned.1 This is based on retrospective findings in some large clinical trials showing a reduced beneficial effect on mortality of angiotensin converting enzyme (ACE) inhibitors in patients treated with aspirin.2 3 Moreover, improvement in central haemodynamic indices and pulmonary diffusion capacity in patients with congestive heart failure during short term ACE inhibitor treatment was impaired when aspirin was added,4-6 though there was no interaction between antiplatelet treatment with ticlopidine and ACE inhibitor treatment.6
We retrospectively analysed data from a study on calf capillary fluid filtration and microvascular blood flow in 22 patients with congestive heart failure (20 men and two women; mean age 45 years (range 27 to 64); mean (SD) ejection fraction 22 (8)%; mean arterial blood pressure 88 (15) mm Hg) in New York Heart Association (NYHA) class II (n = 14), class III (n = 6), and class IV (n = 2), to see whether resting calf skeletal muscle blood flow and capillary filtration of water differed in six patients on long term treatment with 75–150 mg aspirin and 16 patients not on treatment with aspirin.
To test the effect on heart failure alone and to avoid influence of atherosclerosis, we only included patients with idiopathic dilated cardiomyopathy. The groups compared did not differ with respect to NYHA class, ejection fraction, mean arterial pressure, sex, or age and all were treated with an ACE inhibitor.
Calf skeletal muscle blood flow was measured by the local133xenon washout method and capillary filtration by venous occlusion strain gauge plethysmography. Figure 1 shows that patients on aspirin treatment had lower resting skeletal muscle blood flow (and thus increased vascular resistance: 80 (20) mm Hg.min/ml in patients on aspirin treatment v 56 (17) mm Hg.min/ml not on aspirin treatment, p < 0.01) and a higher capillary filtration coefficient for water than patients not on aspirin treatment. There was no significant difference in calf skeletal muscle blood flow or capillary fluid filtration coefficient in relation to other medication.
Aspirin impedes platelet aggregation and blocks prostaglandin formation, including the formation of the vasoconstrictor and platelet aggregation inducer thromboxane A2. Our data suggest that patients with congestive heart failure on long term treatment with aspirin and an ACE inhibitor have increased peripheral precapillary to postcapillary resistance, with increased afterload and increased susceptibility to oedema formation. These findings add to the growing evidence that aspirin may not be beneficial in patients with congestive heart failure on treatment with an ACE inhibitor. However, our study was small, retrospective, and non-randomised, and the subject is controversial as there are also data showing an absence of interaction between aspirin and ACE inhibitor treatment in congestive heart failure.7 The data therefore need to be confirmed in a larger study specifically designed for the purpose before a deleterious effect of aspirin can be considered proven.