The Effect of Different Antithrombotic Regimens on Platelet Aggregation After Myocardial Infarction

Abstract

Platelet aggregate ratio (PAR) was measured according to the method of Wu & Hoak in 143 patients after acute myocardial infarction (AMI) and in 54 controls. A PAR < 1 expresses the presence of platelet aggregates. The patients were randomized to aspirin 160 mg/d, or warfarin, or aspirin 75 mg/d + warfarin. In patients on aspirin, PAR was measured 24 h after aspirin intake, and in 76 patients also 2 h after aspirin. The median PAR in patients on warfarin was 0.85, on warfarin + aspirin 0.91 and on aspirin alone 0.94, all significantly lower than the median PAR of 0.97 in the controls. In 14 patients on aspirin the PARs were below a cut-off point of 0.82 (secondary aspirin non-responders). PAR increase significantly 2 h after aspirin intake. In two patients, however, PAR remained low (primary aspirin non-responders). It is concluded that some patients do not seem to respond to aspirin, the clinical implication of which has yet to be determined.

Current evidence and clinical implications of aspirin resistance

“…49 Even though an across-the-board consensus on the ideal aspirin dosage for primary and secondary prevention of atherothrombotic events seems to be lacking, 87,88 higher doses seem to be more effective in clinical trials that use laboratory endpoints to measure aspirin resistance. 7,19,26,28,[89][90][91][92][93][94][95][96] However, these findings were not confirmed in studies with clinical outcome endpoints 97 and meta-analyses of studies assessing the clinical significance of laboratory-identified ASA resistance have failed to demonstrate a similar dose-dependent effect. 98 Variability in aspirin pharmacodynamics and pharmacokinetics (absorption, bioavailability, metabolism, and excretion).…”

Aspirin resistance in stroke: 2004

“…The Rapid Platelet Function Assay-ASA is an automated turbidimetric-based optical detection system employing fibrinogen-coated beads and platelet agonist. Other methods to measure platelet function include wholeblood aggregometry [13], activated clotting time, and determination of the platelet aggregates ratio [14] or platelet reactivity index [15]. The skin bleeding time test lacks clinical benefit for several reasons, including its inability to reliably identify individuals who have recently ingested aspirin, its poor reproducibility, and operator dependency.…”

Antiplatelet resistance with aspirin and clopidogrel: Is it real and does it matter?

“…Aspirin's antiplatelet effect is usually quantified by assays of platelet aggregation or measurements of markers of platelet activation. Using different methodologies and varied definitions, the prevalence of hyporesponsiveness (ie, resistance) to aspirin has been reported to vary from 5% to 60% among patients with atherosclerotic diseases involving different vascular beds [11][12][13][14][15][16][17][18][19][20][21][22]. The mechanisms of aspirin resistance are not clearly defined.…”