Non-compliance is the predominant cause of aspirin resistance in chronic coronary arterial disease patients.

Background: Our previous publication showed that 9% of patients with a history of myocardial infarction MI. could be labeled as aspirin resistant; all of these patients were aspirin resistant because of non-compliance. This report compares the relative frequency of aspirin resistance between known compliant and non-compliance subjects to demonstrate that non-compliance is the predominant cause of aspirin resistance.

Monitoring platelet inhibition after clopidogrel with the VerifyNow-P2Y12(R) rapid analyzer: the VERIfy Thrombosis risk ASsessment (VERITAS) study.

Introduction: Clopidogrel inhibits platelet P2Y12 ADP receptors, while ADP, as an inductor of aggregation, stimulates both P2Y12 and P2Y1 platelet receptors. Despite a clinical loading dose routine with clopidogrel, some patients still experience coronary stent thrombosis suggesting persistent platelet activation. The VerifyNow-P2Y12 is a rapid assay that test platelet activity over 3 min and uses of the combination of ADP and prostaglandin E1 (PGE1) to directly measure the effects of clopidogrel on the P2Y12 receptor.

Compliance as a critical consideration in patients who appear to be resistant to aspirin after healing of myocardial infarction.

The hypothesis that aspirin resistance is often due to noncompliance was investigated. One hundred ninety patients with a history of myocardial infarction were evaluated using arachidonic acid-stimulated light aggregometry at 3 different time points: while receiving their usual daily aspirin, after not receiving aspirin for 7 days, and 2 hours after the observed ingestion of aspirin 325 mg. At the first time point, 17 patients (9%) failed to show aspirin inhibition of platelet aggregation, but 2 hours after observed aspirin ingestion, aspirin inhibition was observed in all but 1 patient.

Earliest cardiac toxicity induced by iron overload selectively inhibits electrical conduction.

Female guinea pigs were injected intraperitoneally with 0.083 g/kg iron dextran (Fe-D) to achieve progressively increasing levels of iron load; controls received dextran. Delayed and blocked cardiac conductivity at the Purkinje fiber-papillary muscle junction was initially observed with Fe-D loads of 0.

A new method for measuring inhibition of platelet function by nonsteroidal antiinflammatory drugs.

Aspirin is widely used to help prevent vascular occlusion caused by atherosclerotic vascular disease. We used a platelet-aggregation assay (PAA) to evaluate the reliability of a proprietary platelet agonist, platelet prostaglandin agonist (PPA), to detect the amount of platelet inhibition induced by four different classes of nonsteroidal antiinflammatory drugs (NSAIDs) with antiplatelet effects. Twenty normal donors were evaluated before and 24 hours after ingestion of 325 mg of aspirin.