Platelet activation and thrombus formation relates to the presence of myocardial inflammation in patients with cardiomyopathy.

Background: Patients with cardiomyopathy show a significantly increased risk for thromboembolic events due to a hypercoagulable state and platelet dysfunction. The pathophysiologic mechanism underlying the increasing platelet activity in patients with cardiomyopathy remains unclear. We performed a clinical study to elucidate the link between myocardial tissue alterations and platelet activation in patients with cardiomyopathy.

Abciximab therapy is associated with increased platelet activation and decreased heparin dosage in patients with acute myocardial infarction.

The inhibition of the glycoprotein (GP) IIb/IIIa receptor for reducing periprocedural ischemic events in patients undergoing coronary intervention is known to influence platelet reactivity. Suboptimal doses of GP IIb/IIIa antagonists have been suggested to be prothrombotic and proinflammatory. This study was performed to observe platelet activation markers, whole blood aggregation and the dosage of unfractionated heparin (UFH) in the presence or absence of the GP IIb/IIIa inhibitor abciximab.

ADP induced platelet degranulation in healthy individuals is reduced by clopidogrel after pretreatment with atorvastatin.

Statins inhibit platelet reactivity and reduce blood thrombogenicity. The effectiveness of clopidogrel in inhibiting platelet reactivity was suggested to be reduced in the presence of atorvastatin due to shared enzymes in metabolism. Healthy individuals, 17 pretreated with atorvastatin (20 mg/d for 3 days) and 17 without pretreatment, as well as 15 patients with stable coronary artery disease (CAD) and concurrent atorvastatin therapy were started on clopidogrel (loading dose 300 mg, then 75 mg/d).

Platelet activation is increased in patients with cardiomyopathy: myocardial inflammation and platelet reactivity.

Thrombotic events are a major complication in patients with cardiomyopathy, in which inflammation is often found within the heart. We examined the platelet activation in patients with cardiomyopathy with and without myocardial infiltrates. Endomyocardial biopsies of 45 patients with cardiomyopathy (CM) were immunohistologically assessed for infiltrates.