Key result
Cardiomyopathy was associated with significantly increased platelet activation compared to healthy controls (thrombospondin 13.5% vs 10.6%, P=0.002), particularly in those with myocardial infiltrates.
Why the study?
Is platelet activation increased in patients with cardiomyopathy and myocardial inflammation compared to those without inflammation and healthy controls?
Observational (n=90)
Is platelet activation increased in patients with cardiomyopathy and myocardial inflammation compared to those without inflammation and healthy controls?
Patients with cardiomyopathy, particularly those with myocardial inflammation, exhibit increased platelet reactivity, which may contribute to their higher risk of thrombotic events.
May warrant heightened thrombotic vigilance in cardiomyopathy with inflammation; leaves open whether antiplatelet strategies merit prospective testing.
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. Twenty-three patients had myocardial infiltrates (>/= 2 CD3(+) cells/high power field (HPF), CM+) and 22 patients had no inflammation (< 2 CD3(+) cells/HPF, CM-). Platelet adhesion proteins were flow cytometrically quantified (thrombospondin, P-selectin, CD 41) and platelet activation in CM compared to 45 healthy controls. Significantly more activated platelets were detected in patients with cardiomyopathy than controls (for thrombospondin 13.5% [10.3; 22.0] median [25; 75 quartile] vs. 10.6% [8.2; 16.0], P = 0.002; for P-selectin 12.6% [10.0; 18.6] vs. 7.7% [5.8; 10.9], P < 0.001). Platelet activation was higher in patients with cardiomyopathy and myocardial infiltrates (for thrombospondin 19.0% [11.0; 26.3]) compared to patients without inflammation (12.3% [9.9; 16.0], P = 0.018). Platelet GPIIb/IIIa expression was also increased in patients with inflammation (290 arbitrary units [268, 338]) compared to the controls (215 [188, 248], P < 0.001). In conclusion, platelet reactivity was increased in patients with cardiomyopathy and myocardial infiltrates. Measurement of platelet reactivity may be useful to identify patients with cardiomyopathy at risk for thrombotic events.
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Weikert et al. (2002) conducted an observational in Cardiomyopathy (n=90). Cardiomyopathy vs. Healthy controls was evaluated on Platelet activation (thrombospondin) (p=0.002). Cardiomyopathy was associated with significantly increased platelet activation compared to healthy controls (thrombospondin 13.5% vs 10.6%, P=0.002), particularly in those with myocardial infiltrates.
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