Platelet Survival in Patients with Dilated Cardiomyopathy

Summary Dilated cardiomyopathy is associated with thromboembolic complications, which correlate poorly, however, with a visible left ventricular thrombus. Therefore, this study was performed to assess whether an abnormality of platelet function in vivo can be detected in patients with dilated cardiomyopathy. Platelet survival was measured after autologous labeling with indium-111 oxine in 28 patients with dilated cardiomyopathy and angiographically normal coronary arteries (mean ejection fraction 21 ± 9% [standard deviation], range 4 to 39%) and in nine patients with coronary artery disease and similar left ventricular dysfunction (mean ejection fraction 21 ± 10%). Plasma levels of beta-thromboglobulin and platelet factor 4 were measured in patients with idiopathic cardiomyopathy (n = 15) and platelet scintigraphic images of the heart (n = 24) were obtained in subsets of both patient groups. Platelet survival was significantly and similarly shortened in patients with idiopathic and ischemic cardiomyopathy (67 ± 34 and 55 ± 24 h, respectively) compared to controls (209 ± 9 h, n = 12; p <0.001). Of the two platelet-specific proteins, beta-thromboglobulin was increased in the patients compared with controls (42 ± 17 versus 22 ± 6 ng/ml, p <0.001). Platelet scintigraphy 24 h (n = 24) and/or 48 h (n = 9) after labeling showed a diffuse pattern of enhanced platelet uptake over the heart which varied in intensity among patients, but which was never seen in controls (n = 6). This increased platelet uptake was similar in patients with idiopathic and ischemic cardiomyopathy but did not correlate with either ejection fraction or cardiothoracic ratio. Patients taking Coumadin (n = 9) had lower values of quantitative and qualitative scintigraphic platelet uptake than patients without Coumadin (n = 14; p <0.05). Thus, platelet survival is markedly shortened and cardiac platelet uptake diffusely enhanced in patients with dilated cardiomyopathy of either idiopathic or ischemic origin. Whether enhanced platelet activation per se contributes to the risk of systemic embolization in this patient population requires further investigation.