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The platelet collagen receptor glycoprotein (GP) VI is critical for the formation of arterial thrombosis. GPVI platelet surface expression was examined in patients with stable angina and in patients with acute coronary syndrome (ACS). Surface expression of platelet activation markers such as P-selectin, GPIbalpha, and platelet GPVI was determined by flow cytometry. Patients with ACS showed a significantly enhanced GPVI expression compared with patients with stable angina and healthy controls. The expression of GPVI correlated well with CD62P. Elevated platelet GPVI expression was associated with ACS independent of markers of myocardial necrosis such as troponin and creatine kinase. In ACS, platelet surface GPVI expression was already elevated several hours before troponin and creatine kinase indicated myocardial injury. We conclude that the determination of the platelet-specific thrombotic marker GPVI may help to identify patients at risk before myocardial ischemia is evident.

Serious cardiovascular events frequently arise from rupture of vulnerable atherosclerotic plaques. Not infrequently, these plaques are clinically silent and suddenly cause acute complications such as myocardial infarction, which in a high percentage are fatal. Thus, identifying individual patients with vulnerable plaques at high risk for plaque rupture is a central challenge in clinical medicine. This review highlights noninvasive scintigraphic techniques, which use radiolabeled molecules to detect functional aspects in atherosclerotic plaques by visualizing their biological activity. One major principle is the molecular imaging of inflammation with radionuclide tracers, including detection of metabolic activity, chemotaxis, cell recruitment, and lipoprotein enrichment. Additional studies focus on visualization of apoptosis, angiogenesis, or proteolysis. A central feature of plaque vulnerability is its thrombogenicity. Therefore, detection of thrombogenic plaques is another promising principle of molecular imaging. If a reliable protocol to image vulnerable plaques, which are prone to rupture, can be established and introduced into clinical practice, the required measures such as atheroprotective medication or revascularization could be undertaken to prevent serious cardiovascular events.

Several lines of evidence suggest a viral infection as the initiating event for the development of myocarditis (MC). Especially enteroviruses like coxsackie B3 virus have been shown to induce MC in humans and strains of MC-prone mice after an infection. The further course of the disease is, however, determined not only by the viral infection but also by the host's immune system. Both the humoral and the cellular immune system can modify the extent of the damage caused by the disease. The humoral immune system mounts an anti-viral immune response immediately after the infection; however, during the course of the disease, autoantibodies against a variety of different autoantigens emerge. The epitopes recognized by the anti-viral antibodies and those of several autoantibodies have been identified using synthetic peptides. The human disease could be transferred into SCID mice using peripheral blood leukocytes of patients, suggesting a pathophysiological significance of the autoimmune reaction. However, the significance of the humoral immune responses needs to be tested in randomized, prospective studies using immunoadsorption of autoantibodies in patients with inflammatory cardiomyopathy.