Emerging evidence supports a role for platelets in the progression of atherosclerosis in addition to an involvement in thrombotic vascular occlusion. Platelet Factor 4 (PF4), a chemokine released by activated platelets, stimulates several pro-atherogenic processes. Therefore, we examined the localization of PF4 and the homologous protein, Neutrophil Activating Protein-2 (NAP-2) in lesions representing the evolution of human atherosclerotic plaques. Carotid plaques from 132 patients with critical carotid stenosis and 6 autopsy specimens were studied. Clinical, histologic and immunohistochemical data were analyzed using a chi(2)-test. PF4 was detected in the cytoplasm of luminal and neovascular endothelium, in macrophages and in regions of plaque calcification. The presence of PF4 in macrophages and neovascular endothelium correlated with lesion grade (p = 0.004; p = 0.044). Staining of macrophages for PF4 correlated with the presence of symptomatic atherosclerotic disease (p = 0.028). In early lesions, PF4 was commonly found in macrophages of early lesions (Grade I/II), whereas NAP-2 was rarely present. In conclusion, correlation between PF4 deposition, lesion severity and symptomatic atherosclerosis suggests that persistent platelet activation may contribute to the evolution of atherosclerotic vascular lesions. These studies support the rationale for the chronic use of anti-platelet therapy in patients at risk for developing symptomatic atherosclerosis.

Background and Purpose-Bone formation and dystrophic calcification are present in carotid endarterectomy plaques.The clinical significance of these findings is unknown. The purpose of this study was to determine whether bone formation and extensive dystrophic calcification are associated with stable plaques and protective against ischemic vascular events. Methods-Carotid endarterectomy plaques were collected from 142 patients (94 men) with carotid stenosis. The specimens were evaluated for lamellar bone formation, dystrophic calcifications, inflammatory infiltrates, neovascularization, and histological type or grade of plaque according to a standard AHA grading system. Immunohistochemical staining was performed to identify vascular endothelial cells in neovascularization (factor VIII) and lymphocytes. Clinical data, including history of cerebrovascular and cardiovascular events, were recorded at the time of surgery. Results-Patients with calcification of carotid plaques had fewer symptoms of stroke and transient ischemic attack (Pϭ0.042) than those without calcification. Stroke and transient ischemic attack occurred less frequently in patients with plaques with large calcific granules (Pϭ0.021). Of the patients, 13% had lamellar bone formation, which directly correlated with the presence of sheetlike calcifications (Pϭ0.0001) and inversely correlated with ulcerated lesions (Pϭ0.048). The presence of bone also correlated with diabetes (PϽ0.01) and coronary artery disease (PϽ0.01). Of the 20 patients with bone, 6 had a history of stoke and transient ischemic attack (Pϭ0.5). Conclusions-The results indicate that bone formation tends to occur in heavily calcified carotid lesions devoid of ulceration and hemorrhage. Patients with extensive calcification of the carotid plaques are less likely to have symptomatic disease.

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Background Patients with single ventricle physiology and Fontan circulation are at increased risk for late complications and reduced survival. The aim of the study was to investigate the correlation between ventricular geometry and systolic regional function in different underlying anatomic conditions in adolescent and adult Fontan‐palliated patients. Method In a retrospective cross‐sectional study, we measured 2D strain, ventricular diameters, ventricular volumes, ejection fraction (EF), global and segmental wall stress, and sphericity index. The same analyses were performed in 99 age‐ and gender‐matched healthy individuals. Results One hundred and one patients were included at a mean age of 21 (range 14–59) years. In comparison with healthy subjects, patients with Fontan circulation displayed larger ventricular volumes (153 ± 78 mL vs 116 ± 38 mL P < 0.05), reduced EF (43% ± 15% vs 55% ± 8% P < 0.05), reduced longitudinal (−13% ± 6% vs −21% ± 4% P < 0.05) and circumferential strain values (−15% ± 7% vs −22% ± 4% P < 0.05). Functionally single ventricles were more spherical (ratio of longitudinal to short‐axis diameters 1.3 ± 0.3 vs 1.7 ± 0.2 P < 0.05). Circumferential strain correlated well with global wall stress and the degree of sphericity (R2 = 0.320), while segmental strain did not correlate with segmental wall stress. The percentage of segments with akinesia was relatively high (16 ± 16% vs 0 ± 0% P < 0.05) indicating reduced segmental contractile function. Conclusion Functionally single ventricles after Fontan palliation have significantly reduced systolic regional and global function with a high intersegmental inhomogeneity. The underlying pathological mechanisms might be multifactorial, including ventricular geometry, sphericity, and regional contractile properties. Future studies are needed to investigate the role of ventricular geometry for clinical performance and outcome.