Hugh S. Weily

Platelet Function Studies in Coronary Artery Disease

Platelets have been implicated and abnormal platelet function proposed in the pathogenesis of coronary artery disease (CAD). This investigation examines platelet function in men with stable, arteriographically defined CAD and correlates results with lipid pattern, history of angina or myocardial infarction and smoking habits. Platelet survival (51Chromium method), adhesiveness, and aggregation were measured in 21 men with CAD. Twelve patients had Type IV hyperlipoproteinemia and nine patients had normal lipoprotein level. Eighteen had angina and 13 had had infarction.The average platelet survival for the total group was normal (6.8 ± 0.24 days, avg ± SEM), but survival was shortened in 11 and normal in ten. There was no significant difference between: (1) patients with hyperlipoproteinemia (6.8 ± 0.30 days) and those with normal lipoproteins (6.9 ± 0.41 days); (2) patients with angina (6.8 ± 0.28 days) and without (6.6 ± 0.26 days); (3) patients with infarction (6.8 ± 0.26 days); and without (6.8 ± 0.50 days); (4) patients with varying patterns of arteriographic involvement; and (5) with varying smoking histories. Adhesiveness was normal in all. Aggregation was normal in 14. Neither adhesiveness nor aggregation correlated with platelet survival or defined the subgroups of CAD. Results suggest an abnormal short platelet survival frequently occurs in patients with CAD, but there is no discernible difference in platelet survival among the various clinical subgroups of CAD.

Altered Platelet Function in Patients with Prosthetic Mitral Valves Effects of Sulfinpyrazone Therapy

Platelet survival time and platelet adhesiveness and aggregation were examined in 16 patients with prosthetic mitral valves. Subsequently, nine patients were treated with sulfinpyrazone in doses of 400 mg and 800 mg/day, and the studies were repeated after a treatment period of 5 to 8 weeks. 51Chromium survival time was shortened in 15 of 16 patients, and the mean value for the entire group was 5.49 ± 0.23 days (normal, 6.73 ± 0.21 days; P < 0.001). Mean platelet adhesiveness in glass bead columns was 53 ± 5% (normal, 30 to 60%). Platelet aggregation (turbidometric technic of Born) was normal. Treatment with 400 mg of sulfinpyrazone daily reduced platelet adhesiveness to 40 ± 5% (P < 0.05), but effected no change in platelet survival time or platelet aggregation. Therapy with 800 mg of sulfinpyrazone daily corrected platelet survival time to normal, 6.68 ± 0.57 days (P < 0.01), but it produced no further decrease in adhesiveness and no change in aggregation. It is concluded that platelet abnormalities regularly occur in patients with prosthetic mitral valves and may contribute to thromboembolism in this group. Platelet survival time is a more sensitive measure of altered platelet kinetics than platelet adhesiveness or platelet aggregation. Therapy with 800 mg of sulfinpyrazone per day corrects demonstrated abnormalities and may be useful for prevention of thromboembolism in patients with prosthetic mitral valves.

Platelet Survival in Patients with Substitute Heart Valves

Abstract To determine the relation of thromboembolism to the presence of substitute heart valves platelet studies were performed in 55 patients. Average platelet survival was normal in patients wit...

Platelet Survival and Adhesiveness in Recurrent Venous Thrombosis

Abstract Of 28 patients with idiopathic recurrent venous thrombosis, platelet survival time was abnormally shortened in 18 and normal in 10, and platelet adhesiveness was increased in eight and normal in 20. Platelet survival time was normal in nine anticoagulant-responsive patients, but was significantly shortened in 15 patients who were refractory to anticoagulants or who had had arterial thrombosis. Platelet adhesiveness did not distinguish these patients, nor did it correlate with platelet survival time. Platelet-inhibitor therapy with sulfinpyrazone was effective in the control of thrombosis in seven patients with shortened platelet survival time, increasing platelet survival time and decreasing platelet adhesiveness. These results suggest that shortened platelet survival or increased platelet adhesiveness is present in a high proportion of patients with recurrent venous thrombosis. Platelet-inhibitor therapy may prove useful in such cases. (N Engl J Med 288:1148–1152, 1973)

Platelet Survival in Patients with Rheumatic Heart Disease

Abstract Platelet studies were carried out in patients with valvular heart disease to determine the correlation of results with thromboembolism. Platelet survival was normal in 11 patients with aor...

Platelet survival time following aortic valve replacement.

Thromboembolism continues to complicate the course of patients following aortic valve replacement. In patients with prosthetic and homograft mitral valves, platelet survival time has been shown to correlate with occurrence of thromboembolism. This study extends these observations to patients with aortic valve disease. Platelet survival time was measured (by the chromium-51 method) in 73 patients with aortic valve disease. Eighteen patients were studied preoperatively and had platelet survival times of 3.4 ± 0.14 days (mean ± standard error of the mean), almost the same as normal (3.7 ± 0.4 days). Platelet survival time was shortened (P < 0.001) following aortic valve replacement with Starr-Edwards prostheses — Model 1000: 2.5 ± 13 days (N = 6); Model 1200-1260: 3.0 ± 0.10 (N = 14); Model 2300-2320: 3.0 ± 0.15 days (N = 9) — and with stented aortic homografts: 3.0 ± 0.10 days (N = 16). Platelet survival time was normal following aortic valve replacement in patients with directly sewn aortic homografts 3.7 days ± 0.24 days (N = 10). Eleven patients with Starr-Edwards prostheses had a history of thromboembolism and all also showed shortened platelet survival time (2.7 ± 0.12 days, P < 0.001), a measurement which was significantly different (P < 0.01) from the 18 patients with Starr-Edwards prostheses and no thromboembolism (3.0 ± 0.09 days). Platelet suppressant therapy prolonged platelet survival in eight patients with Starr-Edwards devices, thromboembolism, and shortened platelet survival time. These results suggest that insertion of Starr-Edwards valves and stented aortic homografts alter platelet survival time but that direct homografts do not. A correlation between occurrence of thromboembolism after aortic valve replacement and shortened platelet survival time has been shown.

Platelet survival time in patients with hypoxemia and pulmonary hypertension.

Platelet survival time (autologous labeling with 85chromium) was measured in 63 patients in order to evaluate the role of platelets in the thromboembolic complications of patients with hypoxemia and pulmonary hypertension. Thirty-eight of these patients had chronic obstructive airways disease; 13, primary pulmonary hypertension; seven, recurrent pulmonary embolism; four, the Eisenmenger syndrome; and one, multiple pulmonary arteriovenous fistula. Forty-three patients were hypoxemic and 41 (95%) had shortened platelet survival. Platelet survival was weakly associated with arterial oxygen tension (r = 0.50), but not with the arterial carbon dioxide tension or the level of pulmonary artery pressure. Sulfinpyrazone lengthened platelet survival in 12 of 24 (50%) treated patients but this drug did not alter either arterial oxygen tension, arterial carbon dioxide tension, or pulmonary artery pressure. Our results suggest that hypoxemia is associated with shortened platelet survival time and that platelets may, therefore, be involved in the thromboembolic complications that develop in patients with hypoxemia.

Platelet survival in patients with a Beall valve. Relation to low incidence of thromboembolism.

Recent investigations demonstrating short platelet survival time in patients with prosthetic heart valves have suggested that platelets contribute to thromboembolism in this group. New prostheses have proved less thrombogenic than those previously employed, but platelet survival studies in patients with these valves are lacking. In this study, the Beall mitral prosthesis, known to be infrequently associated with thromboembolism, was used as a model, and platelet survival time and its relation to hemolysis, thrombosis and the surface area of the disc were determined in 9 patients. Platelet survival time was normal in 6 of 9 patients, and mean survival time (6.5 ± 0.29 days) did not differ significantly from normal (6.73 ± 0.21 days; P > 0.50). Platelet survival time was inversely related to increasing disc surface area but did not correlate with the presence or degree of hemolysis. The fact that platelet abnormalities were not demonstrable in patients with Beall valves may explain the low incidence of thromboembolism in this group. Platelet survival studies may be useful for determining the thrombogenic potential of valvular prostheses and for evaluating newer prosthetic materials and designs.

Altered platelet function in patients with prosthetic mitral valves: Effects of sulfinpyrazone therapy

Platelet survival time and platelet adhesiveness and aggregation were examined in 16 patients with prosthetic mitral valves. Subsequently, nine patients were treated with sulfinpyrazone in doses of 400 mg and 800 mg/day, and the studies were repeated after a treatment period of 5 to 8 weeks. 51Chromium survival time was shortened in 15 of 16 patients, and the mean value for the entire group was 5.49 + 0.23 days (normal, 6.73 + 0.21 days; P < 0.001). Mean platelet adhesiveness in glass bead columns was 53 + 5% (normal, 30 to 60%). Platelet aggregation (turbidometric technic of Born) was normal. Treatment with 400 mg of sulfinpyrazone daily reduced platelet adhesiveness to 40 5% (P < 0.05), but effected no change in platelet survival time or platelet aggregation. Therapy with 800 mg of sulfinpyrazone daily corrected platelet survival time to normal, 6.68 + 0.57 days (P < 0.01), but it produced no further decrease in adhesiveness and no change in aggregation. It is concluded that platelet abnormalities regularly occur in patients with prosthetic mitral valves and may contribute to thromboembolism in this group. Platelet survival time is a more sensitive measure of altered platelet kinetics than platelet adhesiveness or platelet aggregation. Therapy with 800 mg of sulfinpyrazone per day corrects demonstrated abnormalities and may be useful for prevention of thromboembolism in patients with prosthetic mitral valves.