We studied the relationship of cigarette smoking to the severity of coronary and thoracic aortic atherosclerosis in 116 men who received coronary angiography and transesophageal echocardiography. Severity of coronary atherosclerosis was assessed in terms of Gensini’s score (GS), and that of thoracic aortic atherosclerosis was assessed by the average sclerotic length (ASL) and average sclerotic area (ASA). The plasma fibrinogen levels were significantly positively correlated with smoking, and fasting blood sugar levels tended to be positively associated with smoking. GS was inversely associated with serum levels of high density lipoprotein (HDL) cholesterol. ASL and ASA were positively associated with age, fasting blood sugar levels and plasma fïbrinogen levels, and these associations were statistically significant. Analysis of covariance was used to examine the net association between cigarette smoking and GS, ASL or ASA controlling for age, total cholesterol, HDL cholesterol, fasting blood sugar and plasma fibrinogen. We found that GS, ASL and ASA were all significantly increased with increasing number of cigarette years. Additional adjustment for other risk factors (triglyceride, uric acid, body mass index, alcohol use and hypertension) also showed a strong independent contribution of smoking to GS, ASL and ASA. We concluded that the cumulative exposure to cigarette smoking was an independent indicator of the severity of coronary atherosclerosis as well as thoracic aortic atherosclerosis.

The authors evaluated elements of the coagulation and fibrinolytic systems in 18 male patients with intermittent claudication vs 19 men matched for risk factors who served as controls. Prothrombin time and activated partial thromboplastin time did not significantly differ in the patients and the controls. The plasminogen level in the two groups was not significantly different. The level of lipoprotein(a) was significantly higher in the patients than in the controls. The levels of antigen and the activity of protein C did not differ significantly between the two groups. The thrombomodulin level was significantly higher in the patients than in the controls. There were no significant differences between the two groups in the levels of alpha 2-macroglobulin, C1-inactivator, or antithrombin III. The levels of fibrinogen and alpha 1-antitrypsin were significantly higher in the patients vs the controls. Significantly lower levels of alpha 2-plasmin inhibitor and higher levels of alpha 2-plasmin inhibitor/plasmin complex and thrombin/antithrombin III complex were found in the patients vs the controls. These findings suggest that the levels of thrombin/antithrombin III complex, alpha 2-plasmin inhibitor/plasmin complex, and thrombomodulin may perhaps serve as indicators for injury to the peripheral endothelium and that the coagulation and fibrinolytic systems may be activated in patients with intermittent claudication.

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Cycloadditions of 2-diphenylphosphinoyl-2-methyl-3,4-dihydro-2H-pyrrole N-oxide (DPhPMPO), 3,4-dihydro-2H-pyrrole N-oxide having a diphenylphosphinoyl group at the C2 position with thioketones afforded the corresponding 1,4,2-oxathiazolidines. Dissociation constants of these 5-membered ring products were determined. The cycloadducts were stabilized by the diphenylphosphinoyl group. The reaction of DPhPMPO with di-tert-butyl selenoketone gave the corresponding selenoamide under microwave irradiation. The formation of the selenoamide indicated that the cycloaddition of DPhPMPO with the selenoketone analogue also proceeded through the formation of the corresponding 5-membered ring product.

Although endothelial dysfunction is associated with cardiovascular risk factors and is improved by choles