Physical activity and the risk of acute myocardial infarction

The relationship between physical activity and acute myocardial infarction (AMI) was examined in a case-control study conducted in Italy in 1988 to 1989 within the framework of the GISSI-2 trial of streptokinase versus alteplase and heparin versus no heparin in the treatment of AMI. A total of 916 case patients admitted to coronary care units from various Italian regions for AMI were interviewed. Control subjects were 1106 patients admitted to the same network of hospitals for a broad spectrum of acute diseases not related to known or potential risk factors for myocardial infarction. Among various types of physical activity (occupational activity, walking, stair climbing, and sport and leisure-time physical activity), occupational physical exercise emerged as the most protective. Multivariate odds ratios (ORs) were 1.4 (95% confidence interval (CI), 1.0 to 2.0) and 1.6 (95% CI, 1.2 to 2.1) for the two lowest levels of occupational physical activity. The trends of increasing risk with decreasing activity were consistent, although less strong, when other types of activity were considered. The protection conveyed by occupational physical activity was similar across various strata of sex, age, education, smoking habits, and diabetes, and was not explained by serum cholesterol, body weight, or hypertension. This study therefore confirms that low physical activity is an indicator of subsequent risk of AMI

PTX3, A Prototypical Long Pentraxin, Is an Early Indicator of Acute Myocardial Infarction in Humans

Background: Inflammation is an important component of ischemic heart disease. PTX3 is a long pentraxin whose expression is induced by cytokines in endothelial cells, mononuclear phagocytes, and myocardium. The possibility that PTX3 is altered in patients with acute myocardial infarction (AMI) has not yet been tested. Methods and results: Blood samples were collected from 37 patients admitted to the coronary care unit (CCU) with symptoms of AMI. PTX3 plasma concentrations, as measured by ELISA, higher than the mean+2 SD of age-matched controls (2.01 ng/mL) were found in 27 patients within the first 24 hours of CCU admission. PTX3 peaked at 7.5 hours after CCU admission, and mean peak concentration was 6.94+/-11.26 ng/mL. Plasma concentrations of PTX3 returned to normal in all but 3 patients at hospital discharge and were unrelated to AMI site or extent, Killip class at entry, hours from symptom onset, and thrombolysis. C-reactive protein peaked in plasma at 24 hours after CCU admission, much later than PTX3 (P64 years old and women had significantly higher PTX3 concentrations at 24 hours (P<0.05). PTX3 was detected by immunohistochemistry in normal but not in necrotic myocytes. Conclusions: PTX3 is present in the intact myocardium, increases in the blood of patients with AMI, and disappears from damaged myocytes. We suggest that PTX3 is an early indicator of myocyte irreversible injury in ischemic cardiomyopathy

PTX3, A prototypical long pentraxin, is an early indicator of acute myocardial infarction in humans

Background: Inflammation is an important component of ischemic heart disease. PTX3 is a long pentraxin whose expression is induced by cytokines in endothelial cells, mononuclear phagocytes, and myocardium. The possibility that PTX3 is altered in patients with acute myocardial infarction (AMI) has not yet been tested. Methods and results: Blood samples were collected from 37 patients admitted to the coronary care unit (CCU) with symptoms of AMI. PTX3 plasma concentrations, as measured by ELISA, higher than the mean+2 SD of age-matched controls (2.01 ng/mL) were found in 27 patients within the first 24 hours of CCU admission. PTX3 peaked at 7.5 hours after CCU admission, and mean peak concentration was 6.94+/-11.26 ng/mL. Plasma concentrations of PTX3 returned to normal in all but 3 patients at hospital discharge and were unrelated to AMI site or extent, Killip class at entry, hours from symptom onset, and thrombolysis. C-reactive protein peaked in plasma at 24 hours after CCU admission, much later than PTX3 (P64 years old and women had significantly higher PTX3 concentrations at 24 hours (P<0.05). PTX3 was detected by immunohistochemistry in normal but not in necrotic myocytes. Conclusions: PTX3 is present in the intact myocardium, increases in the blood of patients with AMI, and disappears from damaged myocytes. We suggest that PTX3 is an early indicator of myocyte irreversible injury in ischemic cardiomyopathy