Enhanced Expression of CD40L and MCP-1 in Acute Myocardial Infarction: A Study on Patients with Type II Diabetes Mellitus

Acute myocardial infarction is one of the consequences of complete coronary artery occlusion which is commonly diagnosed by measuring markers of cardiac necrosis. These markers reflect the extent of cardiac damage but failed to provide direct information about plaque disruption or platelet activation. Because the outcome of acute myocardial infarction is highly dependent on inflammation and thrombosis, it is possible that assessment of these two processes will allow better information about plaque instability. Patients with type II diabetes mellitus have a high risk of myocardial infarction (MI) than non diabetic patients. The aim of this work was to study the established link between thrombosis and inflammation represented by CD40L expression on platelets and Monocyte chemotatic protein 1 (MCP-1) expression on monocytes respectively. Flowcytometric detection of CD40L and MCP- 1 expression was carried out on 60 patients presenting with MI which were further subdivided to 30 diabetic patients and 30 non diabetic patients in addition to 20 healthy subjects. CD40 L and MCP-1 expression were significantly higher in all patients compared to control group (p=0.0001); with a higher level in diabetic patients compared to non diabetics yet not reaching a significant level. Regarding diabetic patients there was a significant positive correlation between CD40L expression and some cardiovascular risk factors as admission hyperglycemia and a significant negative correlation with Ejection Fraction (EF%) and left ventricular diastolic function represented by E/A ratio. Similarly MCP-1 level was significantly positively correlated with some cardiovascular risk factors as glycosylated hemoglobin level. A stepwise multiple logistic regression analysis was done to test whether CD40L and MCP1 were associated independently with cardiovascular risk factors thus increasing risk of developing MI; where CD40L was associated with glycosylated hemoglobin, MCP- land EF% while MCP-1 was associated with admission blood glucose, glycosylated hemoglobin level and CD40L. Regarding non diabetic patients there was a significant positive correlation between CD40L expression and some cardiovascular risk factors as hypertension. CD40L expression showed a significant negative correlation with EF%. MCP-1 was significantly positively correlated with glycosylated hemoglobin level and significantly negatively correlated with E/A ratio. CD40L was associated independently with total cholesterol, MCP-1 and EF% while MCP-1 was associated with glycosylated hemoglobin level, EF% and CD40L. In conclusion increased expression of CD40L and MCP-1 are encountered in patients with MI especially in the presence of other risk factors; they may be used as valuable markers for risk stratification of patients more liable to develop MI together with becoming important therapeutic targets.