Acute coronary syndrome, including myocardial infarction, can occur as a result of ischaemia-reperfusion injury caused by acute occlusion of the coronary vessel/s following the rupture of an atherosclerotic plaque. Superimposed thrombosis at the lesion obstructs blood supply to the myocardium causing myocardial necrosis and ischaemic inflammation. Although not fully described, researchers believe that this process is initiated by a dysfunctional endothelium that activates the nearby leukocytes in the blood stream, thus attracting them to the arterial wall and initiating a cascade of complex mechanisms that lead to myocardial infarction. Interestingly, this process is two sided as the leaking soluble factors from a damaged and/or necrotic myocardium enter the systemic circulation, activating the innate and adaptive cell-mediated immune responses, which include increasing cytotoxic mediators. We hypothesize that this unwanted side effect of increase in proinflammatory mediators can lead to harmful systemic immune reactions directed towards various dysfunctional endothelia. Additionally, a strong inflammatory response, caused by myocardial damage, can impair ventricular function, on top of baseline necrosis. To evaluate this hypothesis, we propose to use in vivo tests to measure endothelial dysfunction, as well as ventricular dysfunction by ultrasound methods, and their correlation with immunological and/or biochemical parameters. These tests will be useful in assessing the risk and therapeutic outcome in patients with acute coronary syndrome.