Disruption of vulnerable or high-risk plaques is the common pathophysiological mechanism of acute coronary syndromes with or without ST elevation. The reflection of the same pathophysiological mechanism differs in non-ST-elevation acute coronary syndromes and ST-elevation myocardial infarction (STEMI) in terms of clinical presentation, prognosis and therapeutic approach. Diagnostic and therapeutic evolution had come along together from the beginning of the acute myocardial infarction (MI) concept. Pathological appearance of acute MI is classified as acute, healing and healed phases as a time related phenomenon. Clinical presentation of STEMI, is different than the other ischaemic cardiac events with the sudden onset, the duration and the severity of chest pain or discomfort. Although the old markers creatine kinase and the MB fraction, lactate dehydrogenase are also used for the diagnosis of acute MI, cardiac troponins are very sensitive and specific, and myoglobin is an early marker for acute MI. In electrocardiogram; new or presumed new ST segment elevation at the J point in two or more contiguous leads or Q wave in established MI are typical changes. Echocardiographic or nuclear techniques have been used widely to rule out or confirm STEMI. In conclusion; all clinical, pathological, biochemical, electrocardiographic analysis methods and new imaging techniques have their own unique contribution for evaluating STEMI.