ST-segment elevation myocardial infarction (STEMI) is an acute cardiac condition characterized by myocardial necrosis due to prolonged ischemia, caused by the complete and persistent occlusion of a coronary artery. This is a medical emergency that requires immediate treatment to reduce mortality and prevent long-term complications.
Pathogenesis and Pathophysiology
The pathophysiological mechanism of STEMI is related to the rupture or erosion of an unstable atherosclerotic plaque, which leads to the formation of an occlusive thrombus within the coronary vessel. The total obstruction of blood flow causes ischemic injury of the myocardium downstream from the occlusion, resulting in myocyte necrosis.
The ischemic cascade involves several stages:
Ischemia: reduction in oxygen supply with metabolic and functional alterations.
Myocardial injury: progressive cellular damage with loss of contractile function.
Necrosis: irreversible cell death if reperfusion does not occur promptly.
The extent of the damage depends on several factors, including the duration of occlusion, the presence of collateral circulation, and the individual response to ischemia.
Clinical Presentation
The main symptom of STEMI is acute chest pain, often described as severe retrosternal pressure, which may radiate to the left arm, jaw, back, or upper abdomen. The pain lasts more than 20 minutes and does not subside with rest or nitroglycerin.
Other associated symptoms may include:
Dyspnea, profuse sweating, and pallor.
Nausea and vomiting, more frequent in diabetic and elderly patients.
Palpitations or syncope in case of arrhythmias.
Signs of acute heart failure in the most severe cases.
Diagnosis
The diagnosis of STEMI is based on three key elements:
Electrocardiogram (ECG)
The ECG is the first-line diagnostic test and should be performed within 10 minutes of arrival at the emergency department. The main diagnostic criterion is persistent ST-segment elevation in at least two contiguous leads, indicating acute coronary occlusion.
Cardiac biomarkers
High-sensitivity troponins are the gold standard for confirming myocardial necrosis. In the early phase, levels may be normal, so repeat testing after a few hours is necessary.
Cardiac imaging
Echocardiography is useful for detecting regional wall motion abnormalities, assessing ventricular ejection fraction, and identifying complications such as pericardial effusion.
Treatment
The goal of STEMI treatment is to restore coronary blood flow as quickly as possible to limit the extent of myocardial necrosis.
1. Myocardial revascularization
The therapy of choice is primary angioplasty with stent implantation, ideally performed within 90–120 minutes from symptom onset. If not available, fibrinolytic therapy is used, effective only within the first 12 hours.
2. Pharmacological therapy
Medical management includes:
Antiplatelet agents: aspirin and P2Y12 inhibitors.
Anticoagulants: unfractionated heparin or enoxaparin.
The prognosis of STEMI depends on the promptness of treatment. In patients who undergo early revascularization, in-hospital mortality is less than 5%, while in untreated cases it may exceed 20%. Secondary prevention, based on the control of cardiovascular risk factors and adherence to pharmacological therapy, is essential to reduce the risk of recurrence.
References
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