ST-Segment Elevation Myocardial Infarction (STEMI)

Introduction

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. It is a medical emergency requiring immediate treatment to reduce mortality and prevent long-term complications.

Pathogenesis and Pathophysiology

The pathophysiology of STEMI is linked to the rupture or erosion of an unstable atherosclerotic plaque, leading to the formation of an occlusive thrombus within the coronary artery. The total obstruction of blood flow results in myocardial ischemic injury, followed by myocardial cell necrosis.

The ischemic cascade involves several phases:

• Ischemia: reduction in oxygen supply leading to metabolic and functional alterations.
• Myocardial injury: progressive cellular damage with loss of contractile function.
• Necrosis: irreversible cell death if reperfusion is not achieved promptly.

The extent of myocardial damage depends on several factors, including the duration of occlusion, the presence of collateral circulation, and the individual's ischemic response.

Clinical Presentation

The primary symptom of STEMI is acute chest pain, often described as intense retrosternal pressure, which may radiate to the left arm, jaw, back, or upper abdomen. The pain lasts more than 20 minutes and does not resolve with rest or nitroglycerin.

Other associated symptoms may include:

• Dyspnea, profuse sweating, and pallor.
• Nausea and vomiting, more common in diabetic and elderly patients.
• Palpitations or syncope in cases of arrhythmia.
• Signs of acute heart failure in severe cases.

Diagnosis

The diagnosis of STEMI is based on three fundamental criteria:

1. Electrocardiogram (ECG)

   The ECG is the first diagnostic test and should be performed within 10 minutes of emergency department arrival. The primary criterion for diagnosis is a persistent ST-segment elevation in at least two contiguous leads, indicating acute coronary occlusion.

2. Cardiac Biomarkers

   High-sensitivity troponins are the gold standard for confirming myocardial necrosis. In early stages, levels may be normal, requiring repeated testing within a few hours.

3. Cardiac Imaging

   Echocardiography helps identify wall motion abnormalities, assess left ventricular ejection fraction, and detect complications such as pericardial effusion.

Treatment

The goal of STEMI treatment is to restore coronary blood flow as quickly as possible to minimize myocardial necrosis.

1. Myocardial Revascularization

The preferred therapeutic strategy is primary percutaneous coronary intervention (PCI) with stent placement, ideally performed within 90–120 minutes of symptom onset. If PCI is unavailable, fibrinolytic therapy is considered, but it is only effective within the first 12 hours.

2. Pharmacological Therapy

Medical management includes:

• Antiplatelet agents: aspirin and P2Y12 inhibitors.
• Anticoagulants: unfractionated heparin or enoxaparin.
• Beta-blockers: reduce myocardial oxygen consumption.
• ACE inhibitors: improve prognosis by reducing ventricular remodeling.
• Statins: stabilize atherosclerotic plaques.

Complications

The risk of post-infarction complications is high and includes:

• Ventricular arrhythmias (ventricular fibrillation, ventricular tachycardia).
• Cardiogenic shock with acute ventricular failure.
• Post-infarction heart failure.
• Myocardial wall rupture or ventricular aneurysm.

Prognosis

The prognosis of STEMI depends on the timeliness of treatment. In patients undergoing early revascularization, in-hospital mortality is less than 5%, whereas in untreated cases, it can exceed 20%. Secondary prevention, focusing on cardiovascular risk factor control and adherence to medical therapy, is essential to reduce recurrence risk.

Bibliografia
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