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INTRODUCTION

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  • Acute coronary syndrome (ACS) includes all syndromes compatible with acute myocardial ischemia resulting from imbalance between myocardial oxygen demand and supply.

  • ACS is classified according to electrocardiographic (ECG) changes into: (1) ST-segment-elevation myocardial infarction (STEMI) or (2) non–ST-segment-elevation ACS (NSTE-ACS), which includes non–ST-segment-elevation MI (NSTEMI) and unstable angina (UA).

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PATHOPHYSIOLOGY

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  • Endothelial dysfunction, inflammation, and formation of fatty streaks contribute to development of atherosclerotic coronary artery plaques.

  • With rupture of an atherosclerotic plaque, exposure of collagen and tissue factor induces platelet adhesion and activation, promoting release of adenosine diphosphate (ADP) and thromboxane A2 from platelets, leading to vasoconstriction and platelet activation. A change in the conformation of the glycoprotein IIb/IIIa surface receptors of platelets occurs that cross-links platelets to each other through fibrinogen bridges.

  • Simultaneously, activation of the extrinsic coagulation cascade occurs as a result of exposure of blood to the thrombogenic lipid core and endothelium, which are rich in tissue factor. This leads to formation of a fibrin clot composed of fibrin strands, cross-linked platelets, and trapped red blood cells.

  • Subtypes of MI are based on etiology:

    • ✓ Type 1: Rupture, fissure, or erosion of an atherosclerotic plaque (90% of cases);

    • ✓ Type 2: Reduced myocardial oxygen supply or increased demand in the absence of a coronary artery process;

    • ✓ Type 3: MI resulting in death without the possibility of measuring biomarkers;

    • ✓ Type 4: MI associated with percutaneous coronary intervention (PCI; Type 4a) or stent thrombosis (Type 4b); and

    • ✓ Type 5: MI associated with coronary artery bypass graft (CABG) surgery.

  • Ventricular remodeling after MI is characterized by left ventricular (LV) dilation and reduced pumping function, leading to heart failure (HF).

  • Complications of MI include cardiogenic shock, HF, valvular dysfunction, arrhythmias, pericarditis, stroke secondary to LV thrombus embolization, venous thromboembolism, LV free-wall or septal rupture, aneurysm formation, and ventricular and atrial tachyarrhythmias.

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CLINICAL PRESENTATION

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  • The predominant symptom is midline anterior chest pain (usually at rest), severe new-onset angina, or increasing angina that lasts at least 20 minutes. Discomfort may radiate to the shoulder, down the left arm, to the back, or to the jaw. Accompanying symptoms may include nausea, vomiting, diaphoresis, and shortness of breath.

  • No specific features indicate ACS on physical examination. However, patients with ACS may present with signs of acute decompensated HF or arrhythmias.

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DIAGNOSIS

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  • Obtain 12-lead ECG within 10 minutes of presentation. Key findings indicating myocardial ischemia or MI are STE, ST-segment depression, and T-wave inversion. Appearance of a new left bundle-branch block with chest discomfort is highly specific for acute MI. Some patients with myocardial ischemia have no ECG changes, so biochemical markers and other risk factors for coronary artery disease (CAD) should be assessed.

  • Diagnosis of MI is confirmed with detection of rise and/or fall of cardiac biomarkers (mainly troponin T or I) with at least one value above the 99th percentile of ...

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