A 58-year-old man with a history of hypertension and hyperlipidemia presents to the emergency department with 3 hours of acute-onset substernal chest pain radiating to his left arm. Vital signs are: BP 102/68 mmHg, HR 108 bpm, RR 20/min. Electrocardiography shows ST elevation in leads V1-V4 with reciprocal ST depression in leads II, III, and aVF. Troponin I is 2.4 ng/mL (normal <0.04). Emergent coronary angiography reveals complete occlusion of the left anterior descending (LAD) artery with TIMI 0 flow. Percutaneous coronary intervention is performed with aspiration thrombectomy and drug-eluting stent placement, successfully restoring TIMI 3 flow. However, angiography also demonstrates severe diffuse atherosclerotic disease throughout the entire LAD with multiple areas of 70-90% stenosis in non-culprit segments. Despite anatomically successful reperfusion, myocardial salvage remains limited. Which of the following best explains the primary mechanism limiting myocardial salvage in this clinical scenario?
- A)Failure to revascularize the right coronary artery and left circumflex artery
- B)Mechanical rupture of the left ventricular free wall due to transmural necrosis
- C)Microvascular dysfunction and the no-reflow phenomenonGABARITO
- D)Progressive thrombosis within the stented LAD segment despite adequate antiplatelet therapy
- E)Inadequate collateral blood flow from non-LAD coronary vessels
Explicação
The no-reflow phenomenon represents the inability to reperfuse the myocardium at the microvascular level despite restoration of epicardial TIMI 3 flow. This occurs as a result of microvascular injury from ischemia-reperfusion, distal embolization of atherothro... Ver explicação completa e trilha adaptativa →