3-vessel coronary disease and an acute event | Figure 1

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3-vessel coronary disease and an acute event

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A 56 year-old man with a history significant for hypertension and hyperlipidemia reported to the emergency department with rapid onset of severe, pressure like chest pain radiating to his left arm and jaw that was accompanied by diaphoresis, and lightheadedness. On examination, he was hypotensive, tachycardic and diaphoretic with cool extremities and raised jugular venous pressure. ECG was characterised by massive anterior ST-segment elevation consistent with acute anterior wall infarct. Cardiogenic shock persisted, despite early resuscitative therapy with intravenous fluids and vasopressors.

The patient had urgent coronary angiography, which demonstrated a severe multivessel disease. The LAD had 100% stenosis, left main coronary artery 90% stenosis and circumflex artery 75% stenosed. An emergency percutaneous coronary intervention was performed in the LAD and left main arteries, with balloon angioplasty followed by insertion of drug-eluting stents. Following the procedure, the patient was transferred to the coronary care unit with inotropic and vasodilator support, dual antiplatelet therapy, anticoagulation and full medical management.

His hemodynamic condition continued to improve over the following 7 days, and he regained some left ventricular function. A repeat echocardiogram 2 weeks after the procedure showed an ejection fraction of 38% with multifocal areas of myocardial dyskinesis and akinesis in anterior and apical segments. He was clinically improved with persistent fatigue and mild exercise dyspnea, but otherwise continued to ambulate well and he advanced to formal cardiac rehabilitation.

The patient continued to improve functionally after 1 month of intensive rehabilitation and medical treatment. His ejection fraction was improved to 45% and he could climb a few steps of stairs without dyspnea or chest pain. On repeat echocardiography, there was no change in EF, but mild diastolic noncompliance with post-infarction ventricular remodeling were documented. Lifelong follow-up was scheduled to maximize medical therapy, assess recovery of ventricular function and minimize risk for recurrent ischemic events.

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Cardiogenic shock

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