A 56-year-old man comes to the office due to exertional dyspnea for the past month. He has great difficulty walking half a block without experiencing shortness of breath. He also has palpitations, dry cough, and lower extremity swelling. He has no chest pain, lightheadedness, or syncope. The patient was hospitalized 4 months ago for myocardial infarction after having 2 days of chest pain. He also has a history of hypertension, type 2 diabetes mellitus, hyperlipidemia, intermittent asthma, and gout. He is a current smoker with a 35-pack-year history. His father suffered a myocardial infarction at age 50 and died of heart disease at age 55. Blood pressure is 144/86 mm Hg, pulse is 72/min, and oxygen saturation is 96% on room air. BMI is 32 kg/m2. He does not appear to be in acute distress. Physical examination shows distended jugular veins while sitting up. Bibasilar crackles are heard on lung auscultation. There is moderate lower extremity pitting edema. ECG performed in the office is shown in the exhibit. Which of the following is the most likely diagnosis?
Left ventricular aneurysm | |
Etiology |
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Clinical presentation |
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Diagnosis |
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MI = myocardial infarction. | |
This patient has developed heart failure likely due to a left ventricular aneurysm. Ventricular aneurysm is a late complication of myocardial infarction (MI) that can occur up to several months following a transmural (ST elevation) MI; a delay in coronary reperfusion increases the risk. The healing process following MI results in replacement of necrosed myocardium with fibrous scar tissue, which in the case of a large MI can result in convexity of a large portion of the left ventricular wall (most commonly in the perfusion field of the left anterior descending artery). The aneurysm is dyskinetic with the remaining healthy ventricular wall, resulting in impaired ejection fraction.
Although heart failure (eg, jugular venous distension, pulmonary crackles) is the most common presentation, angina may also occur due to increased oxygen demand caused by elevated wall stress in the setting of an enlarged left ventricle. Ventricular arrhythmia or systemic embolization (due to mural thrombus inside the aneurysm) is possible as well. Classical ECG findings include persistent ST-segment elevation and deep Q waves in the leads corresponding to the previous MI, and diagnosis is confirmed by echocardiogram showing a thinned and dyskinetic myocardial wall.
(Choice A) Post-cardiac injury syndrome (Dressler syndrome) is an immune-mediated pericarditis that may occur several weeks or months following MI, often with accompanying pericardial effusion. Large pericardial effusion can cause tamponade; however, hypertension and evidence of pulmonary edema (typically absent in tamponade) make tamponade extremely unlikely. The persistent ST-segment elevation and deep Q waves suggest ventricular aneurysm.
(Choice C) Pulmonary embolism (PE) usually causes pleuritic chest pain, dyspnea, and hypoxemia. ECG abnormalities (eg, sinus tachycardia, ST and T-wave changes) are usually nonspecific. Absence of tachycardia or significant hypoxemia makes PE unlikely.
(Choice D) Right ventricular infarction presents with hypotension, elevated jugular venous pressure, and clear lung fields, with ECG findings of ST-segment elevation in the inferior leads (II, III, aVF). Evidence of pulmonary edema makes right ventricular infarction less likely.
(Choice E) An acquired ventricular septal defect can occur as a mechanical complication of MI, typically 3-5 days post-infarction. Patients have sudden-onset hypotension and biventricular failure. Presentation several months following MI would be extremely unusual.
Educational objective:
Ventricular aneurysm occurs as a late complication (ie, several months) following transmural myocardial infarction, and is suggested by ECG demonstrating persistent ST-segment elevation with deep Q waves. Patients most commonly have progressive left ventricular enlargement and dyskinetic wall motion leading to heart failure.