A 60-year-old man is brought to the emergency department due to 2 weeks of progressive exertional dyspnea and fatigue. He has difficulty falling asleep and can hardly walk to the bathroom without becoming short of breath. The patient has had no chest pain, syncope, cough, or extremity edema. Two months ago, he was hospitalized with an anterior wall myocardial infarction but was not revascularized due to late presentation. The patient was discharged home with aspirin, clopidogrel, metoprolol, lisinopril, and atorvastatin. Temperature is 36.6 C (97.9 F), blood pressure is 100/67 mm Hg, and pulse is 67/min and regular. Examination shows bilateral crackles in the lower lung fields. The apical impulse is displaced to the left. A faint systolic murmur is heard over the apex. ECG reveals normal sinus rhythm and deep Q waves in leads I, aVL, and V2-V5, with a 2-mm ST-segment elevation; the ECG tracings are unchanged compared to those at discharge 2 months ago. Which of the following is the most likely underlying cause of this patient's symptoms?

Question

A 60-year-old man is brought to the emergency department due to 2 weeks of progressive exertional dyspnea and fatigue.  He has difficulty falling asleep and can hardly walk to the bathroom without becoming short of breath.  The patient has had no chest pain, syncope, cough, or extremity edema.  Two months ago, he was hospitalized with an anterior wall myocardial infarction but was not revascularized due to late presentation.  The patient was discharged home with aspirin, clopidogrel, metoprolol, lisinopril, and atorvastatin.  Temperature is 36.6 C (97.9 F), blood pressure is 100/67 mm Hg, and pulse is 67/min and regular.  Examination shows bilateral crackles in the lower lung fields.  The apical impulse is displaced to the left.  A faint systolic murmur is heard over the apex.  ECG reveals normal sinus rhythm and deep Q waves in leads I, aVL, and V2-V5, with a 2-mm ST-segment elevation; the ECG tracings are unchanged compared to those at discharge 2 months ago.  Which of the following is the most likely underlying cause of this patient's symptoms?

Quizplus · Accepted Answer

11ec25c8_d359_b0e9_bc81_15d55916a64b_MD0003_00 This patient likely has progressive decompensated heart failure due to a left ventricular (LV) aneurysm, which is a delayed complication of transmural (ST-elevation) myocardial infarction (MI) resulting from scarring and fibrosis of a large portion of the LV wall. It most commonly complicates anterolateral MI affecting the perfusion field of the left anterior descending artery. anterolateral MI ST-segment elevation on ECG usually normalizes within a few weeks of MI. LV aneurysm presents with ECG findings of persistent ST-segment elevation and deep Q waves in the same leads. Large LV aneurysm can lead to progressive LV enlargement, causing heart failure, refractory angina, ventricular arrhythmias, and mitral annular dilation with secondary mitral regurgitation (explaining this patient's murmur). A mural thrombus can also develop within the aneurysm, creating risk of systemic arterial embolization (eg, stroke). The diagnosis is confirmed by echocardiography showing a thinned, dyskinetic LV wall in the area of the prior MI. ECG findings (Choices A and C) Acute pericarditis, which can present in the first several days after MI, can cause diffuse ST-segment elevation. Postcardiac injury syndrome (Dressler syndrome), an immune-mediated pericarditis, can occur weeks to months after MI. This patient does not have features of pericarditis (eg, pleuritic chest pain, fever, pericardial friction rub) or an associated pericardial effusion. (Choice B) Papillary muscle rupture, a mechanical complication typically occurring acutely or within 3-5 days after MI, usually presents dramatically with acute, severe mitral regurgitation (eg, hypotension, pulmonary edema, cardiogenic shock). (Choice D) Recurrent ischemia is a consideration with ST-segment elevation, but is less likely as this patient has no chest pain and ECG tracings are unchanged since the MI. (Choice E) Right ventricular infarction typically involves ischemic changes in the inferior ECG leads (II, III, and aVF). It causes acute right ventricular failure and usually presents with hypotension, elevated jugular venous pressure, and clear lung fields. (Choice G) LV free wall rupture is a potential complication of transmural MI, usually occurring within 5 days (but can occur up to 2 weeks) following the event. Affected patients rapidly develop cardiac tamponade with abrupt-onset hypotension, shock, and often cardiac arrest. Educational objective: Left ventricular (LV) aneurysm occurs as a late complication of transmural (ST-segment elevation) myocardial infarction. ECG typically reveals persistent ST-segment elevation along with deep Q waves. Progressive LV enlargement can cause heart failure, refractory angina, ventricular arrhythmias, and secondary mitral regurgitation, and patients can develop a mural thrombus with risk of systemic arterial embolization. References: Electrocardiographic ST segment elevation: left ventricular aneurysm. (http://www.ncbi.nlm.nih.gov/pubmed/11992347) Left-ventricular aneurysms: from disease to repair. (http://www.ncbi.nlm.nih.gov/pubmed/15853602)

A 60-Year-Old Man Is Brought to the Emergency Department Due