A 54-year-old homeless man comes to the emergency department 24 hours after the onset of substernal chest pain and is diagnosed with an anterior wall myocardial infarction. The patient has no history of hypertension or diabetes mellitus and has had no previous chest pain, dyspnea, palpitations, syncope, or leg swelling. He has a 40-pack-year smoking history. Echocardiography shows normal left ventricular size and left ventricular anterior wall hypokinesis, as well as an ejection fraction of 40%. The patient refuses pharmacologic therapy on discharge and is scheduled for an outpatient clinic visit but never shows up. Two years later, the patient is found dead in the street. Autopsy reveals a dilated left ventricle with a globular shape and thinned walls with a scar on the anterior wall. Which of the following would most likely have helped prevent this patient's pathologic findings?

Question

A 54-year-old homeless man comes to the emergency department 24 hours after the onset of substernal chest pain and is diagnosed with an anterior wall myocardial infarction.  The patient has no history of hypertension or diabetes mellitus and has had no previous chest pain, dyspnea, palpitations, syncope, or leg swelling.  He has a 40-pack-year smoking history.  Echocardiography shows normal left ventricular size and left ventricular anterior wall hypokinesis, as well as an ejection fraction of 40%.  The patient refuses pharmacologic therapy on discharge and is scheduled for an outpatient clinic visit but never shows up.  Two years later, the patient is found dead in the street.  Autopsy reveals a dilated left ventricle with a globular shape and thinned walls with a scar on the anterior wall.  Which of the following would most likely have helped prevent this patient's pathologic findings?

Quizplus · Accepted Answer

This patient's myocardial infarction (MI) 2 years ago resulted in left ventricular (LV) systolic dysfunction, and autopsy shows a dilated left ventricle with thinned walls and evidence of scarring. These findings are consistent with eccentric hypertrophy due to ischemic heart disease. Both infarction and LV systolic dysfunction induce deleterious cardiac remodeling with pathologic cardiomyocyte hypertrophy and collagen deposition; these changes commonly progress to cause severe LV systolic dysfunction and create an increased risk for fatal cardiac arrhythmia (eg, ventricular tachycardia or fibrillation), which was the likely cause of death in this patient. eccentric hypertrophy Cardiac remodeling is mostly driven by neurohormonal pathways, including the renin-angiotensin-aldosterone pathway; inhibition of this pathway with an ACE inhibitor (eg, enalapril, lisinopril) has been shown to reduce cardiac remodeling and improve survival in patients who have had MI, especially those with an LV ejection fraction of ≤40% and/or anterior wall MI. Cardioselective beta blockers (eg, metoprolol) have demonstrated similar benefit in all patients following MI, likely through inhibition of sympathetically driven cardiac remodeling pathways. Aldosterone antagonists (eg, spironolactone) have shown survival benefit in patients with MI and LV ejection fraction of ≤40%. (Choice A) Dihydropyridine calcium channel blockers (eg, amlodipine) are appropriate for treating hypertension and may reduce a component of cardiac remodeling that is stimulated by increased LV pressure load. However, these drugs have not shown the degree of survival benefit following MI that ACE inhibitors and other neurohormonal-inhibiting drugs have shown. (Choice B) Anticoagulation agents (eg, apixaban) are not routinely used following MI. These are appropriate to prevent systemic embolization (eg, stroke) in patients with LV aneurysm and mural thrombus, of which this patient has no evidence on autopsy. (Choice C) Low-dose aspirin is beneficial for secondary prevention of further cardiovascular events in patients who have had MI, but it is not known to benefit cardiac remodeling. (Choice E) Isosorbide dinitrate is useful in treating symptomatic angina, but it has not shown survival benefit following MI. (Choice F) P2Y12 inhibitors (eg, prasugrel, clopidogrel), in combination with aspirin, have been shown to reduce cardiovascular events within the first year after MI; however, these drugs do not reduce cardiac remodeling. Educational objective: Following myocardial infarction (MI), deleterious cardiac remodeling is mostly driven by neurohormonal mechanisms. ACE inhibitors (eg, enalapril, lisinopril), cardioselective beta blockers (eg, metoprolol), and aldosterone antagonists (eg, spironolactone) improve survival following MI, likely due to inhibition of neurohormonal-mediated cardiac remodeling. References: Effect of ramipril on morbidity and mode of death among survivors of acute myocardial infarction with clinical evidence of heart failure. A report from the AIRE Study Investigators. (http://www.ncbi.nlm.nih.gov/pubmed/9049514)

A 54-Year-Old Homeless Man Comes to the Emergency Department 24