AND THE ANSWER:
A. Acute myocardial infarction complicated by ventricular septal defect (VSD)
This patient has risk factors for coronary heart disease including diabetes, hypertension, and hyperlipidemia. Her history of atypical angina symptoms (nausea, fatigue, chest pressure at rest) in combination with territorial q-waves / ST elevations, and positive biomarkers for myocardial necrosis is highly suggestive of anteroseptal acute myocardial infarction (MI). In this case, a thorough physical examination is crucial, as this patient has also suffered a rare and devastating “mechanical complication” to acute MI: rupture of the ventricular septum. Classic risk factors for VSD after MI, which are present in this case, include female sex, age >60, hypertension, and late-presentation. Auscultation of a new systolic murmur (especially holosystolic) in the setting of a recent acute MI is concerning for VSD or papillary muscle rupture resulting in acute mitral regurgitation. These two mechanical complications can be difficult to differentiate on physical examination but the murmur of mitral regurgitation is often best heard at the apex and radiates to the axilla, which was not found in this case. A VSD is best heard at the 3rd, 4th, and 5th interspaces at the left sternal border. Acute mitral regurgitation often results in significant pulmonary edema and hypoxemia, whereas this patient’s pulmonary findings were mild. Furthermore, acute MR is seen more often in inferior wall MI given the posteromedial papillary muscle’s dependence on a single blood supply. This patient’s anteroseptal EKG changes suggestive of ischemia in that territory make papillary muscle rupture less likely.
The murmur of aortic stenosis is best heard at the right 2nd interspace and is crescendodecrescendo with radiation to the carotids, characteristics not present in this case. Aortic stenosis is a progressive condition over many years and has neither an acute onset nor direct result from MI. LV free wall rupture is also a devastating mechanical complication to acute myocardial infarction but this is not associated with a new holosystolic murmur. This patient’s echocardiogram with Doppler studies confirmed the presence of a new anteroapical VSD 0.6cm in size with anteroseptal and apical wall motion abnormality and decreased systolic function (EF: 35%). New LV dysfunction (due to MI) explains her symptoms of heart failure (dyspnea on exertion and rales) and the signs of heart failure (elevated JVP with lower extremity edema). Mild CHF is further supported by the X-ray findings and elevated proBNP level. This patient refused aggressive interventions (including cardiac catheterization) and she died within several days of progressive cardiogenic shock despite medical therapy.