Coronary angiography and right heart catheterization in a 56-year-old male with DKA and NSTEMI revealed an occlusion MI and a post-infarct VSD with an O2 saturation step-up from 56% to 89%.
Case Report (n=1)
This case highlights the importance of avoiding anchoring bias on supply-demand mismatch in DKA and maintaining a high index of suspicion for occlusion MI and mechanical complications like VSD.
Introduction: Ventricular septal defect (VSD) is a rare but fatal complication of acute myocardial infarction (MI), resulting from a full-thickness injury to the myocardium. The incidence is ~0.21% in ST elevation MI (STEMI) and ~0.04% in non-STEMI (NSTEMI) cases. The prognosis is poor, with 70-80% mortality within 2 weeks of diagnosis. This case illustrates the diagnostic complexity of concurrent metabolic and cardiovascular emergencies. Description: A 56-year-old African American male with type 2 diabetes mellitus, hypertension, and hyperlipidemia presented with retrosternal chest pain, nausea, vomiting, and generalized weakness for 2 days. Electrocardiogram (ECG) showed T-wave inversions in the inferior leads with troponin peaking at 9490 ng/L, indicating NSTEMI. He also had diabetic ketoacidosis (DKA) (glucose 560 mg/dL, anion gap 18.5, positive serum acetone). He was treated with aspirin, heparin, insulin, and fluids. While DKA resolved, persistent chest pain raised concern for type I NSTEMI. Initial echocardiogram revealed a hyperdynamic left ventricle with normal ejection fraction, without wall motion deficit or shunt. On day 3 of hospitalization, coronary angiography revealed a total occlusion of the proximal right coronary artery, which was successfully revascularized with two drug-eluting stents. However, persistent tachycardia and a new systolic murmur prompted further investigation. Transesophageal echocardiography on day 8 suggested apical septal wall thinning with a potential left-to-right shunt. Right heart catheterization confirmed this, with oxygen saturation increasing from 56% in the right atrium to 89% in the right ventricle. The patient underwent successful surgical repair of the VSD. Discussion: While DKA often causes Type II NSTEMI due to supply-demand mismatch, underlying coronary artery disease must be considered. Anchoring bias toward NSTEMI mechanism can delay recognition. In this patient, persistent symptoms, subtle ECG changes, and elevated troponin levels raised concern for an occlusion MI (OMI), necessitating urgent coronary angiography. This underscores the importance of the OMI paradigm, which prioritizes acute coronary occlusion over ST-segment elevation. The case further emphasizes recognizing post-infarct VSD in hemodynamically unstable post-PCI patients.
Maheshwari et al. (Sun,) conducted a case report in Ventricular septal defect complicating acute myocardial infarction with concurrent diabetic ketoacidosis (n=1). Coronary angiography and surgical repair was evaluated. Coronary angiography and right heart catheterization in a 56-year-old male with DKA and NSTEMI revealed an occlusion MI and a post-infarct VSD with an O2 saturation step-up from 56% to 89%.