Virginia Research Day 2021

Medical Resident Research Case Reports

03 COVID-19 Fears May Be Worse Than the Virus: A Case of Cardiogenic Shock Secondary to Post-Myocardial Infarction Ventricular Septum Rupture

Salem Gaballa; Kyaw Hlaing; Jane Lindsay; Avan Aljaf; Kashyap Patel; Asamoah Owusu; Safa Moursy; Ameenjamal Ahmed; Brijesh Patel Corresponding author: Salem.gaballa@hcahealthcare.com

LewisGale Medical Center-Salem

Introduction: Ventricular septal rupture (VSR) is an uncommon but fatal mechanical complication of a Myocardial infarction (MI). The event occurs 2-8 days after infarction and often precipitates cardiogenic shock. The incidence of Postinfarct VSR had declined over the years due to early reperfusion capabilities but is a surgical emergency even if the patients are hemodynamically stable. Case Presentation: An 87 years old Caucasian woman with a known history of hypertension and arthritis presented to the emergency department with non-exertional epigastric, non-radiating sharp chest pain for the past several days. The patient states that her chest pain was relieved by sublingual nitroglycerine. The patient stated that she was scared to come to the ED, as she doesn’t want to catch COVID-19 from the hospital. The patient denied any shortness of breath or palpitation. Physical Examination was unremarkable. Laboratory data on admission were noted for WBC – 15.19 cells/mcL, D-Dimer 3.08 mg/L, and Troponin 3.66 ng/ml and 30 ng/ml in 2nd recheck. EKG showed normal sinus rhythm with T wave inversion in the lateral leads

Discussion: Risk factors for higher mortality from acute VSD are female sex, advanced age, arterial hypertension, anterior wall AMI, absence of previous AMI, and late arrival at the hospital. Surgical repair for VSR should be carried out on an emergency basis, even if the patient is hemodynamically stable. Conclusions: VSR is a surgical emergency but patients who develop VSR with multiorgan failure may not be a candidate for surgery and should consider palliative care.

(Figure 1). The patient was initiated on a heparin drip according to ACS protocol and titrated with aPTT results. A loading dose of aspirin was received with atorvastatin 40mg and metoprolol tartrate 25mg BID. Cardiology was consulted, and subsequently, cardiac catheterization showed significant stenosis of LAD s/p placement of Drug-eluting stent (Figure 2). She was given DAPTs (Aspirin 81mg + Clopidogrel 75mg daily) post-PCI. Echocardiogram showed a reduced ejection fraction (EF) 35-40% with wall motion abnormality on LAD territory. Few hours post-cardiac catheterization, the patient acutely decompensated and became less responsive. Her lab data were showing acutely worsening of leukocytosis 23.48 cells/mcL, Na 147 mmol/L, Creatinine 2.40 mg/dl, and troponin 96.1ng/ ml. EKG found out new ST-T waves abnormality in the anteroseptal and lateral leads. Stat Echocardiogram showed a new membranous ventricular septal defect (Figure 3). The patient developed a cardiogenic shock, requiring three vasopressors (Epinephrine, dobutamine, and vasopressin) but continued to deteriorate and triggered code blue. The family was notified for the goal of care and switched for palliative care before the patient passes away.

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