A Case of Acute Myocarditis Complicated by Refractory Cardiogenic Shock with Complete Native Heart Recovery
Presenter
Natthapon Angsubhakorn, MD, Loma Linda University, Loma Linda, CA
Natthapon Angsubhakorn, MD1, Nicolas Kang, MD2, Joshua Chung, MD2, Jason Hoff, MD3, Liset Stoletniy, MD2, Antoine Sakr, MD2 and Dr. Aditya Bharadwaj, M.B.B.S., FSCAI4, (1)Loma Linda University, Loma Linda, CA, (2)Loma Linda University Health, Loma Linda, CA, (3)Loma Linda University Medical Center, Loma Linda, CA, (4)Loma Linda University Medical Center, Riverside, CA
Title
A Case of Acute Myocarditis Complicated by Refractory Cardiogenic Shock with Complete Native Heart Recovery
Introduction
Cardiogenic shock is a life-threatening syndrome characterized by low cardiac output and end‐organ hypoperfusion. Efforts to reduce the high morbidity and mortality focus on improvement of hemodynamic parameters by mechanical circulatory support (MCS) and team-based management. Here we report a case of refractory cardiogenic shock due to acute myocarditis in an otherwise healthy man, who required percutaneous left ventricular assist device (pVAD) and veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for 7 days with full myocardial recovery.
Clinical Case
A previously healthy 45-year-old man presented to an outside facility with a three-day history of shortness of breath and chest tightness. He was found to have LVEF of 15% on focused cardiac ultrasound and was promptly transferred to our institution for further management of cardiogenic shock. On arrival, he was intubated, sedated, and on high doses of intravenous dobutamine and norepinephrine. Examination revealed jugular venous distention and cold extremities. Laboratory testing showed serum creatinine 3.9 mg/dL, serum lactate 3.0 mMol/L, pro–B-type natriuretic peptide 17,279 pg/mL, and high-sensitivity troponin T 10,906 ng/L. Respiratory viral panel was negative. ECG showed sinus tachycardia and chest x-ray showed pulmonary vascular congestion. Coronary angiogram revealed no obstructive epicardial disease. Invasive hemodynamic evaluation revealed significantly elevated filling pressures (right atrial pressure 17 mmHg; pulmonary capillary wedge pressure 27 mmHg), reduced cardiac index of 1.45 L/min/m2, reduced cardiac power output (CPO) of 0.33 Watts, and reduced pulmonary artery pulsatility index (PAPI) of 0.5. This confirmed SCAI Stage D shock with biventricular failure. The patient was immediately evaluated by our multidisciplinary shock team and decision was made to proceed with transfemoral pVAD (Impella CP, Abiomed, Inc, Danvers, MA) placement. Subsequently, given biventricular failure and persistently reduced CPO, cardiac surgeon performed peripheral VA-ECMO cannulation. Evaluation for cardiac transplantation was initiated. Patient responded well to MCS, intravenous immunoglobulin, and medical optimization. He was supported on VA-ECMO and unloaded with pVAD for 7 days before uneventful decannulation. LVEF had improved to 70% before discharge.
Discussion
Cardiogenic shock requires immediate diagnosis and multidisciplinary management with a goal for complete heart recovery. Hemodynamic criteria utilizing CPO and PAPI should guide decisions regarding choice of MCS and the need to escalate support. We utilized a multidisciplinary team approach with hemodynamic criteria to successfully manage a patient with acute myocarditis with refractory cardiogenic shock. Unloading the left ventricle with pVAD in the presence of VA-ECMO helps with native heart recovery.