Abstract
Viral infections may lead to myocarditis, which is inflammation of the myocardium. This inflammation, when severe enough, can result in left ventricular dysfunction and potentially reduce the left ventricular ejection fraction (LVEF). In rare cases, the effects of this inflammation lead to hemodynamic changes that can be life-threatening. We discuss a case of a 38-year-old female recently diagnosed with influenza A (H3 subtype) who presented to our institution's emergency department for evaluation after an episode of syncope, as well as intermittent chest pressure and dyspnea on exertion. Initial vitals displayed a heart rate of 87 bpm and blood pressure of 105/66 mmHg. The physical examination demonstrated a regular rhythm, no lower extremity edema, and lungs that were clear to auscultation. She was found to have an elevated pro-B-type natriuretic peptide level of 6152 pg/mL and a positive influenza A polymerase chain reaction (PCR) test. A transthoracic echocardiogram (TTE) was obtained and demonstrated globally reduced left ventricular systolic function with an estimated ejection fraction of 28%, as well as reduced right ventricular systolic function. Over the next six hours, the patient became progressively tachycardic and hypotensive, with a heart rate of 135 bpm and a blood pressure measured at 46/28 mmHg. She was initially admitted to the cardiovascular ICU and started on dobutamine and vasopressin. Pulmonary artery catheterization was completed for better evaluation of cardiogenic shock, and it demonstrated a severely reduced cardiac index of 0.9 L/min/m(2). Due to concerns of worsening cardiogenic shock and impending circulatory collapse, mechanical circulatory support was initiated via veno-arterial extracorporeal membrane oxygenation (VA-ECMO), and she was admitted to the cardiothoracic surgery ICU. Several days later, a biventricular assist device (BiVAD) was implanted with the goal of discontinuing ECMO as a bridge to transplant. Shortly afterwards, a repeat echocardiogram demonstrated a normalized left and right ventricular systolic function, and the BiVAD was removed. Ten days after the initiation of ECMO, it was able to be discontinued, and the patient was decannulated. The patient was discharged home in stable condition. This case exemplifies how fulminant myocarditis (FM) can have positive outcomes, even in critically ill patients, when the timing of intervention is early and aggressive.