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A 72-year-old Hispanic male with a history of hypertension was brought to the emergency department complaining of persistent fatigue and malaise and watery diarrhea associated with lightheadedness for 2 days. He has recently returned from Europe. He tried home remedies to control the diarrhea, but they did not help. No recent antibiotic use and he takes amlodipine for hypertension. Family history and social history were noncontributory. In the emergency department he was found to be febrile, otherwise, he had normal vitals. Physical examination was unremarkable. Laboratory data showed prerenal azotemia, elevated lactate dehydrogenase (LDH), and low leukocyte count. He was transferred to the medical floor for intravenous hydration and further workup. On the floor, SARS-CoV-2 polymerase chain reaction was confirmed. The next day he suddenly became hypotensive and developed severe respiratory distress. Chest radiograph (CXR) showed acute pulmonary edema. He was moved to critical care and started on noninvasive ventilation. His pro-brain natriuretic peptide (BNP) and troponin were elevated, and his renal function further worsened. Transthoracic echocardiogram (TTE) showed moderately reduced left ventricular (LV) function with global wall motion abnormalities. No prior echocardiogram was available. He was later mechanically ventilated and started on pressors. The patient underwent right heart catheterization that showed low cardiac output and elevated pulmonary capillary wedge pressure indicating cardiogenic shock. He continued to require inotropes and vasopressors. The patient also received tocilizumab and remdesivir for a total of 5 days, broad-spectrum antibiotics for a total of 7 days, as well as supportive measures. After 5 days of mechanical ventilation, the patient started to show improvement and was weaned off from the ventilator and renal function started to improve. After 12 days of hospitalization the patient was discharged home on carvedilol 6.25 mg and lisinopril 5 mg. Two months postdischarge, he presented to the cardiology clinic for a follow-up; repeat echocardiogram showed improved LV function.


COVID-19 has been associated with various cardiovascular complications that may include subclinical myocardial injury, de novo heart failure (HF), and worsening of existing HF. Several observational studies from China, Europe, and the United States have reported the prevalence of HF in COVID-19 patients ranging from 4%-12%.1 HF in COVID-19 patients has been associated with exceedingly high mortality. Older age group and people with preexisting HF has a higher chance of complications with this infection. In a recent global observational study, coronary artery disease (CAD) and congestive heart failure (CHF) are considered the predictors of inpatient mortality. Although the data on difference in outcomes in heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF) are limited, clinical progression of disease remains similar in both cohorts. (1-3)


COVID-19 infection can lead to acute inflammatory response like other viral infections and may lead to decompensated HF. The cytokine storm can cause further worsening of cardiac function by demand-supply ...

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