ABSTRACT
A 66-year-old male patient with coronavirus disease-19 (COVID-19) developed cardiogenic shock with echocardiographic evidence of decreased left ventricular ejection fraction and global hypokinesia concomitant with a robust systemic inflammatory response. Following the administration of convalescent plasma therapy and inotropic support, left ventricular function recovered fully in accordance with the decrease in the concentration of the inflammatory markers. Thus, we demonstrate the presence of transient reversible cardiomyopathy in a patient with severe COVID-19 and illustrate the association of acute cardiac dysfunction with profound systemic inflammation among COVID-19 patients.
Subject(s)
Betacoronavirus , Cardiomyopathies/therapy , Coronavirus Infections/therapy , Pneumonia, Viral/therapy , Aged , COVID-19 , Cardiomyopathies/complications , Cardiomyopathies/immunology , Coronavirus Infections/complications , Coronavirus Infections/immunology , Coronavirus Infections/metabolism , Humans , Immunization, Passive/methods , Male , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , SARS-CoV-2 , Stroke Volume , Treatment Outcome , Ventricular Function, Left , COVID-19 SerotherapyABSTRACT
Recent reports have suggested an increased risk of QT prolongation and subsequent life-threatening ventricular arrhythmias, particularly torsade de pointes, in patients with coronavirus disease-2019 (COVID-19) treated with hydroxychloroquine and azithromycin. In this article, we report the case of a 75-year-old female with a baseline prolonged QT interval in whom the COVID-19 illness resulted in further remarkable QT prolongation (>700 ms), precipitating recurrent self-terminating episodes of torsade de pointes that necessitated temporary cardiac pacing. Despite the correction of hypoxemia and the absence of reversible factors, such as adverse medication effects, electrolyte derangements, and usage of hydroxychloroquine/azithromycin, the QT interval remained persistently prolonged compared with the baseline with subsequent degeneration into ventricular tachycardia and death. Thus, we highlight that COVID-19 illness itself can potentially lead to further prolongation of QT interval and unmask fatal ventricular arrhythmias in patients who have a prolonged QT and low repolarization reserve at baseline.