Recurrent Takotsubo Cardiomyopathy Triggered by COVID-19 Infection Complicated by Ventricular Tachycardia Arrest and Cardiogenic Shock: A Case Report.

Takotsubo cardiomyopathy is a transient stress-induced cardiomyopathy typically triggered by emotional or physical stress. Since the emergence of coronavirus disease 2019 (COVID-19), several cardiovascular complications have been reported, including stress cardiomyopathy. Recurrent Takotsubo cardiomyopathy complicated by malignant ventricular arrhythmias and cardiogenic shock remains uncommon. A 73-year-old Hispanic female with a prior history of Takotsubo cardiomyopathy in 2013, subclinical hyperthyroidism, and hyperlipidemia presented with worsening malaise and subjective fever. She tested positive for COVID-19. Initial troponin was 0.070 ng/mL, with a peak value of 0.143 ng/mL. Pro-BNP (pro B-type natriuretic peptide) was markedly elevated at 11,250 pg/mL, reflecting significant myocardial wall stress. The initial electrocardiogram showed sinus rhythm with nonspecific T-wave abnormalities in leads III and aVF and a QTc interval of 452 ms. A repeat electrocardiogram six hours later revealed clear T-wave inversions in leads II, III, aVF, and V6. She was transferred to a tertiary care center, where she developed pulseless ventricular tachycardia due to an R-on-T phenomenon, requiring nine minutes of advanced cardiovascular life support. COVID-19 was considered the primary trigger after exclusion of alternative physical stressors. Coronary angiography demonstrated no obstructive coronary artery disease. Right heart catheterization revealed elevated filling pressures and low cardiac output consistent with cardiogenic shock. Transthoracic echocardiography showed an ejection fraction of 10% with apical ballooning typical of Takotsubo cardiomyopathy. Mechanical circulatory support with an intra-aortic balloon pump, inotropes, and vasopressors was required. The patient gradually improved; a repeat echocardiogram on day 9 demonstrated complete normalization of ejection fraction to 70%, cardiac magnetic resonance imaging revealed no late gadolinium enhancement, and sustained recovery was confirmed at outpatient follow-up with an ejection fraction of 60%-70%. Due to the malignant ventricular arrhythmia, a secondary prevention implantable cardioverter-defibrillator was placed. A follow-up electrocardiogram showed sinus rhythm with no ischemic changes, no Q waves, and a QTc of 428 ms. This case illustrates a recurrent Takotsubo episode temporally associated with COVID-19 infection and complicated by R-on-T ventricular tachycardia and cardiogenic shock. The prior normal myocardial perfusion study and full functional recovery support the diagnosis. A large national database study has shown that COVID-19 patients with stress cardiomyopathy have significantly higher mortality and complication rates. The role of subclinical hyperthyroidism as a potential sensitizer to catecholamine surges is explored. A recently published case of asymptomatic COVID-19 triggering recurrent Takotsubo highlights that the spectrum of this association ranges from subclinical infection to life-threatening presentations. COVID-19 infection was temporally associated with recurrent Takotsubo cardiomyopathy with life-threatening arrhythmias. Early recognition, aggressive hemodynamic support, and individualized decisions regarding implantable cardioverter-defibrillator placement are critical for favorable outcomes.