Opposing forces of cardiogenic shock: left ventricular outflow obstruction, severe mitral regurgitation, and left ventricular dysfunction in Takotsubo cardiomyopathy.

Rates of stress (Takotsubo) cardiomyopathy have increased during the coronavirus pandemic due to social stressors, even in patients who are not infected with the virus. At times, Takotsubo cardiomyopathy (TC) may present as cardiogenic shock. Herein, we present a case during the pandemic of shock from TC secondary to left ventricular outflow tract obstruction (LVOTO), mitral regurgitation (MR), and left ventricular (LV) dysfunction. The contrasting management strategy of LVOTO, MR, and LV failure was cause for clinical challenge, and we highlight the balance of treating these opposing forces.

Right Ventricular Outflow Tract Tachycardia in a COVID-19 Patient: A Case Report and Review of the Literature (preprint)

Objectives: The novel Coronavirus (SARS-CoV2) adversely affects cardiac status and may cause arrhythmias. The objective of this study is to describe the case of a 41 year-old female presenting to the emergency department with Right ventricular outflow tract (RVOT) ventricular tachycardia; as well as to appraise and compare etiologies proposed in the literature with our case. Methods: The study design is a case report and review of the literature. A PubMed/Medline search was conducted including studies published in peer-reviewed journals between December, 2019 and November, 2020. Papers discussing the relationship between COVID-19 and cardiac arrhythmias were included, excluding the pediatric population and papers with major confounding factors to the predisposition of cardiac arrhythmias. Results: 6 papers were included in the qualitative synthesis. These papers discussed different mechanisms by which COVID-19 can cause arrhythmias. These results were compared with the findings in our case in an attempt to better understand the etiology behind our case of RVOT-VT. Proposed etiologies included ACE2-mediated direct damage of cardiomyocytes, raised serum CRP levels, and raised systemic inflammatory markers and activation of the Ca2+/Calmodulin protein kinase I. Conclusion: The lack of associated comorbidities and risk factors in our patient highlights the unique challenge of identifying the clinical sequelae of COVID-19. Proposed pathophysiologies in the literature were not applicable to our case, highlighting the need for clinical monitoring in patients, and the need for further research on the topic.