STUDY OBJECTIVE The objective of the study is to estimate the frequency of cardiac arrhythmias and characterize the mode of death in patients with the novel coronavirus disease (SARS-CoV-2; COVID-19). The study will also evaluate the long term cardiac outcomes in patients previously diagnosed with COVID-19.
INTRODUCTION, RATIONALE The novel coronavirus (SARS-CoV-2) emerged in Wuhan, China, in late 2019 and has quickly become a pandemic, significantly impacting the health and economy of the United States and the rest of the world. There are over 500,000 cases and 24,000 deaths related to COVID-19 worldwide, with an estimated mortality rate ranging from 1-8%. The United States has been impacted by this pandemic significantly with over 80,000 cases and thousands of deaths reported; these numbers will continue to worsen.
Patients infected with COVID-19 can exhibit a wide range of clinical manifestations, ranging from an asymptomatic state to mild upper respiratory symptoms (with low-grade fever) to severe disease with hypoxia and acute respiratory distress syndrome (ARDS) type lung injury. In the setting of hypoxemic respiratory failure, ground glass opacification on chest imaging is found more than 50% of the time.
COVID-19 has the potential to cause myocardial injury with at least 17% found to have an elevated troponin and 23% noted to have heart failure in a study of 191 inpatients from Wuhan, China. The prevalence of heart failure was significantly higher among non-survivors compared with survivors (52% vs. 12%). In a meta-analysis of 4 studies including a total of 341 patients, standardized mean difference of cardiac troponin I levels were significantly higher in those with severe COVID-19 related illness compared to those with non-severe disease (25.6, 95% CI 6.8-44.5). Furthermore, cases of fulminant myocarditis with cardiogenic shock have also been reported, with associated atrial and ventricular arrhythmias. In a recent report from Wuhan, China, 16.7% of hospitalized and 44.4% of ICU patients with COVID-19 had cardiac arrhythmias. Given the potential sampling bias in sicker, hospitalized patients with hypoxia and electrolyte abnormalities in the acute phase of severe illness can potentiate cardiac arrhythmias, the exact arrhythmic risk related to COVID-19 in patients with less severe illness or those who recover from the acute phase of the severe illness is currently unknown.
Furthermore, as it is currently unclear what medications may be beneficial for patients with COVID-19. Several medications eg: chloroquine, hydroxychloroquine, remdesivir, tocilizumab etc. are currently being investigated. Hydroxychloroquine is known to block Kv11.1 (HERG) and can cause drug-induced LQT. As such, these drugs are used concomitantly with other antiarrhythmic drugs such as amiodarone, Tikosyn, sotalol etc. which can be associated with QT prolongation requiring close EKG and cardiac monitoring. Improved characterization of arrhythmia burden and mechanism of death is critical, primarily in guiding the need for developing treatment strategies, additional arrhythmia monitoring and need to consider advanced prevention strategies including the role of implantable cardioverter defibrillator (ICD).
