Background The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses angiotensin-converting enzyme-2 receptors on host cells to enter the cells. These receptors are expressed on heart muscle tissue and the tissues of other major organs, which supports the primary accepted theory for the direct cardiac cell injury of coronavirus disease 2019 (COVID-19) and the associated cardiorespiratory manifestations. The SARS-CoV-2 infection leads to unstable myocardial cell membranes due to hypoxia, myocarditis, myocardial ischemia, and abnormal host immune response. This is the main reason behind arrhythmia and electrocardiogram (ECG) changes during COVID-19. However, the specific effect on QTc has not been studied well. Therefore, this study aimed to examine the association between COVID-19 and QTc changes. Methodology We conducted an observational, retrospective review of hospital medical records of 320 adult participants diagnosed with COVID-19 at our facility. After applying the exclusion criteria, 130 participants were included and distributed into two groups. One group had long QTc, and one group had normal QTc. Data were collected and recorded using Microsoft Excel. We used SPSS Statistics for Windows, Version 20.0. (IBM Corp., Armonk, NY, USA) to analyze the data. Student’s t-tests were performed for independent groups. Quantitative data were summarized using mean and standard deviation. Statistical significance was taken as p < 0.05. Results A total of 63 (48.4%) participants met the criteria for long QTc, and 67 (51.5%) participants had normal QTc (p < 0.001). There was no statistically significant difference in mortality outcomes between long QTc and normal QTc (0.8% vs. 3.8%, respectively; p = 0.21). Conclusions This study aimed to examine the association between COVID-19 and QTc changes. Nearly half of the participants had an increased QTc with COVID-19, and QTc length was not associated with mortality outcomes. Our results indicate that COVID-19 is an independent risk factor for QTc prolongation on ECG. Identifying COVID-19 as an independent risk factor for QTc prolongation is a clinically significant finding, and physicians should consider this when treating cardiac patients and possible COVID-19-positive patients.

Background Objective: What is the association between COVID-19 infection and QTc changes? Coronavirus SARS-COV2 uses angiotensin-converting enzyme receptors 2 (ACE2) on host cells to enter into human cells. These receptors are expressed on the heart cells among other major cells. This is one of the most accepted theories for direct cardiac cell injury of COVID-19disease and associated cardiorespiratory manifestations. COVID-19 infection leads to unstable myocardial cell membranes, by causing hypoxia, myocarditis, myocardial ischemia, and abnormal host immune response. This is the main reason behind Arrhythmia and EKG changes during COVID19 infection. But the specific effect on QTc has not been studied well so far, so our research try to study this connection. Method: This is an observational retrospective hospital chart review involving 320 adult participants diagnosed with COVID-19 infection at our facility. After applying the exclusion criteria, 130 participants remained, who were distributed into two groups. One group with long QTc and one group with normal QTc. Data was collected and demographics were recorded using Excel and SPSS, then compared using a student’s t-test for independent groups. The quantitative data are summarized by the mean and standard deviation (SD). Statistical significance was taken as P <0.05. Result: A total of 63 participants (48.4% of total 130 participants) met the criteria for long QTc, and a total of 67 participants(51.5%) had normal QTc (P < 0.001). There was no statistically significant mortality outcome (0.8% vs. 3.8%, P = 0.21). Conclusion: Our study showed 48.4% participants having an increase in QTc during COVID-19 infection, (20% of 320 total admissions). This observation is very important to help healthcare providers to gaina better understanding of this disease.