Cardiac Corrected QT Interval Changes Among Patients Treated for COVID-19 Infection During the Early Phase of the Pandemic.

Importance: Critical illness, a marked inflammatory response, and viruses such as SARS-CoV-2 may prolong corrected QT interval (QTc). Objective: To evaluate baseline QTc interval on 12-lead electrocardiograms (ECGs) and ensuing changes among patients with and without COVID-19. Design, Setting, and Participants: This cohort study included 3050 patients aged 18 years and older who underwent SARS-CoV-2 testing and had ECGs at Columbia University Irving Medical Center from March 1 through May 1, 2020. Patients were analyzed by treatment group over 5 days, as follows: hydroxychloroquine with azithromycin, hydroxychloroquine alone, azithromycin alone, and neither hydroxychloroquine nor azithromycin. ECGs were manually analyzed by electrophysiologists masked to COVID-19 status. Multivariable modeling evaluated clinical associations with QTc prolongation from baseline. Exposures: COVID-19, hydroxychloroquine, azithromycin. Main Outcomes and Measures: Mean QTc prolongation, percentage of patients with QTc of 500 milliseconds or greater. Results: A total of 965 patients had more than 2 ECGs and were included in the study, with 561 (58.1%) men, 198 (26.2%) Black patients, and 191 (19.8%) aged 80 years and older. There were 733 patients (76.0%) with COVID-19 and 232 patients (24.0%) without COVID-19. COVID-19 infection was associated with significant mean QTc prolongation from baseline by both 5-day and 2-day multivariable models (5-day, patients with COVID-19: 20.81 [95% CI, 15.29 to 26.33] milliseconds; P < .001; patients without COVID-19: -2.01 [95% CI, -17.31 to 21.32] milliseconds; P = .93; 2-day, patients with COVID-19: 17.40 [95% CI, 12.65 to 22.16] milliseconds; P < .001; patients without COVID-19: 0.11 [95% CI, -12.60 to 12.81] milliseconds; P = .99). COVID-19 infection was independently associated with a modeled mean 27.32 (95% CI, 4.63-43.21) millisecond increase in QTc at 5 days compared with COVID-19-negative status (mean QTc, with COVID-19: 450.45 [95% CI, 441.6 to 459.3] milliseconds; without COVID-19: 423.13 [95% CI, 403.25 to 443.01] milliseconds; P = .01). More patients with COVID-19 not receiving hydroxychloroquine and azithromycin had QTc of 500 milliseconds or greater compared with patients without COVID-19 (34 of 136 [25.0%] vs 17 of 158 [10.8%], P = .002). Multivariable analysis revealed that age 80 years and older compared with those younger than 50 years (mean difference in QTc, 11.91 [SE, 4.69; 95% CI, 2.73 to 21.09]; P = .01), severe chronic kidney disease compared with no chronic kidney disease (mean difference in QTc, 12.20 [SE, 5.26; 95% CI, 1.89 to 22.51; P = .02]), elevated high-sensitivity troponin levels (mean difference in QTc, 5.05 [SE, 1.19; 95% CI, 2.72 to 7.38]; P < .001), and elevated lactate dehydrogenase levels (mean difference in QTc, 5.31 [SE, 2.68; 95% CI, 0.06 to 10.57]; P = .04) were associated with QTc prolongation. Torsades de pointes occurred in 1 patient (0.1%) with COVID-19. Conclusions and Relevance: In this cohort study, COVID-19 infection was independently associated with significant mean QTc prolongation at days 5 and 2 of hospitalization compared with day 0. More patients with COVID-19 had QTc of 500 milliseconds or greater compared with patients without COVID-19.

Interpretation of arrhythmogenic effects of COVID-19 disease through ECG.

OBJECTIVE: We aimed to detect the malignant arrhythmic potential of COVID-19 with surface electrocardiographic (ECG) markers. MATERIAL AND METHOD: Of the ECG parameters PR, QT, QTc, QTd, TPe, and Tpe/QTc were measured in 51 COVID-19 patients and 40 in control subjects. RESULTS: Compared to control group mean QTc (410.8 ± 24.3 msec vs. 394.6 ± 20.3 msec, p < .001) and Tpe/QTc (0.19 ± 0.02 vs. 0.18 ± 0.04, p = .036) and median QTd (47.52 vs. 46.5) values were significantly higher in COVID-19 patients. Troponin levels were significantly correlated with heart rate (r = 0.387, p = .006) but not with ECG parameters. CONCLUSION: Several ventricular arrhythmia surface ECG predictors including QTc, QTd, and Tpe/QTc are increased in COVID-19 patients. Since medications used in COVID-19 patients have the potential to affect these parameters, giving importance to these ECG markers may have a significant contribution in decreasing disease-related arrhythmias.

Prolonged QTc in HIV-Infected Patients: A Need for Routine ECG Screening.

BACKGROUND: With HIV-infected patients living longer, there is an increased burden of comorbidities related to aging, HIV itself, and polypharmacy. Cardiac morbidity is of particular importance. METHODS: This 2-group comparison study (156 HIV-positive and 105 HIV-negative patients) investigated the prevalence of abnormalities in and factors associated with an electrocardiogram (ECG) measure, corrected QT interval (QTc), where prolongation can lead to arrhythmia and sudden death. Medications prescribed (antiretroviral therapy, psychiatric medications, methadone, and antibiotics) at the time of ECG were noted. Patient characteristics, medications, QTc, and ECG characteristics were compared between the 2 groups. RESULTS: Prolongation (29% versus 19%) and extreme prolongation (6% versus 1%) in QTc were more frequent in those with HIV. Antiretroviral therapy was associated with lower odds of prolonged QTc (odds ratio [OR] = 0.35; P = .04), while methadone with higher odds (OR = 4.6; P = .01) in HIV-positive patients. With methadone and medication groups adjusted, HIV status was still associated with 17-millisecond longer QTc ( P = .04). CONCLUSION: This study provides evidence that patients with HIV may have clinically relevant longer QTc interval on ECG. Baseline and routine ECG monitoring may be warranted among patients living with HIV in clinical practice based on cumulative evidence.

Risk of QTc prolongation in a cohort of opioid-dependent HIV-infected patients on methadone maintenance therapy.

BACKGROUND: Concern regarding the QTc interval in human immunodeficiency virus (HIV)-infected patients has been growing in recent years, and cases of prolonged QTc interval and torsades de pointes have been described in HIV-infected patients on methadone therapy. This study aimed to determine the prevalence and factors associated with long QTc interval in a cohort of opioid-dependent HIV-infected patients on methadone maintenance therapy. METHODS: A cross-sectional study was conducted in opioid-dependent HIV-infected patients on methadone maintenance therapy at a drug abuse outpatient center. Patients with any cardiac disease, drug-positive urine test, electrolyte abnormalities, and changes in their antiretroviral therapy (ART) or methadone doses in the last 2 months were excluded. Heart rate and QT interval in lead II were measured using the Bazett formula. RESULTS: Ninety-one patients were included: 58 (63.7%) were men with a median age of 44.5 years and 68 of 91 (74.7%) were on ART. Median methadone dose was 70 mg/day (range 15-250 mg/day) and mean QTc interval was 438 ± 34 ms. Prolonged QTc interval (>450 ms) was documented in 33 of 91(36.3%) patients, and 3 of 91 (3.2%) had QTc >500 ms. On multiple linear regression analysis, methadone doses (P = .005), chronic hepatitis C-induced cirrhosis (P = .008), and being ART-naive (P = .036) were predictive of prolonged QTc. CONCLUSIONS: The prevalence of prolonged QTc interval in opioid-dependent HIV-infected patients on methadone maintenance therapy is high. Risk factors for prolongation of the QTc interval are chronic hepatitis C-induced cirrhosis, higher methadone doses, and being ART-naive. Thus, electrocardiographic monitoring is required to minimize cardiovascular morbidity and mortality in this specific HIV group.

Viral load and CD4+ cell count as risk factors for prolonged QT interval in HIV-infected subjects: a cohort-nested case-control study in an outpatient population.

BACKGROUND: QTc interval prolongation is a serious ECG finding which has frequently been reported in HIV-infected patients, but associated risk factors have not been determined in this population. METHODS: Data were collected from the charts of a cohort of 135 consecutive HIV-infected patients from our HIV outpatient clinic. The cohort was divided into two groups, patients with prolonged QTc and those with normal QTc interval. Multiple variables and potential risk factors were analyzed, including the CD4+ cell count and viral load (VL), which were assessed on the same day or within several days of the initial ECG. RESULTS: 23 patients were found to have prolonged QTc (17%). No significant difference in baseline characteristics was observed between the groups; however, statistically significant differences were observed with regard to the CD4+ cell count and VL. CONCLUSION: A low CD4 cell count and a high VL may be risk factors potentially related to QT prolongation in HIV patients in the outpatient setting.

Prevalence and risk factors of prolonged QTc interval in HIV-infected patients: results of the HIV-HEART study.

BACKGROUND: Corrected QT (QTc) prolongation is predictive of cardiovascular mortality in both the general and human immunodeficiency virus (HIV) populations. OBJECTIVE: As part of the HIV-HEART study, we assessed the prevalence and risk factors of a prolonged QTc interval in patients with HIV infection. METHODS: In this cross-sectional cohort study, 802 unselected HIV-infected patients were included. Data were analyzed by the use of gender-specific QTc categories (men abnormal at > 440 ms and women abnormal at >460 ms). Multiple variables related to infection and treatment were collected. Results were analyzed with a multivariable model. RESULTS: The QTc interval was found to be prolonged in 154 patients (19.8%; 95% CI 17-23). The mean (+/-SD) QTc in men (n = 142) presenting with a prolonged QTc interval was 456 +/- 16.3 ms (range 441-548 ms). The mean (+/-SD) QTc in women (n = 12) presenting with a prolonged QTc interval was 479 +/- 9 ms (range 465-498 ms). In the multivariable model, female gender, diabetes mellitus, and arterial hypertension were associated with prolonged QTc. There were no parameters related to HIV independently associated with QT interval prolongation. In particular, no anti-HIV drug was associated with QTc prolongation. CONCLUSIONS: Our study demonstrated that in an HIV-infected population, QTc prolongation had a high prevalence of nearly 20% compared to the general population and was possibly influenced by common factors like gender, diabetes, and arterial hypertension.

HIV and Long QT syndrome--cause or coincidence.

The Long QT syndrome is a disorder characterized by abnormalities of cardiac repolarisation, resulting in a propensity to polymorphic ventricular tachycardia (torsades de pointes) and sudden cardiac death. It remains unclear whether cardiac involvement with the HIV virus itself can cause QT prolongation. We report a case of a HIV infected young female presenting with recurrent syncope due to torsades de pointes.

Acquired QT prolongation associated with esophagitis and acute weight loss: how to evaluate a prolonged QT interval.

When the physician is confronted with a patient having significant QT prolongation, it is critical to determine whether the patient harbors a genetic defect and a transmissible form of long QT syndrome (LQTS) or whether the QT prolongation has an acquired cause. The distinction has profound ramifications for the type of care provided to the patient and family. We report the case of a previously healthy 14-year-old boy who presented with a 10-day history of painful swallowing, a 10-lb weight loss, and chest pain. A 12-lead electrocardiogram (ECG) showed marked QT prolongation. Endoscopy and culture identified a Herpes simplex esophageal ulcer. After treatment with acyclovir, the patient recovered completely. Three weeks after the resolution of his symptoms and recovery from his acute weight loss, a follow-up ECG showed complete normalization of the QT interval. This case illustrates yet another potential mechanism for acquired QT prolongation. We also provide a diagnostic algorithm for the careful evaluation of a prolonged QT interval.