Effect of COVID-19 medications on corrected QT interval and induction of torsade de pointes: Results of a multicenter national survey.

BACKGROUND: There are some data showing that repurposed drugs used for the Coronavirus disease-19 (COVID-19) have potential to increase the risk of QTc prolongation and torsade de pointes (TdP), and these arrhythmic side effects have not been adequately addressed in COVID-19 patients treated with these repurposed medications. METHODS: This is the prospective study of 2403 patients hospitalised at 13 hospitals within the COVID-19 epicentres of the Iran. These patients were treated with chloroquine, hydroxychloroquine, lopinavir/ritonavir, atazanavir/ritonavir, oseltamivir, favipiravir and remdesivir alone or in combination with azithromycin. The primary outcome of the study was incidence of critical QTc prolongation, and secondary outcomes were incidences of TdP and death. RESULTS: Of the 2403 patients, 2365 met inclusion criteria. The primary outcome of QTc ≥ 500 ms and ∆QTc ≥ 60 ms was observed in 11.2% and 17.6% of the patients, respectively. The secondary outcomes of TdP and death were reported in 0.38% and 9.8% of the patients, respectively. The risk of critical QT prolongation increased in the presence of female gender, history of heart failure, treatment with hydroxychloroquine, azithromycin combination therapy, simultaneous furosemide or beta-blocker therapy and acute renal or hepatic dysfunction. However, the risk of TdP was predicted by treatment with lopinavir-ritonavir, simultaneous amiodarone or furosemide administration and hypokalaemia during treatment. CONCLUSION: This cohort showed significant QTc prolongation with all COVID-19 medications studied, however, life-threatening arrhythmia of TdP occurred rarely. Among the repurposed drugs studied, hydroxychloroquine or lopinavir-ritonavir alone or in combination with azithromycin clearly demonstrated to increase the risk of critical QT prolongation and/or TdP.

Comparison between rosuvastatin and atorvastatin for the prevention of contrast-induced nephropathy in patients with STEMI undergoing primary percutaneous coronary intervention.

Introduction: There is some controversy over the efficacy of statins for the prevention of contrastinduced nephropathy (CIN). There have also been reports on varying efficacies of different statins. Hence, in this study the efficacy of atorvastatin and rosuvastatin for the prevention of CIN was assessed. Methods: This single-blind randomized clinical trial was performed on 495 random patients with myocardial infarction with ST-segment elevation undergoing primary percutaneous coronary intervention (PCI) in a training referral hospital in 2015. Patients were randomly assigned to receive either atorvastatin 80 mg at admission and daily or rosuvastatin 40 mg at admission and daily. CIN was defined based on serum creatinine elevation after 48 hours from the PCI. Results: The incidence of CIN was observed in 63 patients (21.4%) After 48 hours from primary PCI. Of those, 17% (n = 50) were grade 1 CIN, while 4.4% (n = 13) were grade 2 CIN. There was no significant difference between rosuvastatin group compared with atorvastatin group, regarding the CIN grading (P = 0.14). Conclusion: Our results indicate that atorvastatin and rosuvastatin have similar efficacy for the prevention of CIN.

QT Dispersion after Thrombolytic Therapy.

BACKGROUND: QT dispersion (QTd) is equal to longer QTc minus shorter QTc measured by 12-lead electrocardiogram (ECG). QTd reflects inhomogeneity in repolarization of ventricular myocardium and because of easy and fast measurement of QTd, it can be used to predict high-risk patients for dysrhythmia after Acute Myocardial Infarction (AMI). OBJECTIVES: This study aimed to assess the effect of thrombolytic therapy on QTd before and 1 hour and 4 days after beginning of thrombolytic therapy. PATIENTS AND METHODS: The patients with chest pain and ST Elevated Myocardial Infarction (STEMI) that underwent thrombolytic therapy were enrolled into this study. Streptokinase was the thrombolytic agent in all the patients. Standard 12-lead (ECG) was evaluated before beginning of thrombolytic therapy (QTd 1) and 1 hour (QTd2) and 4 days (QTd3) after thrombolytic therapy. First, ECG was magnified × 10 for exact calculation of QT and QTd. After all, the variables were compared using one-way analysis of variance (ANOVA). Besides, P ≤ 0.05 was considered as statistically significant. RESULTS: This study was conducted on 160 patients. The results revealed no significant differences among QTd 1, QTd 2, and QTd 3 (P > 0.05). At inferior AMI, however, a significant difference was observed among QTd1, QTd2, and QTd3 (P = 0.031). CONCLUSIONS: Thrombolytic therapy had no significant effects on QTd. Thus, thrombolytic therapy does not increase the risk of arrhythmia.