WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • The risks of torsade de pointes and QTc prolongation in HIV patients have been reported. • Authors have shown that four protease inhibitors (PIs) blocked human ether‐a‐go‐go‐related gene (hERG), the current that underlies QTc prolongation and drug‐induced proarrhythmia, and have also reported cases of torsades and suggested that PIs were responsible for these adverse events. • This earlier paper has had a major impact on the perception of the arrhythmogenic risk associated with PIs, and regulatory agencies in Europe and the USA have modified the labelling of PIs accordingly. WHAT THIS STUDY ADDS • The present study provides alternative explanations for QTc prolongation in a cohort of HIV patients and reports ECG abnormalities found in such patients. • It does not confirm that PIs play a significant role in QTc interval prolongation in HIV patients. • In contrast, it shows that QTc prolongation is related to common causes and to the duration of HIV infection rather than to anti‐HIV treatments. AIMS QTc interval prolongation and torsades de pointes have been reported in HIV‐infected patients. Protease inhibitors (PIs) are suspected to contribute to this adverse reaction. However, many factors can prolong QTc interval. We examined factors influencing QTc duration in HIV‐infected patients. METHODS Unselected HIV‐infected patients (n = 978) were enrolled in this prospective, single‐centre cross‐sectional study. Variables related to infection and treatments were collected. A digital electrocardiographic record was recorded in each patient and QT interval duration was measured and corrected using both Bazett's (QTcB) and Fridericia's (QTcF) formula. Results were analysed with a multivariable linear model. RESULTS After excluding arrhythmias and complete bundle branch blocks, QT interval was measured in 956 patients. The mean (SD) QTcB was 418 ms (23) and QTcF was 405 ms (20). QTc was found prolonged (>450 ms in women and >440 ms in men) in 129 [13.5%; 95% confidence interval (CI) 11.5, 15.8] and 38 (4%; 95% CI 2.9, 5.4) patients using Bazett and Fridericia corrections, respectively. On multivariable analysis, incomplete bundle branch block, ventricular hypertrophy, signs of ischaemic cardiopathy, female gender, White ethnic origin and age were significantly associated with QTc prolongation. The only HIV variable independently associated with QTc prolongation was the duration of infection (P = 0.023). After adjustment, anti‐HIV treatment, in particular PI (P = 0.99), was not associated with QTc prolongation. CONCLUSIONS Although PIs block in vitro hERG current, they are not independently associated with QTc interval prolongation. Prolonged QTc interval in HIV‐infected patients is primarily associated with factors commonly known to prolong QT and with the duration of HIV infection.

One in every 10 HF patients with permanent AF may experience SRR after CRT. Baseline EDD