Abstract
Drug-induced QT prolongation is one of the most common side effects of drug use and can cause fatal outcomes such as sudden cardiac arrest. This study adopts the data-driven approach to assess the QT prolongation risk of all the frequently used drugs in a tertiary teaching hospital using both standard 12-lead ECGs and intensive care unit (ICU) continuous ECGs. We used the standard 12-lead ECG results (n = 1,040,752) measured in the hospital during 1994-2019 and the continuous ECG results (n = 4,835) extracted from the ICU's patient-monitoring devices during 2016-2019. Based on the drug prescription frequency, 167 drugs were analyzed using 12-lead ECG data under the case-control study design and 60 using continuous ECG data under the retrospective cohort study design. Whereas the case-control study yielded the odds ratio, the cohort study generated the hazard ratio for each candidate drug. Further, we observed the possibility of inducing QT prolongation in 38 drugs in the 12-lead ECG analysis and 7 drugs in the continuous ECG analysis. The seven drugs (vasopressin, vecuronium, midazolam, levetiracetam, ipratropium bromide, nifedipine, and chlorpheniramine) that showed a significantly higher risk of QT prolongation in the continuous ECG analysis were also identified in the 12-lead ECG data analysis. The use of two different ECG sources enabled us to confidently assess drug-induced QT prolongation risk in clinical practice. In this study, seven drugs showed QT prolongation risk in both study designs.
Highlights
The prolongation of the QT interval refers to the extension of the interval between the start of the QRS complex and the end of the T wave by external factors
As the administration of all drugs was recorded in the intensive care unit (ICU), we accurately identified the exact time point of drug exposure and the time until the QT prolongation event
The age, incidences of diabetes, sudden cardiac arrest, sepsis, and congestive heart failure were higher in the patients who ever have experienced QT prolongation at least one time
Summary
The prolongation of the QT interval refers to the extension of the interval between the start of the QRS complex and the end of the T wave by external factors. The delay in ventricular repolarization caused by a reduction in the outward potassium current results in the broadening of ventricular action potentials and, the prolongation of the QT interval [1]. QT prolongation may cause diverse arrhythmic conditions, including torsade de pointes, which is a type of ventricular tachycardia known to cause sudden cardiac death [2–4]. Drug-induced QT prolongation is the most common cause of acquired QT prolongation [5,6]. A drug’s propensity to cause QT interval prolongation may cause its withdrawal from the market [7]. The early detection of drug-induced QT prolongation is crucial from the medical and socioeconomic perspectives
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