Related Experiment Video
Updated: Jul 3, 2026

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
Published on: June 7, 2018
Moxifloxacin-induced torsades de pointes
Saadia Sherazi1, Michael DiSalle, James P Daubert
1Unity Health System, Department of Medicine, University of Rochester Medical Center, Rochester, NY 14626, USA.
Abstract:
Torsade de pointes (TdP) is increasingly recognized as a complication of drug therapy. The most common cause of drug-induced QT prolongation is inhibition of the rapidly activating component of the delayed potassium current (I(Kr)). Moxifloxacin, a widely used fluoroquinolone, is a weak I(Kr) inhibitor and has been associated with QT prolongation. We report a case of marked QT prolongation (618 ms) and TdP associated with moxifloxacin use. Although it is difficult to predict which patients are at risk from TdP, careful assessment of the risk/benefit ratio is important before prescribing drugs known to cause QT prolongation.
Related Concept Videos
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers
Inhibitors of Bacterial DNA Synthesis
Depolarizing Blockers: Pharmocokinetics
Drug toxicity: Idiosyncratic Reactions
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Drug Toxicity: Risk factors