Previous use of macrolides and metronidazole is associated with H. pylori resistant to these antimicrobial agents. Clarithromycin resistance is associated with a greater risk for failure with clarithromycin-based treatments.

Electrophysiological abnormalities of the QT interval of the standard electrocardiogram are not uncommon. Congenital long QT syndrome is due to mutations of several possible genes (genotype) that result in prolongation of the corrected QT interval (phenotype). Abnormalities of the QT interval can be acquired and are often drug-induced. Torsades de Pointes (TP) is an arrhythmia that is a result of aberrant repolarization/QT abnormalities. If not recognized and corrected quickly, QT interval abnormalities may precipitate potentially fatal ventricular dysrhythmias. The main mechanism responsible for the development of QT prolongation is blockade of the rapid component of the delayed rectifier potassium current (I kr), encoded for by the human-ether-a-go-go-related gene (hERG). The objectives of this review were (1) to describe the electrical pathophysiology of QT interval abnormalities, (2) to differentiate congenital from acquired QT interval abnormalities, (3) to describe the currently known risk factors for QT interval abnormalities, (4) to identify current drug-induced causes of acquired QT interval abnormalities, and (5) to recommend immediate and effective management strategies to prevent unanticipated dysrhythmias and deaths from QT abnormalities in the perioperative period.