Polymorphic ventricular tachycardia (PMVT) is a rapid ventricular tachycardia in which the QRS complexes vary in coupling interval, morphology, and axis on a beat-to-beat basis. PMVT occurs in two distinct forms: PMVT without QT interval prolongation and PMVT with QT interval prolongation. The two types differ in important ways with respect to their differential diagnosis and treatment. PMVT without QT interval prolongation usually emerges in the setting of an unstable structural heart disorder, such as acute ischaemia or decompensated heart failure. Treatment is directed at the underlying heart disorder, correction of acid–base disturbances, hypoxia, and electrolyte abnormalities along with beta-blocking therapy and amiodarone. Invasive antiarrhythmic interventions, such as sympathetic denervation and transcatheter ablation, are occasionally required. Long-term treatment often includes an implantable cardioverter defibrillator. PMVT with QT interval prolongation, known as torsade de pointes VT, occurs when repolarization reserve has been exhausted by either inherited or acquired factors that prolong the QT interval. Classical features of the ‘twisting-of-the-points’ polymorphism and the short–long–short initiation sequence are common but are not universal. Treatment is directed at removal of the cause of the QT interval prolongation, correction of electrolyte disturbances (hypokalaemia and hypomagnesaemia), supplemental magnesium therapy, and treatments to shorten the QT interval such as isoproterenol, pacing, or lidocaine. Long-term treatment is focused on avoidance of QT interval prolonging factors. If the likelihood of subsequent recurrence is not low, consideration is given to placement of a permanent pacemaker or implantable cardioverter defibrillator.
Voriconazole-Induced QT Interval Prolongation and Ventricular Tachycardia: A Non--Concentration-Dependent Adverse Effect
