Premature Ventricular Contractions strike Back

Address for reprints: Dr. Carlos Labadet Av. Almirante Brown 240 CABA e-mail: [email protected] A BIT OF HISTORY Historically, premature ventricular contractions (PVCs) were considered precursors of sudden cardiac death and, for many years, their mere presence was taken as an indication for prescribing antiarrhythmic agents. The concept that ventricular fibrillation (VF) and ventricular tachycardia (VT) are preceded by PVCs arose when coronary care units were created to treat the complications of acute myocardial infarction (AMI). For many years, this concept of premonitory arrhythmias was extended, despite the lack of evidence, to other heart diseases. In addition, the traditional studies evaluating AMI outcome showed that PVCs were independent predictors of sudden and nonsudden death. (1) Studies in the post-thrombolytic era concluded that ventricular arrhythmia was associated with adverse outcome. (2) Finally, studies in ischemic heart disease showed that PVC scould be suppressed with antiarrhythmic agents but at the expense of greater all-cause mortality. (3) Subsequent studies using amiodarone in ischemic heart disease, as the EMIAT or the CAMIAT trials, failed to demonstrate any benefit with this drug. (4, 5) Since then, no significant progress or working hypothesis has emerged about the role of PVCs in the outcome of patients. No new agents were developed in this field and the treatment of PVCs with drugs has remained as something trivial for the past 20 years. The concept of optimizing the treatment of the underlying condition has prevailed, especially with beta blockers, together with implantation of cardioverter defibrillator devices in patients at high risk of sudden death, with or without sustained ventricular tachycardia.