What is the prognosis of premature ventricular contractions (PVCs) in patients with underlying chronic structural heart disease or complex ectopy?

Updated: Jan 13, 2017
  • Author: James E Keany, MD, FACEP; Chief Editor: Erik D Schraga, MD  more...
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Answer

In patients with underlying chronic structural heart disease (eg, cardiomyopathy, infarction, valvular disease) and complex ectopy (eg, >10 PVCs/hr), mortality is significantly increased. The following points should be kept in mind.

First, understanding of the role of antiarrhythmic therapy in the months after MI is poor. The Cardiac Arrhythmia Suppression Trial (CAST) studied patients with ventricular ectopy after MI to see if antiarrhythmic therapy improved survival rates. [6]  Despite suppression of ectopy on Holter monitoring, patients treated with encainide, flecainide, or moricizine had increased rates of sudden death and death from all causes. Findings have suggested a role for amiodarone in this patient population and have had significant reductions in rates of post-MI ventricular arrhythmias and death. Moricizine was discontinued in July 2007 because of diminished market demand.

Second, left ventricular dysfunction has a stronger association with increased mortality rate than do PVCs. Many now believe that PVCs reflect the severity of heart disease rather than contribute to arrhythmogenesis. Some studies in recent years suggest that increased variability of the PVC coupling interval in patients with underlying heart diseases, including left ventricular dysfunction, is a predictor of cardiac death; however, this remains a matter of debate. [7, 8]

Third, EPS has a primary role in risk stratification of patients with frequent or complex PVCs. Patients with PVCs that are noninducible (ie, unable to trigger ventricular tachycardia during stimulation) have a low risk of sudden death.

Frequent PVCs may be associated with increased risk of stroke in patients who do not have hypertension and diabetes. [9]


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