What is the prognosis of ventricular premature complexes (VPCs)?

Updated: Nov 26, 2016
  • Author: Jatin Dave, MD, MPH; Chief Editor: Jose M Dizon, MD  more...
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Answer

The prognosis depends on the frequency and characteristics of VPCs and on the type and severity of associated structural heart disease. Overall, VPCs are associated with an increased risk of death, especially when CAD is diagnosed, but the relationship between VPC frequency and mortality, even in this group, is not robust. Importantly, no survival benefit in in any population has been convincingly demonstrated as a consequence of suppressing VPCs .

In asymptomatic patients, frequent ventricular ectopy (defined as a run of 2 or more consecutive premature ventricular depolarizations or with premature ventricular depolarizations constituting over 10% of all ventricular depolarizations on any of the ECG recordings with the subject at rest, during exercise, or during recovery) recorded during exercise testing was associated with 2.5-fold increased risk of cardiovascular death. [6] Less frequent VPCs did not increase the risk.

In general, multimorphic VPCs connote a poorer prognosis than uniform morphologic VPCs. In patients post-MI, frequent VPCs (>10/h) are associated with increased mortality in the prethrombolytic era, but the association in patients receiving thrombolysis is weak.

In 2 studies, frequent or complex ventricular ectopy (defined as the presence of 7 or more ventricular premature beats per minute during any given stage, ventricular bigeminy, ventricular trigeminy, ventricular couplets, ventricular triplets, sustained or nonsustained ventricular tachycardia, ventricular flutter, torsade de pointes, or ventricular fibrillation) during exercise was an independent predictor of death. [6, 7] However, in another study, frequent VPCs only during exercise did not independently predict an increased risk; instead frequent VPCs during recovery was a stronger predictor of death. [8]

Frequent VPCs, especially when they occur in a bigeminal pattern, can cause or contribute to tachycardia-induced cardiomyopathy, which reversed by elimination of the PVCs through catheter ablation. [6, 9, 10, 11]  However, the extent to which this can be generalized to larger populations remains uncertain. Caution is in order, primarily because prior attempts at pharmacologic suppression were associated with unexpected and deleterious outcomes. [12]


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