Review Article
Ventricular Ectopy in Patients With Left Ventricular Dysfunction: Should It Be Treated?

https://doi.org/10.1016/j.cardfail.2012.11.004Get rights and content

Abstract

Ventricular premature complexes (VPCs) are commonly encountered in patients with congestive heart failure (CHF). Frequent ventricular ectopy can be associated with deterioration of cardiac function and may lead to VPC-induced cardiomyopathy. VPC-induced inter- and/or intraventricular dyssynchrony has been postulated as the main mechanism underlying VPC-induced left ventricular dysfunction. For risk stratification, VPCs in the setting of CHF can not be regarded to be a benign arrhythmia as in an apparently healthy subject. However, any potential survival benefits to be derived from suppression of VPCs or nonsustained ventricular tachycardia in CHF may be offset by the negative inotropic and proarrhythmic effects of antiarrhythmic drugs and may be masked by the risk of death that is already high in this subgroup of patients. β-Blockers are currently considered to be the first-line therapy, with amiodarone as a back-up. Catheter ablation, although invasive and not without procedural risk, avoids the common adverse effects of currently available antiarrhythmic medications. From a standpoint of preventing or reversing left ventricular dysfunction, frequent VPCs should be treated earlier regardless of their site of origin or the presence of associated symptoms, such as palpitations. Catheter ablation may be the preferable approach in selected patients, particularly when β-blocker therapy has been ineffective or not tolerated.

Section snippets

VPCs are Prevalent in CHF

The frequency of VPCs varies widely depending on the clinical characteristics of the subjects enrolled in the study and the type of recording technique employed (Table 1). In healthy adults free of CHF or CAD, VPC incidence on 0.5–1-minute resting electrocardiographic (ECG) strips is ∼1%.19, 20 VPCs are much more frequent in patients with CHF. In subjects referred for exercise testing, ∼8% of those following a clinical presentation of heart failure presented with ≥1 VPC on the resting ECG

VPCs Can Worsen or Cause Heart Failure

Often, VPCs produce no significant or minimal blood pressure in healthy subjects and in patients with reduced cardiac function (Fig. 1). Frequent VPCs have been demonstrated to be associated with impaired systolic and diastolic function of the heart in subjects without significant structural heart diseases.24, 29, 35, 36, 37

A large community-based cohort study has shown that VPCs were often associated with CHF.24 CHF was seen in 10% of subjects enrolled during an average follow-up period of

Predisposing Factors of VPC-Induced Cardiomyopathy

It can be reasonably expected that a high VPC density is more likely to be associated with tachycardia-induced cardiomyopathy.35 A VPC burden of >24% was independently associated with VPC-induced cardiomyopathy,44 but VPC-induced cardiomyopathy has also been observed even in patients with as few as 5,500 daily VPCs.16

In addition to a high VPC burden, other characteristics such as greater VPC QRS width (≥140 ms), persistent VPC duration, burden of interpolated VPCs, presence of NSVT, multiform

Mechanisms Underlying VPC-Induced LV Dysfunction and CHF

VPCs may contribute to LV dysfunction and development of CHF through several potential mechanisms. Inter- and/or intraventricular dyssynchrony is deemed to be particularly important. The evidence that patients with fascicular VPCs, which excite the ventricles more physiologically with less LV dyssynchrony, rarely had a reduced LVEF45 supports this hypothesis. A study using 2-dimensional speckle tracking imaging found homogeneous reductions in global and segmental strain in the radial and

VPCs Are Associated With Increased Mortality in CHF

Many studies have shown that VPCs are associated with higher arrhythmic risk31, 54, 55 and total mortality rate in patients with LV dysfunction, but this has not been observed by some other investigators.56, 57 A recent meta-analysis study suggests that NSVT contributes to risk stratification for sudden cardiac death (SCD) independently from LVEF.58

It has been shown that preexercise resting VPCs were associated with a 5.48-fold increased risk of cardiovascular mortality in patients with a

Antiarrhythmic Treatment of VPCs Fails to Improve Survival in CHF

In the 2006 American College of Cardiology/American Heart Association/European Society of Cardiology guidelines for management of patients with ventricular arrhythmias and prevention of SCD, VPC suppression for reduction of death is not recommended in either the post–myocardial infarction (MI) patients or patients with nonischemic DCM.1 This recommendation is based on the assumption that ventricular arrhythmias during ambulatory recordings in patients with CHF are not considered to specifically

Elimination of VPCs Can Improve Cardiac Function

A majority of cardiologists may choose to treat VPCs aggressively when VPC-induced cardiomyopathy is suspected. Even for primary cardiomyopathy-induced VPCs, we recommend that these frequent PVCs be aggressively treated as primary arrhythmia, because they can worsen heart failure, contribute (particularly NSVT) to SCD, and be responsible for nonresponse to CRT therapy, as discussed earlier.

Summary

VPCs are one of the most common arrhythmias in the general population, and their incidence increases in the presence of congestive heart failure and/or other forms of structural heart disease. Frequent VPCs are associated with deterioration of cardiac function and may lead to VPC-induced cardiomyopathy. VPC-induced inter- and/or intraventricular dyssynchrony is thought to be responsible for VPC-induced LV dysfunction. In advanced CHF, VPCs and CHF may provoke each other to create a vicious

Disclosure

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    The first 2 authors contributed equally to this work.

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