Ventricular Premature Complexes

Background
Ventricular premature complexes (VPCs) are ectopic impulses originating from an area distal to the His Purkinje system. VPCs are the most common ventricular arrhythmia. Assessment and treatment of VPCs is challenging and complex. The significance of VPCs is interpreted in the context of the underlying cardiac condition.
The approach to the evaluation and management of VPCs has undergone dramatic changes in the last decade. Ventricular ectopy leading to ventricular tachycardia (VT), which, in turn, can degenerate into ventricular fibrillation, is one of the common mechanisms for sudden cardiac death. The treatment paradigm in the 1970s and 1980s was to eliminate VPCs in patients after myocardial infarction (MI). Recent arrhythmia suppression studies have demonstrated that eliminating VPCs with available antiarrhythmic drugs increases the risk of death to patients without providing any measurable benefit.
Pathophysiology
Very few studies have evaluated the pathophysiology of VPCs in human subjects. Most of the information is derived from animal studies. Three common mechanisms exist for VPCs, (1) automaticity, (2) reentry, and (3) triggered activity, as follows:

Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a VPC. In animal models, focal mechanisms without evidence of macro-reentry play a major role in the origin of ventricular arrhythmia associated with ischemic cardiomyopathy. Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium.
Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. The slow-conducting tissue could be due to damaged myocardium, as in the case of a healed MI.
Triggered activity: Afterdepolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a VPC. Afterdepolarization can occur either during (early) or after (late) completion of repolarization. Early afterdepolarizations commonly are responsible for bradycardia associated VPCs, but they also can be present with ischemia and electrolyte abnormalities.
Frequency
United States
The reported prevalence of VPCs varies between studies, depending on the population studied, duration of observation, and method of detection. In asymptomatic patients, VPCs are infrequent when only a single 12-lead ECG is used for screening. The Framingham heart study (with 1-h ambulatory ECG) suggested that the prevalence rate of 1 or more VPCs per hour was 33% in men without coronary artery disease (CAD) and 32% in women without CAD. Among patients with CAD, the prevalence rate of 1 or more VPCs was 58% in men and 49% in women. Other studies using 24-hour ambulatory monitoring showed a VPC prevalence rate of 41% in healthy teenage boys aged 14-16 years, 50-60% in healthy young adults, and 84% in healthy elderly persons aged 73-82 years. VPCs also are common in patients with hypertension, ventricular hypertrophy, cardiomyopathy, and mitral valve prolapse.
International
Data from the Gruppo Italiano per lo Studio della Sopravvivenza dell'Infarto Miocardico 2 study demonstrated that 64% of patients who had MI then had ventricular arrhythmia and 20% of patients had more than 10 VPCs per hour when 24-h Holter monitoring was used.
Mortality/Morbidity
Prognosis depends on the frequency and characteristics of VPCs and on the type and severity of associated structural heart disease. 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 and no benefit results in suppressing VPCs to improve survival in any population.

In asymptomatic patients, frequent ventricular ectopy (defined as a run of 2 or more consecutive premature ventricular depolarizations or with premature ventricular depolarizations constituting >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. 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 a recent study, a frequent VPC (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 recovery from exercise was an independent predictor of death. However, frequent VPCs only during exercise did not independently predict an increased risk.

Frequent VPCs, especially when they occur in a bigeminal pattern, can precipitate tachycardia-induced cardiomyopathy that can be reversed by elimination of the PVCs through catheter ablation.
Sex
The Framingham heart study demonstrated increased prevalence of VPCs in men compared with women. The difference was especially higher in men with CAD than in women with CAD.
Age
VPCs are uncommon in children (suggested prevalence rate of 0.8-2.2% from the Vanderbilt Medical Center; exact prevalence not known). Prevalence increases with age.
History
Various symptoms are associated with VPCs, but the exact prevalence of symptoms is not known. Typical symptoms include palpitations, light-headedness, syncope, atypical chest pain, or fatigue. Palpitations are due to an augmented post-VPC beat and may be sensed as a pause rather than an extra beat.
Physical
VPCs frequently are associated with variable or decreased intensity of heart sounds. The augmented beat following a dropped beat is heard frequently. Bounding jugular pulse (cannon A wave) from a loss of atrioventricular (AV) synchrony may be present. The follow-up beat after a VPC is stronger due to the postextrasystolic compensatory pause, allowing greater left ventricular (LV) filling, which usually causes greater intensity of that beat. This is known as extrasystolic potentiation.
Lab Studies
Look for correctable causes of VPCs, such as medications, electrolyte disturbances, infection, and myocardial ischemia or MI.
Obtain serum electrolyte and magnesium levels.
Imaging Studies
Look for underlying structural heart abnormalities that can predispose to VPCs.
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Assess the degree of LV dysfunction by noninvasive techniques such as echocardiography or radionuclide imaging.
Echocardiography may be preferable because it also provides structural information about the heart.
Other Tests
In high-risk patients, ie, those with reduced ejection fraction (EF) and VPCs, a 24-hour Holter monitor may help establish the degree of electrical instability.
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The severity of LV dysfunction, along with the complexity and frequency of the VPC, determines the aggressiveness of management.
Suppressing the VPCs themselves is not the focus of treatment unless patients are extremely symptomatic; rather, treatment may be implemented if the patient is felt to be at high risk of sudden cardiac death.
Treatment of the underlying structural heart disease also is extremely important. This includes acute syndromes, such as ischemia and infarction, the treatment of which involves reperfusion.
ECG should be performed to look for structural cardiac abnormalities. Diagnostic criteria include the following:
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Wide (duration exceeding the dominant QRS complexes) and bizarre QRS complexes are present.
No preceding premature P waves occur, and, rarely, a sinus P wave is conducted.
The T wave usually is in the opposite direction from the R wave.
Full compensatory pause is common.
VPCs originating from the left ventricle typically produce a right bundle-branch block (BBB) pattern on QRS.
VPCs originating from right ventricle typically produce left BBB-like pattern on QRS.
Idiopathic VPCs often originate from the right ventricular outflow tract and have a left bundle rightward axis morphology.
Electrophysiologic study
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Electrophysiologic study (EPS) may be indicated for 2 types of patients with VPCs, (1) those with a structurally normal heart with symptomatic VPCs, for whom pharmacological treatment or catheter ablation is indicated and (2) those with VPCs and structural heart disease, for whom risk stratification for sudden cardiac death is indicated.
According to current American College of Cardiology/American Heart Association guidelines, class I indications for EPS are patients with CAD, low EF (<0.36), and nonsustained VT on ambulatory ECG. Class II indications for catheter ablation apply to patients with a highly symptomatic uniform morphology of VPC, couplets, and nonsustained VT.
Exercise stress testing should be performed to look for coronary ischemia, exercise-induced arrhythmia, or both.