eMedicine Specialties > Cardiology > Arrhythmias
Ventricular Premature Complexes
Updated: Aug 24, 2009
Introduction
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). The CAST and other 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.1
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.
Clinical
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. Conversely, the VPC itself may be underperfused and consequently not perceived by radial pulse, resulting in a spurious documentation of bradycardia.
Causes
- Cardiac causes include the following:
- Acute myocardial infarction
- Valvular heart disease, especially mitral valve prolapse
- Cardiomyopathy (eg, ischemic, dilated, hypertrophic, infiltrative)
- Myocardial stretch
- Cardiac contusion
- Bradycardia
- Tachycardia (high-catecholamine state)
- Noncardiac causes include the following:
- Electrolyte disturbances (hypokalemia, hypomagnesemia, or hypercalcemia)
- Medications (eg, digoxin, tricyclic antidepressants, aminophylline, amitriptyline, pseudoephedrine, fluoxetine)
- Other drugs (eg, cocaine, amphetamines, caffeine, alcohol)
- Anesthetics
- Surgery
- Infection
- Stress
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Further Reading
Keywords
ventricular premature complexes, ventricular extrasystole, ventricular ectopic beats, benign ventricular arrhythmia, missed beats, VPC, PVC, premature ventricular complex, VPD, ventricular premature depolarization, VPB, ventricular premature beat, ventricular arrhythmia, beta-blockers, myocardial infarction, MI, postmyocardial infarction, post-MI, congestive heart failure, CHF, coronary artery disease, CAD, ventricular ectopy, ventricular tachycardia, VT
