Background
Premature ventricular complexes (PVCs) (also known as ventricular premature complexes [VPCs]) are ectopic impulses originating from an area distal to the His Purkinje system. PVCs are the most common ventricular arrhythmia. [1] Assessment and treatment of PVCs is challenging and complex, and these are highly dependent on the clinical context. The prognostic significance of PVCs is variable and, again, best interpreted in the context of the underlying cardiac condition.
The approach to the evaluation and management of PVCs has undergone dramatic changes in the last decade. Observational studies and inferences from typical electrophysiology studies were initially focused on ventricular ectopy triggering ventricular tachycardia which, in turn, can degenerate into ventricular fibrillation, as a mechanisms for sudden cardiac death—particularly post myocardial infarction (MI). [1] The treatment paradigm in the 1970s and 1980s was to eliminate PVCs in patients after MI. The Cardiac Arrhythmia Suppression Trial (CAST) and other arrhythmia suppression studies have demonstrated that eliminating PVCs with available antiarrhythmic drugs increases the risk of death to patients without providing any measurable benefit. [2]
Pathophysiology
The fundamental underlying etiology of PVCs remain to be determined. [3] Very few studies have evaluated the pathophysiology of PVCs in human subjects; most of the information is derived from animal studies. However, what is known is that ventricular monocytes at the cellular level spontaneously depolarize, leading to a cardiac cycle that is an out-of-sync extrasystole. [1] The most prevalent PVCs are from the outflow tract and appear to be due to triggered activity from excess calcium and afterdepolarizations. [4]
Three common mechanisms exist for PVCs: automaticity, reentry, and triggered activity. [3, 4]
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Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a PVCs. 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.
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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.
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Triggered activity: After depolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a PVC Afterdepolarization can occur either during (early) or after (late) completion of repolarization. Early afterdepolarizations commonly are responsible for bradycardia associated PVCs, but they also can be present with ischemia and electrolyte abnormalities.
Etiology
Cardiac causes of PVCs include the following:
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Acute myocardial infarction
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Valvular heart disease, especially mitral valve prolapse
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Cardiomyopathy (eg, ischemic, dilated, hypertrophic, infiltrative) [5]
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Myocardial stretch
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Cardiac contusion
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Bradycardia
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Tachycardia (high-catecholamine state)
Noncardiac causes of PVCs include the following:
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Electrolyte disturbances (hypokalemia, hypomagnesemia, or hypercalcemia)
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Medications (eg, digoxin, tricyclic antidepressants, aminophylline, amitriptyline, pseudoephedrine, fluoxetine)
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Other drugs (eg, cocaine, amphetamines, caffeine, alcohol)
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Anesthetics
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Surgery
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Infection
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Stress
Epidemiology
United States data
Although the reported prevalence of PVCs varies between studies, depending on the population studied, duration of observation, and method of detection, PVCs are very common in most patients with long-term ambulatory monitoring. [1, 3] PVCs appear on standard electrocardiograms (ECGs) in an estimated 1% of clinically normal individuals and in 40-75% of healthy people evaluated by short-term ambulatory monitoring. [1, 6] The Atherosclerosis Risk in Communities (ARIC) trial found a higher PVC prevalence with increasing age, Black ethnicity, male sex, and lower education, as well with the presence of structural heart disease, hypertension, and lower levels of serum magnesium or potassium. [1, 7]
In asymptomatic patients, PVCs are infrequently noted when only a single 12-lead ECG is used for ascertainment. The Framingham heart study (with 1-h ambulatory ECG) suggested that the prevalence rate of 1 or more PVCs 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 PVCs was 58% in men and 49% in women. Other studies using 24-hour ambulatory monitoring showed a PVC 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. PVCs also are common in patients with hypertension, ventricular hypertrophy, cardiomyopathy, and mitral valve prolapse.
International data
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 PVCs per hour when 24-h Holter monitoring was used. [8, 9]
In a study evaluating the features of frequent idiopathic PVCs in the Korean, investigators reported a mean patient age of 54.7 ± 16.8 years and a slight female preponderance (54.8%). [10] The most common typical PVCs-related symptoms/signs were palpitation and a dropped beat (59.2%), whereas the most common ECG features were left bundle branch block, an inferior axis, and late precordial R-wave transition.
Sex- and age-related demographics
The Framingham heart study demonstrated increased prevalence of PVCs in men compared with women. The difference was especially higher in men with CAD than in women with CAD.
In a 2024 report, of 1067 participants from the Women's Health Initiative Strong and Healty (WHISH) trial without a history of atrial fibrillation (AF) but had a 5-year predicted risk of incident of at least 5% by CHARGE-AF score, 4.3% of postmenopausal women had at least 1 patch of frequent PVCs, and 1.1% had at least 1 episode of nonsustained ventricular tachycardia.(NSVT). [11] Gomez et al found a direct correlation between CHARGE-AF score and NSVT and PVC frequency. Sequential monitoring increased identification of PVC frequency.
The ARIC trial found that over 6% of middle-aged adults have PVCs on 2-minute ECGs. [7] As noted above, the study also showed Black ethnicity and male sex are associated with a greater prevalence of PVCs.
PVCs 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.
Prognosis
The prognosis depends on the frequency and characteristics of PVCs and on the type and severity of associated structural heart disease. [1, 3, 12] Overall, PVCs are associated with an increased risk of death, especially when CAD is diagnosed, but the relationship between PVC 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 PVCs.
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. [13] Less frequent PVCs did not increase the risk.
In general, multimorphic PVCs connote a poorer prognosis than uniform morphologic PVCs. In patients post-MI, frequent PVCs (>10/h) are associated with increased mortality in the prethrombolytic era, but the association in patients receiving thrombolysis is weak.
In two 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. [13, 14] However, in another study, frequent PVCs only during exercise did not independently predict an increased risk; instead frequent PVCs during recovery was a stronger predictor of death. [15]
Frequent PVCs, 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. [13, 16, 17, 18] 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. [19]
In a study that evaluated the prognostic value of PVC burden in 1767 individuals with persistent atrial fibrillation (AF), Yen et al reported a significant association of 24-hour PVC burden and the presence of consecutive PVCs, with an independent association with all-cause and cardiovascular mortality in the presence of persistent AF. [12] Multivariate analysis determined significant baseline predictors of all-cause and cardiovascular mortality were increasing age; the presence of heart failure and/or stroke; the use of ACEIs/ARBs, beta blockers, digoxin, and/or anticoagulants; and lower estimated glomerular filtration rate. [12]
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Premature Ventricular Complexes (PVCs). Ventricular trigeminy is present. Note that the PVCs are unimorphic and that a compensatory pause follows each PVC. This patient has asymptomatic idiopathic PVCs originating from the right ventricular outflow tract.
Tables
Class |
Arrhythmia |
0 |
None |
1 |
Unifocal; < 30/h |
2 |
Unifocal; ≥ 30/h |
3 |
Multiform |
4A |
2 consecutive |
4B |
≥ 3 consecutive |
5 |
R-on-T phenomenon |
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