Dr. Jose Luis Merino,
Frequent and apparently idiopathic premature ventricular contractions (PVCs) are usually considered a benign condition that can be managed with conservative measures. B-blockers are usually very effective. Radiofrequency catheter ablation therapy has generally been reserved for patients with frequent PVCs whose quality of life is disturbed by bothersome symptoms or patients with sustained ventricular tachycardia.
It is a relatively common occurrence for cardiovascular clinicians to see patients with frequent premature ventricular contractions. They may appear in patients without any overt cardiovascular disease, in which case pathogenesis can be considered idiopathic. However, although largely asymptomatic, patients with PVCs can experience upsetting symptoms and there are occasions when the presence of PVCs signifies susceptibility towards more sinister arrhythmias, especially when heart disease is present. Premature ventricular contraction in certain patients are triggered by the same mechanisms that give rise to ventricular tachycardia, which may be cured with catheter ablation. Appropriate clinical evaluation and investigations are important in assessing patients so that effective treatment can be targeted.
Premature ventricular contractions have been described in 1% of clinically normal people as detected by a standard ECG and 40–75% of apparently healthy persons as detected by 24–48 hour ambulatory (Holter) ECG recordings. Kennedy et al demonstrated that frequent (>60/h or 1/min) and complex PVCs could occur in apparently healthy subjects, with an estimated prevalence of 1–4% of the general population.(1) Further to demonstrationg that frequent and complex ventricular ectopy could occur in healthy subjects, they also showed it could be associated with a benign prognosis. Additionaly, both the incidence and complexity of PVCs is increased in almost all heart disease, and could be 90% in coronary artery disease and dilated cardiomyopathy. (2,3)Other studies such as MRFIT (4) and data from the Framingham Heart Study (5), have linked the frequent occurrence of PVCs with an increased risk of sudden cardiac death and death from any cause. However, these studies have been criticised for the lack of rigorous measures to exclude underlying heart disease confounded, which can halve the outcome regarding death. These irregularities did not interfere with normal lifespan when they were occasional but an ominous prognosis was implied if they were frequent. This was shown to be so in more recent times where patients who have had a myocardial infarction were more prone to sudden death if they had frequent PVCs (5). Nevertheless, recent studies have documented that the LV dysfunction in patients with frequent PVCs could recover after elimination of the PVCs by medical treatment or catheter ablation therapy in certain cases. (6-10)
The length and morphology of PVCs are highly variable and depend on the place of origin, the presence of structural heart disease and treatment with antiarrhythmic drugs. In general, QRS duration is mostly longer than 120 ms, because the activation spread occurs from a ventricle to the contralateral one through non-specialised myocardium (figure 1). However, when activation comes from one of the fascicle through a specific conduction system, both ventricles could be activated "synchronously", which may result in a QRS complex of less than 120 ms. (11) Premature ventricular contractions can be classified in various ways, depending on 1) coupling interval (early and delayed), 2) QRS duration (wide and narrow), 3) morphology and 4) complexity. The morphology of PVCs is of great importance in patients susceptible to be treated by catheter ablation, because the 12-lead EKG can identify the origin of PVCs with a certain degree of precision. As a general rule, PVCs originating in the left ventricle have right bundle branch block morphology, and PVCs originating in the right ventricle, have a left bundle branch block pattern. Frequent PVCs can also be observed in patients with hypertension. (12) In the MRFIT Population cohort of over 10 000 men aged 35-57 years, the level of systolic blood pressure was linked with the prevalence of PVCs. More recent data in the Atherosclerosis Risk in Communities (ARIC) study (13) of more than 15 000 white and African American men and women presented extended findings that showed frequent or complex PVCs that are also associated with hypertension. The Framingham study has indicated that patients with left ventricular hypertrophy by electrocardiographic criteria are at greater risk of sudden death and acute myocardial infarction than subjects with a normal heart. The ARIC study also demonstrated that the prevalence of PVCs Increases with the electrocardiographic Increases of left ventricular mass.
In some cases, PVCs may be the first manifestation of underlying structural heart disease. For this reason, in all patients with PVCs, the clinician must perform a detailed clinical history of 12-lead EKG and chest X-ray. Although the relationship between frequent PVCs originating from the ventricular outflow tract and arrhythmogenic right ventricular cardiomyopathy was once suggested. (14) The indication of a record EKG-Holter, a stress test or echocardiogram, depends on whether PVCs persist after the initial evaluation of suspected structural heart disease or the development of complex forms of ventricular arrhythmias. For more than 20 years now, it has been accepted that the presence of PVCs in the absence of structural heart disease entails a favorable benign prognosis, even when they arise frequently. For this reason and because of the proarrhythmic potential of antiarrhythmic drugs (see later), the physician does not need to treat PVCs in this clinical setting, except when the PVCs are responsible for many symptoms. Nevertheless, in some cases very frequent PVCs can produce ventricular dilation and dysfunction (tachycardiomyopathy), the latter being an indication for treatment (ablation or antiarrhythmic drugs), even in the absence of symptoms. However, the clinical importance of frequent PVCs in patients without any LV dysfunction is still unclear. The prognostic significance of PVCs in ischemic heart disease is less benign. Indeed, in patients who have suffered a myocardial infarction, the presence of PVCs has been associated with an increase of up to 3 times the risk of sudden death. (2,3,15) There are conflicting results as to the meaning of PVCs in stress testing. Frolkis et al, demonstrated that the presence of frequent PVCs during recovery from exercise testing is a better predictor of the risk of sudden death than the isolated presence of PVCs reached during the effort. (16) Caffeine is a central stimulant which can increase sympathetic activity. Clinical impression and anecdotes often associate arrhythmias with consumption of caffeine, alcohol and tobacco has been widely practiced in managing patients with palpitation despite the relative lack of direct evidence. Animal studies have shown that caffeine administration at high doses could induce and increase the frequency of PVCs. Some epidemiological data exist with an association between PVCs activity with caffeine intake, but experimental human studies have not produced consistent results to establish this link.
The thinking behind the necessity to suppress PVCs was studied in the Cardiac Arrhythmia Suppression Trial (CAST).(17) This study hypothesis that the suppression of asymptomatic PVCs or minimally symptomatic after myocardial infarction, would reduce arrhythmic death. The authors concluded that treatment with Flecainide and Encainide was an independent risk factor for arrhythmic cause death, cardiac death and non-arrhythmic mortality. This excess mortality was independent of time post-AMI. This Further study highlights the proarrhythmic effect of these drugs in patients with heart disease and disputes the notion of using drugs simply for the sake of suppressing PVCs.
PVCs originating from the RVOT have been associated with malignant ventricular arrhythmias. The ability of frequent PVCs originating from a focal source in triggering idiopathic ventricular fibrillation (VF) in seemingly normal hearts was first reported by Haissaguerre et al. (18) The PVCs were mapped to sites at the RVOT and also along the distal Purkinje system in both left and right ventricles. Catheter ablation was shown to be effective in acutely eliminating VEBs and reducing the incidence of further VF recurrence. Similar triggers have been shown in selected patients with long QT and Brugada syndromes with report of successful elimination of PVCs with catheter ablation. Further studies in large numbers of patients with longer follow up are required to assess the full prognostic benefit of this approach. Progressive PVCs are induced with exercise or stress which can cause syncope or sudden death with polymorphic VT or VF. Treatment is usually with b blockers and ICD implantation.
Figure 1 : 55 years-old patient with frequent and asymptomatic premature ventricular contractions.
It is a relatively common occurrence for cardiovascular clinicians to see patients with frequent premature ventricular contractions. Frequent and apparently idiopathic PVCs are usually considered a benign condition that can be managed with conservative measures. B-blockers are usually very effective. Radiofrequency catheter ablation has generally been reserved for patients with frequent PVCs whose quality of life is disturbed by bothersome symptoms or patients with sustained VT. Most of the remaining patients exhibit no severe clinical symptoms, and so the condition of those patients with frequent PVCs without any overt symptoms, is believed to be relatively benign.
1. Kennedy HL, Whitlock JA, Sprague MK, et al. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy. N Engl J Med 1985;312:193–7. 2. Bigger J, Dresdale R, Heissenbuttel R, et al. Ventricular arrhythmias in isquemic heart disease: mechanism, prevalence, significance and management. Prog Cardiovascular Dis 1977;19:255-300. 3. Moss A, Davis H, Camilla J, et al. Ventricular ectopic beat and their relation to sudden and non sudden cardiac death after myocardial infarction. Circulation 1979;60:998-1003. 4. Abdalla IS, Prineas RJ, Neaton JD, et al. Relation between ventricular premature complexes and sudden cardiac death in apparently healthy men. Am J Cardiol 1987;60:1036–42. 5. Bikkina M, Larson MG, Levy D. Prognostic implications of asymptomatic ventricular arrhythmias: the Framingham Heart Study. Ann Intern Med1992;117:990–6. 6. Zalzstein E, Wagshal A, Zucker N, et al. Ablation therapy of tachycardia-related cardiomyopathy. Isr Med Assoc J 2003;5:64–5. 7. Redfearn DP, Hill JD, Keal R, et al. Left ventricular dysfunction resulting from frequent unifocal ventricular ectopics with resolution following radiofrequency ablation. Europace 2003;5:247–50. 8. Takemoto M, Yoshimura H, Ohba Y, et al. Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract improves left ventricular dilation and clinical status in patients without structural heart disease. J Am Coll Cardiol 2005;45:1259–65. 9. Bogun F, Crawford T, Reich S, et al. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: Comparison with a control group without intervention. Heart Rhythm 2007;4:863–7. 10. Sekiguchi Y, Aonuma K, Yamauchi Y, et al. Chronic hemodynamic effects alter radiofrequency catheter ablation of frequent monomorphic ventricular premature beats. J Cardiovasc Electrophysiol 2005;16:1057–63. 11. Elizari M. Arritmias cardíacas. En: Bertolasi C Ed. Cardiología 2000. Buenos Aires: Editorial Panamericana, 2001;3051-12. 12. Simpson RJ Jr, Cascio WE, Schreiner PJ, et al. Prevalence of premature ventricular contractions in a population of African American and white men and women: the Atherosclerosis Risk in Communities (ARIC) study. Am Heart J 2002;143:535–40. 13. Almendral J, Villacastin JP, Arenal A, et al. Evidence favoring the hypothesis that ventricular arrhythmias have prognostic significance in left ventricular hypertrophy secondary to systemic hypertension. Am J Cardiol 1995;76:60D–3D. 14. O’Donnell D, Cox D, Bourke J, et al. Clinical and electrophysiological differences between patients with arrhythmogenic right ventricular dysplasia and right ventricular outflow tract tachycardia. Eur Heart J 2003;24:801–10. 15. Coronary Drugs Project Research Group: Prognostic importance of premature beats following myocardial infarction: experience in the Coronary Drugs Project. JAMA 1973:224:1116-24. 16. Frolkis J, Pothier C, Blackstone E, et al. Frequent ventricular ectopy after exercise as a predictor of death. N Engl J med 2003;348:781-90. 17. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989;321:406–12. 18. Haissaguerre M, Shah DC, Jais P, et al. Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation. Lancet 2002;359:677–8 19. G André Ng. Treating patients with ventricular ectopic beats. Heart 2006;92:1707–12.
Our mission: To reduce the burden of cardiovascular disease
© 2017 European Society of Cardiology. All rights reserved