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Premature Ventricular Contractions

2019; Lippincott Williams & Wilkins; Volume: 140; Issue: 8 Linguagem: Romeno

10.1161/circulationaha.119.040015

1524-4539

Edward P. Gerstenfeld, Teresa De Marco,

Atrial Fibrillation Management and Outcomes

HomeCirculationVol. 140, No. 8Premature Ventricular Contractions Free AccessArticle CommentaryPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessArticle CommentaryPDF/EPUBPremature Ventricular ContractionsNot Always Innocent Bystanders Edward P. Gerstenfeld, MD and Teresa De Marco, MD Edward P. GerstenfeldEdward P. Gerstenfeld Edward P. Gerstenfeld, MD, MU-East 4th Floor, 500 Parnassus Ave, San Francisco, CA 94143. Email E-mail Address: [email protected] Division of Cardiology, Department of Medicine, University of California, San Francisco. and Teresa De MarcoTeresa De Marco Division of Cardiology, Department of Medicine, University of California, San Francisco. Originally published19 Aug 2019https://doi.org/10.1161/CIRCULATIONAHA.119.040015Circulation. 2019;140:624–626A 42-year-old woman presents for evaluation of palpitations. An ECG demonstrates sinus rhythm with premature ventricular contractions (PVCs) of left bundle branch, inferior axis morphology (Figure [A]). A monitor reveals a 33% PVC burden, and an echocardiogram is normal. What should she be advised?Download figureDownload PowerPointFigure. ECGs demonstrating narrow and wide premature ventricular contractions (PVCs). A, Patient with a narrow left bundle branch/inferior axis PVC. The patient had normal left ventricular (LV) function but was referred because of symptoms of persistent palpitations despite trials of metoprolol and flecainide. Ablation was performed successfully in the right parahisian region. B, A right bundle branch/superior axis PVC. This PVC is wider, and the patient had developed a cardiomyopathy with an ejection fraction of 42%. This PVC was ablated on the posteromedial papillary muscle and resulted in compete restoration of normal LV function.Isolated PVCs have typically been considered benign, but emerging data suggest that a high PVC burden may have adverse consequences in some patients. Several studies showed convincingly that patients with frequent PVCs after myocardial infarction were at a higher risk of sudden death. This eventually led to the prospective, randomized CAST (Cardiac Arrhythmia Suppression Trial), in which patients were randomized after myocardial infarction to PVC suppression with encainide, flecainide, or placebo.1 As we know from this pivotal trial, pharmacological PVC suppression actually led to an increase in mortality compared with placebo. This established the practice that pharmacological treatment of isolated PVCs should be undertaken only to treat severe symptoms.However, Duffee and colleagues2 noted that in patients with dilated cardiomyopathy (DCM) and frequent PVCs, suppression led to significant improvement in left ventricular (LV) function. A larger study demonstrated not only that frequent PVCs were associated with DCM but also that PVC elimination with catheter ablation led to improvement or normalization of LV function in >80% of patients.3 This study and others have led to increasing enthusiasm in the electrophysiology and heart failure communities for treating PVCs in patients with unexplained DCM.However, there are clearly some patients with DCM in whom PVCs are present and unrelated to the cardiomyopathy. This always raises the proverbial "chicken-and-egg" question of which came first. Several retrospective studies have sought to identify differences in the characteristics of PVCs among patients with versus without reversible cardiomyopathy. The most consistent factor associated with reversible cardiomyopathy was PVC burden. The best cutoff for predicting PVC cardiomyopathy varied among studies from 10% to 24% over a 24-hour period. No patients with PVC burden 10%, studies suggest that the probability of developing DCM is ≈40% over the ensuing 15 years.4 Therefore, there must be other factors in addition to PVC burden that contribute to the development of cardiomyopathy. PVCs with a wider QRS (Figure [B]) have also been found to be associated with a higher incidence of cardiomyopathy. Finally, the coupling interval (duration between the prior conducted sinus QRS and the PVC) may be important, although the data are less clear.What about patients with structurally normal hearts and frequent PVCs? In a study of healthy patients in the Cardiovascular Health Study who underwent baseline Holter monitoring, those in the upper quartile of PVC frequency had an increased risk of incident heart failure and death compared with the lowest quartile during a median follow-up of >13 years.4 This occurred with a median daily PVC burden in the highest quartile ranging from only 0.1% to 17.7%. Therefore, although we recognize that association does not prove causation, the cumulative evidence raises the question of whether the adverse effect of frequent PVCs in the general population may be underestimated.Is it possible that PVCs are simply a forme fruste of disease in patients already destined to develop a cardiomyopathy? Several translational studies have demonstrated that healthy canines or swine subjected to frequent PVCs via an implanted pacemaker develop DCM over only 2 to 3 months. Our group demonstrated that PVC-induced cardiomyopathy was directly related to the dyssynchrony induced by the offending PVC, which was proportional to the PVC QRS duration.5 We also showed that swine with PVC-induced cardiomyopathy developed diffuse fibrosis and molecular markers of sarcoplasmic reticulum calcium depletion, similar to findings described in mouse models of cardiomyopathy. Therefore, we believe there is sufficient evidence that frequent PVCs can be implicated as a cause of DCM.So how should we clinically approach patients with abnormal LV function and PVCs? We all recognize that DCM represents a heterogeneous group of common and largely irreversible forms of heart muscle disease. Therefore, at least one 24-hour Holter or other prolonged continuous monitor should be considered in any DCM of unclear origin, particularly in patients with evidence of PVCs by symptoms or ECG. Most studies have reported that a PVC burden of at least 10% is associated with cardiomyopathy, and reduction to 10% PVCs should initially receive medical therapy to suppress PVCs. This often begins with β-antagonists in addition to other guideline-directed medical therapy for LV dysfunction. Although antiarrhythmic drugs can be used to suppress PVCs, the associated proarrhythmia and side effects often limit their use. Given the low risk and high success rate of catheter ablation, we have a low threshold to perform catheter ablation in any patient with DCM with a continued high burden of PVCs (>10%). In patients whose LV function returns to normal after PVC elimination, we often continue guideline-directed medical therapy for DCM for at least 6 months. Our preclinical data suggest that fibrosis and dyssynchrony may persist even after return to apparently normal LV function.What about patients with normal LV function and frequent PVCs? Patients who are asymptomatic with <5% PVC burden can be reassured with no further follow-up. In patients who are asymptomatic with a higher PVC burden, we typically recommend repeat monitoring, including echocardiography and rhythm monitoring at yearly intervals, seeking evidence of LV dilatation or dysfunction. β-Antagonist therapy may be considered to test for reduction of PVC burden, but only if well tolerated. Analysis of the 12-lead ECG PVC morphology and QRS duration may also be helpful. Those with typical septal right ventricular outflow tract PVCs that are quite narrow (Figure [A]) are likely to be at the lowest risk of developing a cardiomyopathy, whereas those with wider PVCs of epicardial or papillary muscle origin (Figure [B]) may be at higher risk.Further work is needed to determine the mechanism by which PVCs and other forms of dyssynchrony lead to cardiomyopathy. We hope this mechanistic inquiry will lead to treatments that can prevent the development of cardiomyopathy. Future work may also help better quantify the risk factors associated with the development of cardiomyopathy. We anticipate that measures of PVC burden, duration, and coupling interval will be combined into a PVC risk score that would help clinicians decide which patients may benefit from prophylactic treatment. As clinicians, we should recognize that frequent PVCs on a 12-lead ECG are not always benign and should prompt further evaluation.DisclosuresDr Gerstenfeld has received research grants from Biosense-Webster and Abbott, and honoraria from Biosense-Webster, Boston Scientific, and Abbott. Dr De Marco is a consultant to Boston Scientific.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.https://www.ahajournals.org/journal/circEdward P. Gerstenfeld, MD, MU-East 4th Floor, 500 Parnassus Ave, San Francisco, CA 94143. Email edward.[email protected]eduReferences1. 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; 321:406–412.CrossrefMedlineGoogle Scholar2. Duffee DF, Shen WK, Smith HC. Suppression of frequent premature ventricular contractions and improvement of left ventricular function in patients with presumed idiopathic dilated cardiomyopathy.Mayo Clin Proc. 1998; 73:430–433. doi: 10.1016/S0025-6196(11)63724-5CrossrefMedlineGoogle Scholar3. Baman TS, Lange DC, Ilg KJ, Gupta SK, Liu TY, Alguire C, Armstrong W, Good E, Chugh A, Jongnarangsin K, et al. Relationship between burden of premature ventricular complexes and left ventricular function.Heart Rhythm. 2010; 7:865–869. doi: 10.1016/j.hrthm.2010.03.036CrossrefMedlineGoogle Scholar4. Dukes JW, Dewland TA, Vittinghoff E, Mandyam MC, Heckbert SR, Siscovick DS, Stein PK, Psaty BM, Sotoodehnia N, Gottdiener JS, et al. Ventricular ectopy as a predictor of heart failure and death.J Am Coll Cardiol. 2015; 66:101–109. doi: 10.1016/j.jacc.2015.04.062CrossrefMedlineGoogle Scholar5. Walters TE, Rahmutula D, Szilagyi J, Alhede C, Sievers R, Fang Q, Olgin J, Gerstenfeld EP. Left ventricular dyssynchrony predicts the cardiomyopathy associated with premature ventricular contractions.J Am Coll Cardiol. 2018; 72(23 Pt A):2870–2882. doi: 10.1016/j.jacc.2018.09.059CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Wong D, Li Y, Deepu J, Ho W and Heng C An Energy Efficient ECG Ventricular Ectopic Beat Classifier Using Binarized CNN for Edge AI Devices, IEEE Transactions on Biomedical Circuits and Systems, 10.1109/TBCAS.2022.3152623, 16:2, (222-232) Gamilov T, Kopylov P, Serova M, Syunyaev R, Pikunov A, Belova S, Liang F, Alastruey J and Simakov S (2020) Computational Analysis of Coronary Blood Flow: The Role of Asynchronous Pacing and Arrhythmias, Mathematics, 10.3390/math8081205, 8:8, (1205) Yu J, Wang X, Chen X and Guo J (2020) Searching for Premature Ventricular Contraction from Electrocardiogram by Using One-Dimensional Convolutional Neural Network, Electronics, 10.3390/electronics9111790, 9:11, (1790) Yu J, Wang X, Chen X and Guo J (2021) Automatic Premature Ventricular Contraction Detection Using Deep Metric Learning and KNN, Biosensors, 10.3390/bios11030069, 11:3, (69) Suba S, Fleischmann K, Schell-Chaple H, Prasad P, Marcus G, Hu X, Pelter M and Cannatà A (2021) Diagnostic and prognostic significance of premature ventricular complexes in community and hospital-based participants: A scoping review, PLOS ONE, 10.1371/journal.pone.0261712, 16:12, (e0261712) August 20, 2019Vol 140, Issue 8 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.119.040015PMID: 31424993 Originally publishedAugust 19, 2019 Keywordsventricular premature complexesPDF download Advertisement SubjectsAnimal Models of Human DiseaseArrhythmiasCatheter Ablation and Implantable Cardioverter-Defibrillator