syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'Management' and "Ventricular arrhythmias during acute myocardial infarction: Prevention and treatment", section on 'Ventricular premature beats'.) Chronic coronary syndrome In patients who have had past myocardial infarctions, PVCs, particularly if frequent (more than 10 per hour) or complex (ie, repetitive forms, primarily nonsustained ventricular tachycardia), appear to be associated with a worse prognosis. Most patients with a prior myocardial infarction will be taking a beta blocker as part of standard therapy for their underlying disease, which may be associated with a https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 12/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate reduction in PVCs [71,72]. (See "Beta blockers in the management of chronic coronary syndrome" and "Primary pharmacologic therapy for heart failure with reduced ejection fraction".) Amiodarone is the preferred antiarrhythmic drug in patients with symptomatic PVCs despite beta blocker therapy. Attempted suppression of PVCs with class IC antiarrhythmic drugs in patients with coronary artery disease has been associated with increased mortality ( figure 2). (See 'Antiarrhythmic therapy' above and "Amiodarone: Clinical uses", section on 'Amiodarone for ventricular arrhythmias'.) In cases of complex and/or symptomatic ventricular arrhythmia, an electrophysiology study with programmed ventricular stimulation may better guide therapy. In patients with inducible sustained ventricular tachycardia, an ICD will be needed [73]. (See "Implantable cardioverter-defibrillators: Overview of indications, components, and functions", section on 'Secondary prevention'.) Patients with cardiac resynchronization therapy (CRT) Patients with a CRT device need to have effective biventricular pacing greater than 98 percent of all ventricular beats in order to have a mortality reduction [74]. Frequent PVCs compromise effective biventricular pacing and diminish clinical response to CRT [75]. Hence, a more aggressive approach to suppress PVCs is recommended in these patients. (See "Implantable cardioverter- defibrillators: Overview of indications, components, and functions".) Hypertension This is discussed elsewhere. (See 'Manage triggers and risk factors' above.) Long QT syndrome This is discussed elsewhere. (See "Congenital long QT syndrome: Treatment".) Brugada syndrome This is discussed elsewhere. (See "Brugada syndrome or pattern: Management and approach to screening of relatives".) Hypertrophic cardiomyopathy This is discussed elsewhere. (See "Hypertrophic cardiomyopathy: Management of ventricular arrhythmias and sudden cardiac death risk".) Arrhythmogenic right ventricular cardiomyopathy This is discussed elsewhere. (See "Arrhythmogenic right ventricular cardiomyopathy: Treatment and prognosis".) Cardiac sarcoidosis This is discussed elsewhere. (See "Management and prognosis of cardiac sarcoidosis".) https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 13/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate Amyloid cardiomyopathy This is discussed elsewhere. (See "Amyloid cardiomyopathy: Treatment and prognosis".) MANAGEMENT OF LOW-RISK PATIENTS Low-risk patients are those in whom cardiomyopathy and/or inherited arrythmia syndrome has been reasonably excluded. Our approach to treatment in low-risk patients differs according to whether there are significant PVC-related symptoms. Specific PVC-related symptoms are discussed elsewhere. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'Symptoms'.) Asymptomatic patients with low premature ventricular complex burden For patients with a low burden of PVCs (<1 percent or 1000 PVCs/day), no underlying apparent structural heart disease, and no symptoms, neither medical therapy nor catheter ablation are required; observation and reassurance along with eliminating possible triggers are appropriate ( algorithm 2 and algorithm 3) [49]. While PVCs have been associated with increased risk of cardiovascular death and other adverse outcomes, there is no clear evidence that PVC suppression or elimination with beta blockers, non-dihydropyridine calcium channel blockers, antiarrhythmic drugs, or catheter ablation improves overall survival in patients who have no symptoms, no heart disease, and no sustained ventricular arrhythmias. Patient with symptoms and/or high premature ventricular complex burden Most low-risk patients with significant symptoms from their PVCs will require medical therapy or ablation in an effort to reduce or eliminate symptoms ( algorithm 2 and algorithm 3). Patients with high PVC burden (>15 percent or 15,000 PVCs/day) also benefit from treatment even in the absence of bothersome symptoms to lower their risk of PVC-induced cardiomyopathy. PVC-induced cardiomyopathy typically takes several months or a few years to develop. In a study of 240 patients referred for PVC ablation, symptom duration of 30 to 60 months, as well as symptom duration >60 months, independently predicted impaired LV function (odds ratio 4.0, 95% CI 1.1-14.4 and 20.1, 95% CI 6.3-64.1, respectively) [76]. In a low-risk patient who has more noticeable symptoms in a quiet environment, such as at night while lying in bed, counseling them to move around and increase their heart rate may alleviate symptoms and provide reassurance to the patient. https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 14/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate The decision to recommend antiarrhythmic medication or radiofrequency catheter ablation in a particular patient will depend on many clinical factors and also on patient preference. Some patients will not want to undergo an invasive catheter ablation procedure. Potential risks of the catheter ablation are discussed elsewhere. (See "Overview of catheter ablation of cardiac arrhythmias", section on 'Complications'.) Initial therapy Prior to initiating therapy, correctable causes or triggers should be identified and corrected ( table 1). Beta blockers For low-risk patients with symptomatic and/or a high burden of PVCs, we suggest first-line therapy with a beta blocker. (See 'Beta blockers' above.) Non-dihydropyridine calcium channel blockers In patients without a reduced LVEF, a non-dihydropyridine calcium channel blocker can be substituted if beta blockers are not tolerated or are not successful in reducing symptoms. A table lists specific agents with dosages ( table 2). Non-dihydropyridine calcium channel blockers may be particularly effective in patients without apparent structural heart disease when PVCs are often due to triggered activity of calcium-dependent mechanisms. One example of this is PVCs of fascicular origin (relatively narrow QRS, right bundle branch block-like, left axis deviation) ( waveform 6). Calcium channel blockers may also be preferred to beta blockers if hypertension treatment is needed. Patients should be evaluated for PVCs burden with periodic examinations and continuous ECG monitoring, usually for 24 to 48 hours. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'Ambulatory monitoring'.) If symptoms and PVC burden have been reduced and are not high, treatment should be continued. If a patient prefers to stop or reduce their medications, a trial of weaning and/or stopping may be done after 6 to 12 months. (See 'Premature ventricular complex burden' above and 'Beta blockers' above.) A prospective cohort study of 100 untreated adult patients (mean age 51.8 years, 57 percent female) with a median PVC burden of 18.4 percent showed that reduction to <1 percent of PVCs occurred in 44 percent at a median follow-up of 15.4 months. Recurrence was uncommon (9.1 percent) [77]. Hence, the authors suggested that a strategy of active surveillance may be appropriate for the majority of patients with frequent idiopathic PVCs in association with preserved LVEF. One may extrapolate from these studies that in certain patients who respond to https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 15/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate medical treatment, one may trial them off antiarrhythmic drug therapy, possibly at one to two years, and closely observe for arrhythmia recurrences. Subsequent therapy For patients with ongoing PVC-related symptoms and/or high burden following initial medical therapy with beta blockers and/or non-dihydropyridine calcium channel blockers, or for those who do not tolerate medical therapy due to adverse effects, antiarrhythmic medications or catheter ablation are each reasonable next steps. In patients without structural heart disease or coronary artery disease, it is reasonable to start a class 1C antiarrhythmic rather than to pursue catheter ablation if one or more of the following are present: Multiple PVC morphologies. A low frequency of PVCs (<3 percent or 500 PVCs/day). Patients are deemed to be high-risk candidates for catheter ablation, such as those with challenging PVC foci locations that might limit a successful procedure (eg, epicardium, LV summit, intramural site, papillary muscles, and a para-Hisian location) [78]. A strong patient preference to avoid catheter ablation. The use of antiarrhythmic drugs (eg, flecainide and other class IC antiarrhythmic drugs) ( table 3) for PVCs is an off-label use. Whereas proarrhythmia with these drugs is of concern in patients with structural heart disease, there is little to no concern in patients without underlying heart disease [79]. Importantly, class IC antiarrhythmic agents should not be used to treat patients with PVC-induced cardiomyopathy and LV dysfunction due to grave concerns for proarrhythmia [66,80]. Nevertheless, IC agents have been used in such patients with favorable results. However, these agents should only be prescribed in patients who have ICDs to treat life-threatening ventricular arrythmias [68]. Typical antiarrhythmic options among patients without apparent structural heart disease include: Flecainide, starting dose 50 to 100 mg orally twice daily; maximum daily dose 150 mg twice daily (although doses higher than 100 mg twice daily are rarely used). Propafenone 150 mg three times daily; maximum daily dose 300 mg three times daily. In one observational study of 120 patients with frequent PVCs without structural heart disease, antiarrhythmic medications had superior effectiveness in PVC reduction as https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 16/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate compared with beta blockers and calcium channel blockers and conservative therapy [40]. Median initial PVC burden ranged from 16 to 21 percent. The median relative reduction of PVCs in the conservative therapy, beta blockers/calcium channel blockers, and antiarrhythmic medication cohorts was 33, 31, and 81 percent, respectively. PVC reduction to <1 percent was similar across these groups at 35, 17, 33 percent, respectively. Four patients (3 percent) developed LV dysfunction: One patient was on conservative therapy, two were on a bisoprolol, and one was on flecainide. Rates of adverse drug reactions and medication discontinuation were similar between groups, with no serious adverse events noted. If a patient remains symptomatic and/or has a high PVC burden, catheter ablation should be pursued next. PROGNOSIS The presence of PVCs should alert the clinician to potential coexistent cardiac disease, which may require additional clinical assessment or therapy. In patients without a history of cardiac disease, PVCs are associated with increased mortality. However, prophylactic treatment of asymptomatic PVCs in patients without cardiomyopathy has not been shown to improve mortality. An important caveat pertains to patients with potentially problematic PVCs. (See 'Premature ventricular complex characteristics' above.) No apparent heart disease Mortality Data are mixed as to whether the presence of PVCs in patients with apparently normal hearts is associated with increased mortality. In a meta-analysis of five prospective cohort studies (3629 persons) without apparent heart disease, the presence of PVCs was not associated with all-cause mortality (odds ratio 1.34, 95% CI 0.85-2.12) [81]. However, only one study used advanced testing (ie, echocardiography or stress testing) to exclude underlying structural heart disease. In a Taiwanese cohort of 5778 persons, PVC frequency >12 beats per day was associated with mortality (hazard ratio 1.4, 95% CI 1.28-1.59) [82]. Regarding PVC morphology, an observational study indicated that among 3351 individuals with apparently normal hearts, those with multiform PVCs had an increased incidence of mortality (HR 1.6, 95% CI 1.32-2.03) over a mean follow-up period of 10 years [17]. Reduction in LVEF and heart failure A greater frequency of PVCs has been associated with reduced LVEF and heart failure. Among 1139 patients without known heart disease in the Cardiovascular Health Study, the upper quartile of PVCs on 24-hour Holter monitoring https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 17/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate (>0.12 percent of total heart beats) was associated with reduced LVEF (odds ratio 3.1, 95% CI 1.4-6.8) or heart failure (odds ratio 1.5, 95% CI 1.1-2.0) over the next 10 years [4]. Stroke PVCs are associated with increased risk of stroke. In a prospective evaluation of 14,783 participants in the ARIC observational cohort, 6.1 percent had PVCs on a two-minute ECG, and 729 (4.9 percent) had incident stroke [83]. Incident strokes in individuals with any PVC was 6.6 percent compared with 4.1 percent in those without PVCs (HR 1.7, 95% CI 1.3- 2.2). Similar findings were reported by the REGARDS study [84]. Whether this association relates to increased tendency toward formation of thrombi or embolization through cardiac remodeling or possibly atrial fibrillation or other reason, remains unknown. Heart failure or cardiomyopathy Heart failure In a Danish study of 850 patients with nonischemic systolic heart failure (LVEF <35 percent), 350 patients with high-burden PVCs ( 30 PVCs in a 24-hour Holter monitor, 352 patients) had increased mortality (HR 1.38; 95% CI 1.00-1.90) and cardiovascular disease (HR 1.78, CI 1.19-2.66). However, they did not have a survival benefit from ICD implantation [85]. Patients requiring resynchronization therapy According to a MADIT-CRT substudy, among 698 patients with cardiac resynchronization therapy (CRT)-defibrillator (with ischemic and nonischemic cardiomyopathy), those with >10 PVCs per hour, had significantly higher three-year risk of heart failure/death (25 versus 7 percent) and ventricular tachycardia/ventricular fibrillation (24 versus 8 percent) compared with those with a lower burden of ectopy [86]. Patients with >10 PVCs-per-hour burden had approximately threefold increased risk of both heart failure/death (HR 2.8) and ventricular tachycardia/ventricular fibrillation (HR 2.8). Other cardiomyopathy In patients with hypertrophic cardiomyopathy, PVCs are common, but unlike nonsustained ventricular tachycardia, PVCs have not been associated with an increased risk of sudden cardiac death. (See "Hypertrophic cardiomyopathy: Risk stratification for sudden cardiac death".) In patients with arrhythmogenic right ventricular dysplasia, frequent PVCs and/or the presence of nonsustained ventricular tachycardia are markers of increased arrhythmic risk [87]. (See "Arrhythmogenic right ventricular cardiomyopathy: Treatment and prognosis", section on 'Prognosis'.) In patients with cardiac sarcoidosis, PVCs can help identify patients in whom an electrophysiologic study would be helpful in decision-making for implantable cardioverter- https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 18/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate defibrillator placement/sudden cardiac death prevention. (See "Management and prognosis of cardiac sarcoidosis".) Exercise-induced premature ventricular complexes The prognostic significance of exercise- induced PVCs is discussed separately. (See "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Premature ventricular complexes'.) PREGNANCY PVCs occurring during pregnancy constitute a special situation, where antiarrhythmic agents should be avoided if at all possible, especially during the first trimester, due to the risks posed for the embryo [88]. Triggers Some experts counsel patients with palpitations to discontinue potential precipitant factors such as smoking, coffee intake, alcohol intake, and other stimulants [89]. However, the role of caffeine restriction has not been established. Moderate caffeine exposure has not been demonstrated to increase PVCs in patients with or without structural heart disease [90,91], and caffeine restriction was not found to improve symptoms or reduce the frequency of PVCs in a small trial [92]. However, frequent and/or symptomatic PVCs may need treatment, mainly with the use of beta blockers (eg, metoprolol or bisoprolol). Ablation, if at all needed, should be postponed until the postpartum period. It is reasonable to check electrolytes (eg, potassium, magnesium) in pregnant patients with symptomatic and frequent PVCs, as these are not part of the routine prenatal laboratory measurements, and abnormal levels can be treated. The presence of PVCs in pregnancy has not been shown to cause a worse prognosis. Among a cohort of 49 pregnant women with a structurally normal heart and "high" PVC burden (median PVC burden approximately 9 percent), overall maternal outcomes were favorable [93]. Although 11 percent of pregnancies were complicated by a cardiac event, all were successfully managed with medical therapy, mostly with beta blockers. With the exception of one patient requiring ventricular tachycardia ablation postpartum, no further therapy was required in the postpartum period, and PVC burden was found to decrease. The rate of adverse obstetric and fetal/neonatal outcomes in the PVC group was comparable to the normal pregnant population. SOCIETY GUIDELINE LINKS https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 19/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Catheter ablation of arrhythmias" and "Society guideline links: Ventricular arrhythmias" and "Society guideline links: Arrhythmias in adults".) INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." th th The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more th th sophisticated, and more detailed. These articles are written at the 10 to 12 grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.) Basics topic (see "Patient education: Ventricular premature beats (The Basics)") SUMMARY AND RECOMMENDATIONS Introduction Premature ventricular complexes/contractions (PVCs; also referred to as premature ventricular beats, premature ventricular depolarizations, or ventricular extrasystoles) are common and can occur in patients with and without apparent structural heart disease. (See 'Introduction' above.) Risk stratification Risk stratification is important to determine treatment and is based on symptoms, family history, high PVC burden (>15 percent or 10,000 PVCs in 24 hours) and key PVC characteristics. (See 'Risk assessment' above.) All patients should have triggers identified and eliminated ( table 1). Our treatment approach is summarized in an algorithm ( algorithm 2). Patients with PVC-induced cardiomyopathy Management of patients with reduced left ventricular ejection fraction (LVEF; <50 percent) thought to be related to frequent PVCs is as follows (See 'Premature ventricular complex cardiomyopathy' above.): https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 20/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate For patients with PVC-induced cardiomyopathy, we suggest initial therapy with a beta blocker (Grade 2C). There is low threshold to proceeding with catheter ablation if the PVC burden remains high or the LVEF does not improve. (See 'Beta blockers' above.) For patients with signs and symptoms of heart failure due to suspected PVC-induced cardiomyopathy, we suggest initial treatment with catheter ablation (Grade 2C). Heart failure treatment and beta blocker therapy are also appropriate. (See 'Catheter ablation' above.) Patients with cardiac disease For patients in whom underlying structural or electrical heart disease is identified, management focuses on providing appropriate therapy tailored to the specific underlying condition. Components of this therapy (eg, beta blockers) can contribute to a reduction in PVCs. Calcium channel blockers should be avoided in patients with cardiomyopathy and/or heart failure. (See 'Preexisting cardiac disease' above and "Primary pharmacologic therapy for heart failure with reduced ejection fraction".) Asymptomatic patients with low PVC burden and no structural heart disease Asymptomatic patients with low PVC burden and no underlying heart disease generally do not require treatment. (See 'Asymptomatic patients with low premature ventricular complex burden' above.) Low-risk patients with symptoms and/or high PVC burden Initial medical therapy For most patients with symptomatic PVCs, we suggest first- line therapy with a beta blocker (Grade 2C). A non-dihydropyridine calcium channel blocker is a reasonable alternative in patients without cardiomyopathy (See 'Patient with symptoms and/or high premature ventricular complex burden' above.) Subsequent therapy For patients with persistent PVC-related symptoms on initial medical therapy or not tolerating medical therapy due to adverse effects, we suggest catheter ablation, rather than antiarrhythmic drug therapy, as the next treatment (Grade 2C). Catheter ablation likely has greater long-term efficacy and avoids antiarrhythmic drug toxicity. Class IC antiarrhythmic drug treatment is a reasonable alternative for patients without apparent structural heart disease who do not have access to catheter ablation or prefer to avoid an invasive procedure. Off-label use of ranolazine has also been suggested to effectively suppress PVCs without causing proarrhythmia. (See 'Catheter ablation' above and 'Antiarrhythmic therapy' above.) Prognosis The presence of simple, frequent, complex, or exercise-induced PVCs in patients with apparently normal hearts is associated with increased mortality. (See https://www.uptodate.com/contents/premature-ventricular-complexes-treatment-and-prognosis/print 21/50 7/6/23, 3:35 PM Premature ventricular complexes: Treatment and prognosis - UpToDate 'Prognosis' above.) Exercise-induced PVCs are discussed separately. (See "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Premature ventricular complexes'.) ACKNOWLEDGMENT The UpToDate editorial staff acknowledges Philip J Podrid, MD, FACC, Brian Olshansky, MD, and Bernard Gersh, MB, ChB, DPhil, FRCP, MACC, who contributed to an earlier version of this topic review. Use of UpToDate is subject to the Terms of Use. REFERENCES 1. 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