Version May 2024
INTRODUCTION — Premature ventricular complexes/contractions (PVCs; also referred to premature ventricular beats, premature ventricular depolarizations, or ventricular extrasystoles) are common and occur in a broad spectrum of the population. This includes patients without apparent structural heart disease as well as those with any form of cardiac disease, independent of severity.
The approach to risk assessment and treatment of PVCs along with information on prognosis will be presented here. Discussion of the prevalence, mechanisms, clinical presentation, and approach to diagnostic testing for patients with known or suspected PVCs, as well as review of supraventricular premature beats, are presented separately:
●(See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation".)
●(See "Supraventricular premature beats".)
RISK ASSESSMENT — The management of the patient with PVCs depends on whether the initial evaluation indicates that the patient is at high versus low risk of complications including cardiomyopathy, heart failure exacerbation, and ventricular tachyarrhythmias. High-risk features will indicate more intensive treatment and monitoring.
Our approach, outlined below, is in general agreement with the published recommendations of multiple professional societies [1-3].
Symptoms — Most patients with PVCs have no symptoms; only a minority describe bothersome symptoms (usually palpitations). These PVC-related symptoms are described separately. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'Symptoms'.)
●Patients with no or mild PVC symptoms and none of the other risk factors described below can typically be reassured by their providers that PVCs are usually self-limiting, rarely life-threatening, and in most cases do not require treatment. (See 'Asymptomatic patients with low premature ventricular complex burden' below.)
●Patients with significant and/or persistent PVC-related symptoms should be treated to reduce the PVC burden; the treatment approach will depend upon the presence or absence of other risk factors. (See 'Patient with symptoms and/or high premature ventricular complex burden' below and 'Premature ventricular complex burden' below.)
●Symptoms of syncope (especially with no prodrome or preceded by palpitations), chest pain, or dyspnea are uncommonly reported in patients with PVCs and signal underlying cardiac structural or electrical conduction system disease. These symptoms may identify a higher-risk patient and require specific evaluation. (See 'Underlying or associated cardiac disease' below.)
Family history — A detailed family history should be taken regarding coronary heart disease, sudden death, or arrythmia and cardiomyopathy.
A family history of sudden cardiac death or arrest or an inherited arrythmia syndrome identifies the patient to be at higher risk for electrical or structural heart disease, which in turn requires a more specific evaluation. (See 'Further testing in selected patients' below.)
Premature ventricular complex burden — In all patients, it is important to assess and then continue to monitor for reduction in PVC burden throughout treatment. High PVC burden is a predictor of PVC-induced cardiomyopathy, heart failure, and mortality, and therefore requires more aggressive therapy [4].
Monitoring can usually be done with 24- to 48-hour continuous electrocardiographic monitoring. (See "Ambulatory ECG monitoring", section on 'Continuous ambulatory ECG (Holter) monitor'.)
PVC burden is classified as:
●Low: <1 percent or 1000 PVCs/day
●Intermediate burden: >1 to <15 percent PVCs/ day
●High: >15 percent or 15,000 PVCs/day
Premature ventricular complex characteristics — PVC characteristics such as origin and morphology can be considered when determining whether a patient is at high or low risk for cardiomyopathy or malignant arrythmia. Even when the PVCs seem to be idiopathic in a patient with a previously normal heart, some PVCs can still be potentially malignant (ie, cause cardiomyopathy, or trigger sudden death) [5-7]. PVC morphology is also of value as it can predict the ablation target and response to PVC catheter ablation. (See 'Catheter ablation' below.)
Characteristics associated with higher risk include increased QRS duration [8,9] (these are often of epicardial origin [10-12]) (waveform 1), interpolated PVCs [13] (waveform 2), PVCs involving the Purkinje system (these can trigger ventricular fibrillation and have a short coupling interval figure [14-16]), and polymorphic PVCs [17] (waveform 3). PVCs with highly variable coupling interval (>60 ms) have been identified as originating in unusual areas (aortic sinuses of Valsalva, great cardiac vein) and have been associated with a higher risk for cardiac events [18]. In the same context, greater PVC coupling interval heterogeneity has been associated with both reduced LV function and an increased risk of developing heart failure [19]. Right and left ventricular outflow tract PVCs morphologies have also been associated with malignant ventricular arrhythmias [5,20,21] (waveform 4 and waveform 5).
In patients without apparent heart disease, frequent, complex, and polymorphic PVCs have been associated with worse prognosis [22-24]. Older studies suggested these PVCs were associated with a twofold increase in myocardial infarction or death in males [22,24]. A newer study in a Taiwanese population suggested a smaller magnitude of effect; multiform PVCs were associated with a 20 percent increased risk of mortality and 10 percent increased risk for hospitalization [17].
Underlying or associated cardiac disease — PVCs can be the first manifestation of cardiac disease, including coronary artery disease, cardiomyopathy, and inherited arrhythmia syndromes (eg, long QT syndrome, arrhythmogenic right ventricular cardiomyopathy).
In addition, patients with a high PVC burden can develop a cardiomyopathy. In some people with inherited arrythmia syndromes, PVCs can trigger ventricular tachyarrhythmia. (See "Congenital long QT syndrome: Pathophysiology and genetics", section on 'Triggered activity' and "Brugada syndrome: Epidemiology and pathogenesis", section on 'Ventricular arrhythmias and phase 2 reentry' and "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'R-on-T phenomenon'.)
If a patient has a left ventricular ejection fraction (LVEF) <50 percent (regardless of symptoms) and a high PVC burden, the LVEF reduction is assumed to be related to frequent PVCs (also called PVC-induced cardiomyopathy [25,26]). In one series of 245 patients with PVC-induced cardiomyopathy, independent predictors for development of PVC-induced cardiomyopathy were male sex, high PVC burden, lack of symptoms, and epicardial PVC origin [27]. (See 'Premature ventricular complex cardiomyopathy' below.)
Evaluation in most patients — In order to assess PVC burden and the presence of structural heart disease, all patients should undergo:
●A 12-lead electrocardiogram (ECG).
●Twenty-four-hour Holter monitoring.
●An echocardiogram should be performed if there are high-risk symptoms, frequent PVCs, or if there is any suspicion of underlying or new structural heart disease (including PVC cardiomyopathy) and/or high-risk information from other risk assessments such as abnormal 12-lead ECG or family history of heart disease and especially of sudden cardiac death. (See 'Symptoms' above and 'Family history' above and 'Premature ventricular complex burden' above and 'Premature ventricular complex characteristics' above.)
When ambulatory ECG monitoring is indicated, a monitoring period of 24 to 48 hours is typically sufficient to identify PVCs and quantify the overall PVC burden. A variety of ambulatory ECG monitoring techniques are available, but for most patients Holter monitoring or patch monitoring will be the preferred approach. (See "Ambulatory ECG monitoring".)
Further testing in selected patients — Specific symptoms and/or high-risk features are reasons to get further cardiac testing.
If obstructive coronary disease is suspected (on the basis of symptoms or risk factors), or the PVCs are effort related, the patient should also undergo:
●Exercise stress testing – Among patients with effort-related symptoms and who are suspected to have obstructive coronary disease, exercise stress testing can evaluate ischemia [28] and provide useful prognostic information. (See "Prognostic features of stress testing in patients with known or suspected coronary disease".)
PVCs occurring during exercise may be secondary to underlying ischemia or could represent adrenergic or catecholamine-sensitive arrhythmias (eg, inherited channelopathies) [29]. For patients whose PVCs are induced by exercise, exercise testing in conjunction with ambulatory monitoring can be used to assess the effectiveness of antiarrhythmic drug treatment.
For patients with exercise-related PVCs, further cardiac testing for underlying cardiovascular disease should be undertaken that may include additional cardiac tests, such as stress testing with imaging, cardiac magnetic resonance imaging (CMR), and electrophysiology testing [30-32].
More commonly, however, PVCs are suppressed during exercise and reemerge in the ensuing recovery period.
●Cardiac magnetic resonance imaging – Selected patients (ie, those with high-risk PVC features, a family history of sudden death or cardiomyopathy, and/or cardiomyopathy of uncertain etiology) may require CMR [33]. CMR can be particularly useful in diagnosing hypertrophic cardiomyopathy, cardiac sarcoid, arrhythmogenic right ventricular cardiomyopathy, and amyloid cardiomyopathy. CMR is generally obtained if these conditions are suspected based on baseline ECG and/or echocardiogram characteristics, family history, and exercise history. We do not routinely use CMR imaging for all patients with frequent PVCs due to limited availability of this test, high cost, lack of expertise in cardiac MRI imaging, and the lack of prospective randomized trials demonstrating that a CMR-based strategy improves outcomes, including mortality. CMR is used selectively and can be center dependent, based on local availability and expertise. Screening with CMR may be useful before further invasive electrophysiology assessment and therapeutic decision-making are undertaken. For instance, CMR may play a role in evaluating need for implantable cardioverter-defibrillator (ICD) in patients with PVC cardiomyopathy. (See 'Implantable cardioverter-defibrillator' below.)
Observational studies in patients with frequent PVCs have shown that myocardial abnormalities on CMR are commonly seen (ie, in 15 to 35 percent of such patients) and are associated with adverse cardiac outcomes [34-36]. Among an international cohort of 518 patients (mean age 44 years) with frequent (>1000/24 hours) PVCs and otherwise negative diagnostic work-up, myocardial abnormalities were found in 85 patients (16 percent) [34]. In a single-center observational study, 255 patients with frequent PVCs (>5 percent per 24 hours) who had a contrast-enhanced CMR for work-up of PVCs were followed for the composite outcome (mortality, ventricular fibrillation, sustained ventricular tachycardia, or reduction in left ventricular ejection fraction of ≥10 percent) [35]. Thirty-five percent of patients had a myocardial abnormality on CMR, and the composite outcome occurred in 5.9 percent. After a median follow-up of 36 months, the incidence of the composite outcome was higher among patients with myocardial abnormalities versus a normal CMR (20 versus 3.6 percent; hazard ratio 4.35, 95% CI 1.34-14.15).
●Electrophysiology testing – Electrophysiology testing is used only in selected patients with higher-risk PVC features as a risk stratification tool to guide therapy or in patients undergoing catheter ablation procedure (ie, as treatment for frequent symptomatic PVCs refractory to medical therapy or in whom the PVCs have resulted in cardiomyopathy). (See "Invasive diagnostic cardiac electrophysiology studies" and 'Implantable cardioverter-defibrillator' below.)
MANAGE TRIGGERS AND RISK FACTORS — Prior to initiating therapy, correctable causes or triggers should be identified and, where possible, corrected (table 1).
Patients with hypertension often have PVCs, and if there is left ventricular hypertrophy, outcomes are often worse. These patients should have their blood pressure controlled, preferably with a beta blocker and/or an angiotensin converting enzyme inhibitor or angiotensin II receptor blocker, and receive treatment for concurrent left ventricular dysfunction/heart failure if present. Efforts should be made to avoid hypokalemia, which can result from the diuretic class of antihypertensive agents [37]. (See "Choice of drug therapy in primary (essential) hypertension" and "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'Associated conditions'.)
MANAGEMENT OF HIGH-RISK PATIENTS — High-risk patients have any of the following conditions: high (>10 to 15 percent) PVC burden, PVC-induced cardiomyopathy, preexisting cardiac structural or electrical conduction system disease, history of syncope, and abnormalities on cardiac magnetic resonance (CMR) imaging even in the presence of a normal LVEF [34,38,39].
Management in these patients is required to reverse or reduce the risk of developing a cardiomyopathy and to reduce the risk of ventricular arrhythmias and sudden cardiac death (algorithm 1).
Premature ventricular complex cardiomyopathy — If a patient has an LVEF <50 percent (regardless of symptoms), and a high PVC burden, the LVEF reduction is assumed to be related to frequent PVCs, and the diagnosis is PVC-induced cardiomyopathy [25,26]. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'PVC-induced cardiomyopathy' and 'Underlying or associated cardiac disease' above and 'Premature ventricular complex burden' above.)
In such patients, treatment is aimed towards reducing PVC burden, which can in turn avert or reverse the cardiomyopathy. Even patients who already have an implantable cardioverter-defibrillator (ICD) benefit from PVC reduction and ablation.
Some patients with PVC-induced cardiomyopathy will exhibit signs and symptoms of heart failure that may require treatment with heart failure medications. However, the definitive treatment is to suppress or ablate the PVCs. (See "Arrhythmia-induced cardiomyopathy", section on 'Frequent ventricular ectopy' and "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'PVC-induced cardiomyopathy'.)
Calcium channel blockers should generally be avoided in patients with cardiomyopathy. (See "Drugs that should be avoided or used with caution in patients with heart failure", section on 'Calcium channel blockers'.)
Beta blockers — The first-line therapy to reduce PVC burden is beta blockers. An exception may be those with heart failure who may proceed directly to catheter ablation.
Commonly used beta blockers to treat PVCs include metoprolol and carvedilol. Typical starting doses, alternatives, and maximum dosages for PVC treatment are given in a table (table 2). Once given, the patient should be monitored for a reduction in symptoms that correspond with a reduction in PVCs, titrating the medication as necessary. Repeat ambulatory ECG monitoring is typically obtained after three months of treatment to determine if the patient has responded to beta blockers. If symptoms and PVC burden have been reduced and are not high, the beta blocker should be continued.
If after one month of maximal beta blocker therapy there is no symptom relief or decrease in PVC burden, a catheter ablation is usually considered (especially if PVCs are monomorphic, making them more amenable to ablation). Alternatively, some patients are treated with antiarrhythmic drugs.
●Efficacy of beta blockers – Beta blockers are effective at reducing PVC symptoms. This is because beta blockers reduce the post-extrasystolic potentiation via the Starling mechanism (increased inotropy related to the increased stroke volume) associated with the PVC. Beta blockers can also prevent PVC recurrence. However, it should be recognized that they have no direct effects on the ventricular myocardium. Therefore, beta blockers are most likely to suppress PVCs that result from excess sympathetic stimulation or are catecholamine sensitive.
In an observational study, beta blockers were reported to reduce PVC burden in one-third of patients taking them [40]. Similar findings (a 21 to 36 percent PVC reduction) were reported by other studies [41,42].
●Weaning – Sometimes, a patient will prefer to stop the beta blocker after symptom relief is achieved. In this case, one can try to wean the beta blocker after 6 to 12 months of medication treatment. The dose can be gradually reduced and a 24-hour Holter recording can be repeated periodically. It is preferable to keep the patient on at least a low-dose beta blocker if they are willing, as this may prevent PVC reoccurrence. (See 'Premature ventricular complex burden' above.)
Catheter ablation — Catheter ablation is an effective option (algorithm 2) to reduce or eliminate PVCs in patients who do not respond to beta blocker therapy [41,43-49] and may be first-line treatment in those with heart failure. In a multicenter study of 1185 patients undergoing PVC ablation, 85 percent did not require the use of antiarrhythmic medications at two years following ablation [27].
In patients with PVC-induced cardiomyopathy, PVC ablation can lead to left ventricular function recovery. In a multicenter study of 245 patients with PVC-induced cardiomyopathy who underwent ablation, the LVEF increased from 38 to 50 percent after ablation [27].
The decision to recommend radiofrequency catheter ablation versus antiarrhythmic therapy in a particular patient will depend on clinical factors (ie, predictors of procedural success) and on patient preference. Some patients will not want to undergo an invasive catheter ablation procedure. Not all centers have catheter ablation expertise. Reasonable attempts should be made to refer appropriate patients to centers with catheter ablation expertise.
●Predictors of procedural success – Clinical variables that identify patients most likely to respond to catheter ablation and/or less likely to experience complications include [37]:
•Unifocal PVCs.
•High PVC burden. (See 'Premature ventricular complex burden' above.)
•Right ventricular outflow tract (RVOT) origin. PVCs of right ventricular origin (left bundle branch block inferior axis) will have left bundle branch inferior axis morphology on 12-lead ECG (waveform 5). For such patients, we have a lower threshold to do catheter ablation, as ablation of PVCs in the right ventricle requires only venous access. In contrast, PVCs arising in the LV outflow tract or LV require retrograde aortic or transeptal access and have a higher associated procedural risk. In a 2014 meta-analysis of small nonrandomized studies of patients with idiopathic PVCs originating from the RVOT, catheter ablation was associated with a reduction in PVC burden (97 percent mean reduction) along with an improvement in LVEF (mean increase 10 percent) [50]. Heterogeneity across studies limited the certainty of these effect estimates.
The majority of patients with PVC-induced LV dysfunction have a recovery of LV function within four months. In some patients, recovery of LV function may take longer; an epicardial origin of PVCs and/or a significantly longer PVC-QRS width are more often present in patients with delayed recovery of LV function than in patients with early recovery of LV function. In a study of 75 patients with frequent idiopathic PVCs and PVC-induced cardiomyopathy submitted to successful PVC ablation, the majority (68 percent) had a recovery of LV function within four months [48]. Patients with delayed recovery of LV function were more likely to have epicardial origin of PVCs (54 versus 4 percent) and longer PVC-QRS width (170±21 versus 159±16 ms) compared with those with an earlier recovery. Similarly, in a study of 114 patients, mean PVC-QRS was 173 ms for those with irreversible LV dysfunction versus 158 ms for those with reversible LV dysfunction (odds ratio 5) [51].
Predictors of ablation failure include multiple PVC morphologies, epicardial or papillary muscle origins, and decreased/short earliest local activation time [27,52].
●PVC ablation complications – Regardless of whether venous or arterial access is needed, vascular complications are a potential risk of the procedure. Ablation of PVCs originating in the LV require arterial access, and therefore, circulatory complications of stroke, myocardial infarction, and mitral or aortic valve damage can occur. Myocardial perforation and cardiac tamponade or coronary artery injury are potentially lethal complications [53,54].
In a study of 1185 patients undergoing catheter ablation for PVCs, the major complication rate was 2.4 percent, with the most common complications related to vascular access [27]. Nine patients (0.8 percent) had pericardial tamponade requiring pericardiocentesis, and a single patient experienced permanent atrioventricular block. No patients died or experienced stroke. In another study, among 1231 patients undergoing PVC ablation, the overall complication rate was 2.7 percent, with cardiac tamponade being the most common complication (27 percent of all complications or an overall rate of 0.7 percent) [54]. Two ablation-related deaths occurred; one patient died from coronary artery injury during the procedure, and the other died from infectious endocarditis. Location (LV and epicardium) was the main predictor of complications, with RVOT predicting fewer complications. Potential risks of catheter ablation are discussed separately. (See "Overview of catheter ablation of cardiac arrhythmias", section on 'Complications'.)
●Expected timeframe for recovery of LVEF – Repeat cardiac monitoring should be performed post-procedure at approximately three months to assess PVC burden. Also, a repeat echocardiogram should be performed three months after the PVC ablation to assess for LV function recovery.
Most patients experience complete LVEF recovery after three to six months post-ablation [55]. In about one-third of patients, recovery is delayed and can take up to three to four years [48]. Predictors of delayed recovery included epicardial-origin PVCs [27] and increased intrinsic QRS duration [56].
Antiarrhythmic therapy — If a patient is not an optimal candidate for, or prefers not to have, an invasive ablation procedure, an antiarrhythmic agent can be tried.
In patients with structural heart disease, including those with PVC cardiomyopathy, there are limited safe and efficacious antiarrhythmic drugs [37,50].
Preferred agents for patients with underlying heart disease are amiodarone and ranolazine:
●Amiodarone – Amiodarone is the least proarrhythmic agent in patients with structural heart disease, although there are substantial risks of organ toxicities with long-term use.
Trials of amiodarone use in patients with PVCs and prior myocardial infarction or heart failure have demonstrated a reduction in PVCs and in arrhythmic mortality (6.9 versus 4.5 percent; relative risk 0.49; 95% CI 0.05-0.72) but not overall mortality (figure 1) [57]. However, routine amiodarone therapy in asymptomatic patients is not recommended because of the limited benefit and potential side effects [57-59].
Oral loading doses of 400 to 1200 mg/day in divided doses (up to a total loading dose of 6 to 10 grams) can be used. The usual maintenance dose should be the lowest effective dose; this is usually 200 mg daily but can be as low as 100 mg daily. (See "Amiodarone: Clinical uses", section on 'Amiodarone for ventricular arrhythmias'.)
●Ranolazine – Ranolazine, an oral antianginal medication that has INa- and IKr-blocking properties, is approved for patients with chronic stable angina. Observational studies [60] and case reports/series [61-63] suggest that ranolazine may be a safe and effective treatment for PVCs; however, no randomized trials have been performed to confirm these results. In one cohort of 59 patients with ventricular ectopy with or without cardiac disease, ranolazine reduced PVCs by 71 percent (from 13,329 to 3837 per day) [60]. Ventricular bigeminy and couplets were each reduced by 80 percent, and ventricular tachycardia was reduced by 90 percent.
Safety and efficacy of ranolazine for ventricular tachycardia were studied in the MERLIN-TIMI 36 trial (ventricular tachycardia lasting ≥3 beats, 52 versus 61 percent; relative risk 0.86, 95% CI 0.82-0.90) [64] without causing significant proarrhythmia [65].
Starting dose is 500 mg orally twice daily; maximum daily dose 1000 mg twice daily.
Class IC drugs may be proarrhythmic in patients with coronary artery disease and/or significant myocardial dysfunction; therefore, they should not be used in these patients [66,67]. In patients with a prior myocardial infarction, the use of flecainide and other class IC antiarrhythmic drugs (table 3) for PVCs has been associated with increased mortality due to proarrhythmia (figure 2 and figure 3) [66,67]. Flecainide and propafenone (class IC antiarrhythmic drugs (table 3)) have been successfully used in patients with suspected PVC-induced cardiomyopathy who have failed previous catheter ablation attempts [68], but they should not be generally used in this setting due to safety concerns. The use of these drugs in lower-risk patients is discussed below. (See 'Subsequent therapy' below.)
Implantable cardioverter-defibrillator — In patients with PVC-induced cardiomyopathy and very low LVEF (<35 percent) that would otherwise meet primary prevention criteria for an ICD, elimination of the PVCs can generally restore LV function and obviate the need for ICD implantation [69]. (See "Implantable cardioverter-defibrillators: Overview of indications, components, and functions", section on 'Primary prevention'.)
However, when the etiology of nonischemic cardiomyopathy is not clear, which can be the case before PVCs are eliminated and the LVEF normalizes, there remains a concern about the risk of sudden cardiac death. Thus, preprocedural CMR followed by an electrophysiology study with programmed ventricular stimulation, particularly in CMR-positive patients, may be considered [30]. In the absence of CMR-defined myocardial fibrosis/scarring and/or inducible ventricular tachycardia during an electrophysiology study, one can wait for improvement in LVEF following PVC elimination, withholding the ICD and reevaluating the patient within six months of ablation. (See "Determining the etiology and severity of heart failure or cardiomyopathy", section on 'Cardiovascular magnetic resonance' and "Premature ventricular complexes: Clinical presentation and diagnostic evaluation" and "Invasive diagnostic cardiac electrophysiology studies".)
Preexisting cardiac disease — Patients with coronary artery disease, cardiomyopathy, or electrical conduction system disease who have PVCs are considered high risk. High-risk PVC characteristics, including morphology and origin, are discussed above. (See 'Premature ventricular complex characteristics' above.)
For patients with underlying structural heart disease, it is important to reduce the PVC burden if it is high (ie, >15 percent or 15,000 PVCs/day) in order to lower the risk of developing PVC-induced cardiomyopathy.
The first-line therapy for these patients is to reduce PVC burden with beta blockers. If after two to four weeks of beta blocker therapy, there is no decrease in PVC burden and/or there is a persistent reduction in LVEF, catheter ablation is usually considered next [27,37,41,43-50]. (See 'Catheter ablation' above.)
Generally, treating the underlying condition often improves and can reduce PVC burden. For an inherited cardiomyopathy or arrythmia syndrome, referral to a genetic counselor is also appropriate.
●Heart failure – Patients with dilated cardiomyopathy or heart failure have a reported 70 to 95 percent prevalence of PVCs [70]. The evaluation and management of PVCs in such patients are discussed separately. (See "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy".)
●Coronary artery disease – The management of PVCs differs in patients with acute and chronic coronary syndrome.
•Acute coronary syndrome – For persons with PVCs in the setting of acute coronary syndromes, the best antiarrhythmic approach is the use of antiischemic therapies (reperfusion/revascularization) combined with a beta blocker. As mentioned, treatment with ranolazine may significantly lower the incidence of ventricular arrhythmias in patients with a non-ST-elevation acute coronary syndrome, as shown in MERLIN-TIMI 36 trial [64]. (See "Initial evaluation and management of suspected acute coronary 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 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", section on 'Beta blocker'.)
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".)
●Amyloid cardiomyopathy – This is discussed elsewhere. (See "Cardiac amyloidosis: 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.
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 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 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 (>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-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 — 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." The Basics patient education pieces are written in plain language, at the 5th to 6th 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 sophisticated, and more detailed. These articles are written at the 10th to 12th 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.):
•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", section on 'Beta blocker'.)
●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 '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.
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