Management of Premature Ventricular Complexes

Abstract

Premature ventricular contractions (PVCs) are frequently encountered, and management is determined by symptoms, precipitating factors, and the presence of underlying cardiac disease. No treatment is indicated in patients with asymptomatic PVCs in absence of cardiac disease. Symptomatic patients without cardiac disease may be managed by identifying and correcting reversible causes. In patients with cardiac disease, management includes treating the underlying cardiac disease to improve both symptoms and prognosis.

Introduction

Premature ventricular complexes (PVCs) are frequently encountered in the primary care setting. The clinician is often faced with the dilemma of finding PVCs in a patient and deciding whether the PVCs should be treated. Management of PVCs includes discernment of associated heart disease and other predisposing conditions prior to the decision to specifically treat the PVCs.

Prevalence

The prevalence of PVCs in the general population may be as high as 80% in healthy young adults^1,2 and increases with age. ³ PVCs are more common in men, in African-Americans, and in individuals with underlying heart disease, hypertension, hypokalemia or hypomagnesaemia.³ Mechanisms for ectopic electrical activity include reentry from a previous scar or underlying heart disease, triggered activity from afterdepolarizations from a previous action potential precipitated by drugs such as digoxin or QT interval prolonging medications, and enhanced automaticity provoked by catecholamines, electrolyte abnormalities, or ischemia. It is important to investigate these underlying causes because initial management, if needed, is focused on identifying and treating these causes. See Table 1.

Table 1.

Etiologies of PVCs

Anxiety/Stress Drugs Alcohol Amphetamines Caffeine Cocaine Tobacco Cardiac Disease Cardiomyopathy Congenital Abnormalities Hypertensive Heart Disease Valvular Heart Disease Infarction Ischemia Myocarditis Electrolyte Abnormalities Hypercalcemia Hypokalemia Hypomagnesemia Hormonal Hyperthyroidism Pheochromocytoma Idiopathic Medications Aminophylline Digoxin Sympathomimetics Tricyclic Antidepressants Respiratory Abnormalities Hypercapnia Hypoxia

Diagnosis

While the vast majority of individuals are asymptomatic, some patients report palpitations, dizziness, or syncope. In examining a patient with symptoms that could be related to PVCs, simultaneous palpation of the radial artery pulse during cardiac auscultation may reveal a diminished or absent pulse during the auscultated ectopic beat and a more pronounced pulse following the pause after the premature beat. Most important is examination of the patient for signs of structural heart disease such as cardiac murmurs, heart failure, or hypertension because these conditions are associated with an increased incidence of PVCs. The routine electrocardiogram (ECG) may not demonstrate any ventricular ectopy especially if PVCs are infrequent; 24-hour ambulatory ECG monitoring or an event monitor may be needed to temporally correlate PVCs with symptoms. Other scenarios in which PVCs may be diagnosed include hospitalization for myocardial infarction or ischemia, during exercise stress testing, and during sleep studies. Exercise as well as sleep may both increase or decrease the number of PVCs.

After the diagnosis of PVCs has been established, it is important to evaluate for underlying heart disease as the etiology for the ectopy. The standard 12-lead ECG may show old infarction or evidence of hypertrophy. A transthoracic echocardiogram can provide both structural and functional information. PVCs are more frequent in the setting of mitral valve prolapse and left ventricular hypertrophy. ^4,5 There is an increased risk of sudden cardiac death in patients with left ventricular hypertrophy; however, there is no evidence that PVCs are an independent predictor of mortality in this population.⁶ Patients with heart failure also have an increased prevalence of PVCs. In this population, PVCs may be associated with an increased risk of sustained ventricular tachyarrhythmia and sudden cardiac death. Myocardial injury from a myocardial infarct or myocarditis is also associated with an increased incidence of PVCs.⁷ In the setting of myocardial infarction, frequent and especially complex PVCs are associated with an increase in total mortality, although it is unclear if the increase in mortality is independent of left ventricular function.

Prognosis of PVCs

In young healthy patients, isolated PVCs have not been shown to be associated with any increase in mortality compared to the general population. In some studies, frequent and complex PVCs in the absence of coronary heart disease were found to be associated with an increase in sudden cardiac death in an older population.^8,9 Other studies have not demonstrated such an association.¹⁰ Frequent PVCs during exercise in the absence of known cardiovascular disease is predictive of a higher rate of cardiovascular mortality.¹¹ In patients with suspected or known coronary disease, development of frequent ventricular ectopy during the recovery phase after exercise stress testing was found to be associated with increased cardiovascular mortality.¹²

The decision of whether to treat PVCs depends on symptoms and structural heart diseases (See Figure 1). In the absence of symptoms and structural heart disease, no treatment is needed, and reassurance is recommended. There is no evidence that suppression of PVCs with medications in this situation improves mortality.

Figure 1.

Management of PVCs

Treatment of PVCs in Absence of Structural Heart Disease

In the presence of symptoms without structural heart disease, reversible causes of increased ectopy should be addressed. Treatment includes correcting electrolyte abnormalities (hypokalemia, hypomagnesemia, hypercalcemia), improving respiratory status (hypercapnea, hypoxia), treating hyperthyroidism, and avoiding medications that may precipitate ectopy such as digoxin, sympathomimetics, and tricyclic antidepressants. Avoidance of alcohol, amphetamines, caffeine, cocaine, and tobacco is also recommended. As anxiety can result in an increase in catecholamines resulting in increased ectopy, reassurance and treatment of underlying anxiety disorder may help. Daily magnesium supplementation with potassium supplementation has also been shown in a randomized clinical trial to decrease the occurrence of PVCs.¹³ While this trial did not demonstrate any improvement in symptoms, daily magnesium and potassium supplementation may be beneficial by promoting electrical stability and may be considered given the few side effects of additional electrolytes.

With significant, persistent symptoms in the absence of structural heart disease and after failure to identify an underlying cause, medical therapy is indicated with a beta blocker, a class II antiarrhythmic. A beta blocker is started at a low dose and titrated until symptoms are alleviated or better tolerated. Amiodarone, a class III antiarrhythmic agent, can also be used if beta blockade is unsuccessful in suppressing the symptomatic PVCs. During treatment with amiodarone, thyroid, hepatic, and pulmonary function needs to be closely monitored given the side effects of long term amiodarone use. Other antiarrythmics such as flecainide and propafenone may be considered; these agents are associated with increased mortality due to their proarrhythmic potential. Ablation of the responsible ectopic focus may be useful in frequent, symptomatic, monomorphic PVCs refractory to medical therapy.¹⁴ Ablation is not recommended for treatment of asymptomatic PVCs.¹⁴

Treatment of PVCs in Presence of Heart Disease

In the setting of PVCs with left ventricular hypertrophy from hypertension, the goal of therapy should be control of blood pressure. Regression of left ventricular hypertrophy with blood pressure control has been associated with a decrease in frequency of PVCs.¹⁵ Control of blood pressure in hypertension with left ventricular hypertrophy should include both a beta blocker and angiotensin converting enzyme inhibitor.

Patients with known coronary artery disease should be on beta blocker therapy due to their proven benefits on cardiovascular morbidity and mortality; this may also help suppress PVCs. PVCs in the setting of myocardial ischemia or previous infarction is associated with increased mortality; suppression of PVCs with antiarrhythmics other than beta blockers has not demonstrated any survival benefit. In the Cardiac Arrhythmia Suppression Trial (CAST) in post myocardial infarction patients, flecainide, encainide, and moricizine (class I antiarrhythmics) suppressed PVCs; however total mortality was increased compared to placebo.¹⁶ Thus, class I antiarrhythmics are not recommended and may be harmful in this setting. In the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT), patients receiving amiodarone for suppression of PVCs post myocardial infarction had significantly decreased ventricular ectopy as well arrhythmic death, yet had no significant change in overall mortality.¹⁷ This effect was more pronounced in patients also taking a beta blocker. Amiodarone in addition to beta blocker may be beneficial in the patient with a previous MI who has symptomatic PVCs since this drug combination has not been shown to increase mortality. With amiodarone it is recommended to monitor liver, thyroid, and pulmonary function tests. There is no role of amiodarone in asymptomatic patients with frequent PVCs.

PVCs are very common in patients with underlying heart failure and may be a predictor of sudden cardiac death. Patients with frequent symptomatic PVCs with underlying heart failure benefit from beta blockade regardless of the etiology of the cardiomyopathy. Carvedilol, extended release metoprolol succinate, and bisoprolol have all been shown to decrease all-cause mortality in clinical trials of heart failure. Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor antagonists have also been shown to decrease mortality and may also decrease the risk of sudden cardiac death.¹⁸ Aldosterone antagonists such as spironolactone decrease ventricular arrhythmias in the setting of systolic heart failure and improve mortality.¹⁹ This may be due to the potassium sparing properties or direct effect of aldosterone antagonism. If severe symptomatic PVCs persist despite optimal medications for treatment of heart failure, amiodarone may be considered. In clinical trials in patients with heart failure and ventricular ectopy, amiodarone decreased PVCs and did not demonstrate an adverse effect on mortality.²⁰ Ablation is another option for patients with symptomatic PVCs and heart failure despite medical therapy. Ablation may actually improve left ventricular function if the cardiomyopathy is from a tachycardia mediated etiology.

In addition to medical therapy for ventricular ectopy in the setting of systolic heart failure, an implantable cardioverter-defibrillator (ICD) may be an option for primary prevention of sudden cardiac death in patients with an ejection fraction of less than or equal to 35 percent with NYHA class II or III heart failure. While not alleviating the symptoms associated with the PVCs, ICD implantation has been shown to decrease overall mortality as well as sudden cardiac death from ventricular arrhythmias compared to amiodarone or placebo.²¹

Conclusion

Premature ventricular contractions are frequently encountered and management is determined by symptoms, precipitating factors, and the presence of underlying cardiac disease. No specific medical treatment is indicated in asymptomatic PVCs or tolerable symptoms in the absence of cardiac disease; if a reversible cause of PVCs is not determined, reassurance is recommended. With symptomatic PVCs, beta blockers and electrolyte supplementation may be used. Other antiarrhythmics may be considered, but are associated with side effects. In the presence cardiac disease such as cardiac ischemia, infarction, or heart failure and symptoms from PVCs, optimal medical therapy including beta-blockers and ACE inhibitors may improve symptoms. Amiodarone and ablation may be considered for refractory symptoms in all patients. Empiric use of an ICD in patients with persistently reduced left ventricular ejection fraction of less than 35% decreases long-term mortality.

Biography

Albert K. Chan, MD, and Mary L. Dohrmann, MD, are at the University of Missouri Hospital and Clinics, Division of Cardiovascular Medicine.

Contact: chana@health.missouri.edu