Evaluation and Management of Ventricular Premature Beats
ABSTRACT: Ventricular premature beats (VPBs) are extrasystoles that are triggered in the ventricular myocardium. VPBs are extraordinarily common in both healthy patients and those with heart disease, and they are rarely symptomatic. Patients who present to their primary care physician may report the feeling of skipping or missing a heartbeat. VPBs are rarely harmful in healthy asymptomatic patients, but patients with symptomatic, frequent, or repetitive VPBs should be evaluated by looking for structural heart disease and managed accordingly. This article reviews the most current diagnostic work-up for VPBs and presents 6 electrocardiogram waveforms depicting the different types of VPBs. The authors also discuss the prevalence, pathophysiology, and medical management of VPBs.
Ventricular premature beats (VPBs) are ventricular impulses triggered from the ventricular myocardium. VPBs are also called premature ventricular complexes (PVCs), ventricular premature depolarizations, ventricular asystoles, or ventricular ectopic beats. This condition is extremely common in healthy patients and in patients with a heart disorder. VPBs become more prevalent with increasing age and occur in association with a variety of cardiac and noncardiac causes (Table 1).1 VPBs are typically considered harmless when they occur in healthy people without a history of cardiovascular disease, but primary care providers should be aware of when this arrhythmia may become life-threatening. For example, ventricular ectopy leading to ventricular tachycardia, which in turn can degenerate in to ventricular fibrillation, is one of the common mechanisms for sudden death.2 The approach to the evaluation and management of VPBs has undergone dramatic changes in the last decade. This article briefly discusses the prevalence and pathophysiology of VPBs and presents the most current recommendations for evaluating and managing VPBs.
Prevalence and Disease Associations
The prevalence of VPBs is directly related to the study population, study design, and duration of observation. The following findings were noted in a review of 15,792 middle-aged adults (45 to 65 years of age) in the ARIC (Atherosclerosis Risk in Communities) study3:
• The overall prevalence of any VPB on a 2-minute electrocardiogram (ECG) was approximately 6%.
• The prevalence of more frequent or complex VPBs (eg, multiformed, couplets, or non-sustained ventricular tachycardia) was approximately 3% and 0.8%, respectively.
• VPBs are more frequent in men than women, in African-Americans compared with whites, and in those with organic heart disease.
• The prevalence increased with age (34% increase for each 5-year increment in age) and the presence of other factors, such as faster sinus rate, hypokalemia, hypomagnesemia, and hypertension.
All forms of ventricular as well as supraventricular arrhythmia are common in patients with mitral valve prolapse.4 Patients with hypertension are more likely to experience VPBs; as seen in the ARIC study, hypertensive patients had a 23% increase in the prevalence of VPBs.5 VPBs are common in patients after an acute myocardial infarction (MI), with a reported incidence as high as 93%.6 The prevalence of VPBs in patients with coronary heart disease (CHD) varies considerably based upon the method of detection. They are infrequently seen on an ECG; by comparison, they can be detected in approximately 90% of such patients on a 24-hour ambulatory monitor.7 VPBs are increased in patients with dilated cardiomyopathy and heart failure, regardless of the etiology,8,9 as well as in patients with congenital heart disease, in whom VPBs can result from the primary defect or operative repair.10
Pathophysiology
Very few studies have evaluated the pathophysiology of VPBs in humans. Most of the information is derived from animal studies, from which three common mechanisms have been reported2,11:
Automaticity. This is the development of a new site of depolarization in non-nodal ventricular tissue, which can lead to VPBs. Increased automaticity may be due to electrolyte abnormalities or ischemic myocardium.
Re-entry circuit. Re-entry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. Re-entrant VPBs occur in the presence of a conduction delay and unidirectional block. The slow-conducting tissue could be due to damaged myocardium, as in the case of healed MI.
Triggered activity. Triggered activity is a more common mechanism for VPB development in humans than was previously appreciated. Early or late afterdepolarizations may occur in Purkinje cells or in the ventricular myocardium; such electrical activity may arise because of a number of conditions, including hypokalemia, ischemia, infarction, cardiomyopathy, excess calcium, and drug toxicity, such as digoxin or agents that prolong repolarization or the QT interval.
Clinical Evaluation
The presence of VPBs is associated with several characteristic findings on history, physical examination, and ECG. VPBs produce few or no symptoms in the vast majority of patients; however, because many underlying causes of VPBs can be corrected without the use of medication, a thorough work-up is important.
History-Taking
While taking patients’ history, inquire about palpitations or dizziness related to VPBs, which may occur occasionally. VPBs rarely cause true hemodynamic compromise except in patients with frequent ectopy and severely impaired left-ventricular function or when VPBs are concurrent with underlying bradycardia.12 Less often, frequent VPBs can result in a pounding sensation in the neck, lightheadedness, or near syncope.2 Palpitations often provoke a great deal of anxiety that may in turn cause a vicious cycle of anxiety, catecholamine surges, and additional ectopy and palpitations.
Clinicians should ask their patients about their lifestyles and medication regimens as well as any other substances that they ingest. Refer to Table 1 for a list of some medications that are associated with VPBs. Caffeine, nicotine, alcohol, and even over-the-counter cough and cold remedies can cause arrhythmias. Physical exercise and physical or emotional stress may also cause VPBs, in which case an exercise stress test may be useful in identifying VPBs in middle-aged or older patients without other evidence of CHD.13,14
Physical Examination
During the physical examination, check for variable or decreased intensity of heart sounds. The augmented beat following a dropped beat is heard frequently. Bounding jugular pulse (cannon A wave) from a loss of atrioventricular (AV) synchrony may be present.2 The splitting of the second heart sound depending upon whether the VPB has a right or left bundle branch block morphology.1
Electrocardiogram Findings
An ECG should be part of the standard evaluation for any patient with suspected VPBs. In evaluating patients with suspected VPBs, 24 to 48 hours of ambulatory ECG monitoring significantly increases the likelihood of making the diagnosis, given the sporadic nature of VPBs in most patients.12 The ECG may show the following characteristics11: duration of more than 120 milliseconds; bizarre morphology that does not resemble usual aberration (eg, a typical right or left bundle branch block); T wave in the opposite direction from the main QRS vector; and a fully commendatory pause (ie, the P–P interval surrounding the VPB is twice the sinus P–P interval). Less frequently, the VPB is interpolated and does not alter the baseline sinus interval (eg, the P–P interval surrounding the VPB is equal to the sinus P–P interval). As shown in Figure 1, the fourth beat is a VPB. It has a wide, bizarre morphology, with a duration greater than 160 millseconds. Refer to Table 2 for definitions of these ECG terms.
There are notable exceptions to these characteristic findings, and several specific VPB patterns have been described.12 On occasion, the PVC may be interpolated, as shown in Figure 2. It occurs between two normal sinus QRS complexes, and the P–P interval between the QRS complex prior to and after the premature beat is the same as the underlying sinus P–P interval, due to lack of retrograde penetration into the AV node. The third beat is a VPB. It is called an interpolated VPB since it does not alter the underlying sinus R–R interval.
As shown in Figure 3, a ventricular bigeminy is present when a PVC follows each sinus beat. A ventricular beat follows each sinus beat and the coupling interval between the ventricular beat and the previous sinus QRS complex is constant (ie, fixed coupling interval).
As shown in Figure 4, a ventricular trigeminy is present when two sinus beats are followed by the VPB. Thus, every third beat is a VPB. The coupling interval between the VPB and the previous sinus QRS complex is constant (ie, fixed coupling interval).
Ventricular couplets are defined as two PVCs in a row, as shown in Figure 5. There is often a compensatory pause after the second premature beat. The two premature beats may have an identical morphology (unifocal couplet), or their morphology may differ (multifocal couplet). The R–R interval between the two successive PVCs varies widely. Two VPBs occur following 3 normal QRS complexes. This is a unifocal couplet since both VPBs have the same morphology.
Ventricular parasystole represents an independent ectopic ventricular rhythm that has no relationship to the sinus rhythm. As shown in Figure 6, it appears on the ECG as unifocal PVCs with a variable coupling cycle (the interval
between the prior sinus beat and the premature beat varies). Unifocal parasystolic VPBs occur at a rate that is slower than the underlying sinus rhythm and manifest different coupling intervals (ie, the distance between the VPB and the prior QRS complex).
Laboratory Testing
Electrolyte imbalances, in particular low serum potassium (<3.5 mEq/L), may cause palpitations, so it is important to obtain serum electrolyte levels. Checking magnesium levels, especially in patients with low potassium, may also be warranted because the serum potassium level may be difficult to replenish if the serum magnesium level is also low.15
Imaging Studies
Look for underlying structural heart abnormalities that can predispose to VPBs.2 Assess the degree of left-ventricular dysfunction by noninvasive techniques, such as echocardiography or radionuclide imaging. Echocardiography may be preferable because it also provides structural information about the heart.
Electrophysiologic Study
An electrophysiologic study may be indicated for 2 types of patients with VPBs: (1) those with a structural normal heart with symptomatic VPBs, for whom pharmacological treatment or catheter ablation is indicated; and (2) those with VPBs and structural heart disease, for whom risk stratification for sudden cardiac death is indicated.
Medical Care and Management of VPBs
Deciding when to treat VPBs can be difficult because not all patients with VPBs are at risk of sudden death, and treatment is associated with risk. The approach to VPBs depends on the frequency of VPBs, attributable symptoms, the presence or absence of underlying structural heart disease, and the estimated risk of sudden cardiac death.
Patients who are found to have underlying structural heart disease will typically receive medical therapy specific to their disease process, as the occurrence of VPBs can significantly increase the risk of morbidity and mortality.1 In the absence of significant structural heart disease (eg, normal ventricular function, no coronary or valvular heart disease), VPBs are associated with little or no risk of developing a dangerous arrhythmia, however, medication may be warranted in patients with symptomatic VPBs.1
For symptomatic VPBs, recommended treatment usually involves patient education and reassurance, avoidance of aggravating factors (eg, stress, caffeine-containing products), and anxiolytic drugs if education and avoidance of aggravating factors are ineffective. Beta-blockers and nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) can be used to treat symptomatic patients. We suggest using a beta-blocker as the first-line drug for treatment of symptomatic VPBs.2,12
For patients with symptomatic VPBs in whom beta blockers have not resulted in symptomatic improvement, we suggest the use of an antiarrhythmic drug. The antiarrhythmic drug of choice is variable and depends on the presence or absence of underlying structural heart disease, particularly CHD. Flecainide and propafenone, which belong to class Ic antiarrythmics, are highly effective for suppressing VPBs. However, both are contraindicated in patients with pre-existing CHD due to the potential for proarrhythmia and increased mortality.12,16,17
In patients who cannot take class Ic drugs, amiodarone and sotalol (class III antiarrythmics) are effective, alternative agents.18 The primary care provider may need to refer patients to a cardiologist if the patient’s condition is refractory to standard therapy.
Optimal treatment for patients with VPBs should include treatment for CHD, if present, and limiting the risk of transient ischemia. It is important to maintain electrolyte balance and to control hypertension because left-ventricular hypertrophy is associated with increased VPBs.
When Is Ablation Therapy Recommended?
Ablation therapy is a procedure that uses radiofrequency energy to destroy the area of heart tissue that is causing the arrhythmia. This procedure is recommended in several situations, according to the 2006 ACC/AHA/ESC guidelines14:
• Patients with frequent, symptomatic, and monomorphic VPBs that are refractory to medical therapy.
• Patients who choose to avoid long-term medical therapy.
• Patients with ventricular arrhythmia storm that is consistently provoked by VPBs of a similar morphology.
It is important to note that the recommendations put forth in these guidelines were given a level C rating for strength of evidence, indicating only consensus of expert opinion, case studies, or standard-of-care. There are no data from randomized clinical trials or meta-analyses to support the use of ablation therapy in patients with VPBs.
Conclusion
VPBs are generally harmless in patients without cardiovascular disease. Significant risk factors for potential morbidity or mortality include age, hypertension, CHD, heart failure, structural abnormalities or operative repair. Standard evaluation includes a directed history of symptoms, triggers, lifestyle, and medications, a cardiac examination, ECG with 24- to 48-hour ECG monitoring, electrolyte testing (basic metabolic and magnesium) and imaging, preferably echocardiography. Treatment depends on symptoms, risk factors and comorbidities (eg, CHD, heart failure). Healthy patients with structurally normal hearts and minimal symptoms may be managed with lifestyle changes and reassurance. Patients with hypertension, CHD, or other underlying cardiovascular conditions should receive appropriate medical therapy to include beta blockers or nondihydropyridine calcium channel blockers as first-line therapy for their symptoms. Unresponsive patients requiring second-line therapy (class Ic or III antiarrythmics) or ablation warrant referral. ■
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