A ventricular premature beat is an extra heartbeat resulting from abnormal electrical activation originating in the ventricles (the lower chambers of the heart) before a normal heartbeat would occur. VPBs are also called premature ventricular complexes (PVCs), ventricular premature depolarizations, ventricular asystoles, or ventricular ectopic beats.
Ventricular premature beats are common, particularly among older people. This arrhythmia may be caused by physical or emotional stress, intake of caffeine (in beverages and foods) or alcohol, or use of cold or hay fever remedies containing drugs that stimulate the heart, such as pseudoephedrine. Other causes include coronary artery disease (especially during or shortly after a heart attack) and disorders that cause ventricles to enlarge, such as heart failure and heart valve disorders.
Symptoms of Ventricular Premature Beats
Isolated ventricular premature beats have little effect on the pumping action of the heart and usually do not cause symptoms, unless they are extremely frequent. The main symptom is the perception of a strong or skipped beat (palpitations). Ventricular premature beats are not dangerous for people who do not have a heart disorder. However, when they occur frequently in people who have a structural heart disorder (such as a heart valve disorder or a heart attack), they may be followed by more dangerous arrhythmias such as ventricular tachycardia or ventricular fibrillation, which can cause sudden death.
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.
If no associated cardiac disease is present and if the ectopic beats are asymptomatic, no therapy is indicated. Mild symptoms or anxiety from palpitations may be allayed with reassurance to the patient of the benign nature of this arrhythmia. If PVCs are frequent (bigeminal or trigeminal pattern), electrolyte abnormalities (especially hypokalemia or hyperkalemia and hypomagnesemia), hyperthyroidism, and occult heart disease should be excluded.
In addition, an echocardiogram should be performed in patients in whom a burden of PVCs of greater than 10,000 per day has been documented by ambulatory ECG monitoring. Pharmacologic treatment is indicated only for patients who are symptomatic or who develop cardiomyopathy thought due to high burden PVCs (generally greater than 10% of daily heart beats). Beta-blockers or non-dihydropyridine calcium channel blockers are appropriate as first-line therapy.
The class I and III antiarrhythmic agents may be effective in reducing ventricular premature beats but are often poorly tolerated and can be proarrhythmic in up to 5% of patients. Catheter ablation is a well-established therapy for symptomatic individuals who do not respond to medication or for those patients whose burden of ectopic beats has resulted in a cardiomyopathy.