Ventricular premature beats (VPB) are single ventricular impulses caused by reentry within the ventricle or abnormal automaticity of ventricular cells. They are extremely common in both healthy patients and patients with a heart disorder. VPB may be asymptomatic or cause palpitations. Diagnosis is by electrocardiography. Treatment is usually not required.
(See also Overview of Arrhythmias.)
Ventricular premature beats (VPBs), also called premature ventricular contractions (PVC), may occur erratically or at predictable intervals (eg, every 3rd [trigeminy] or 2nd [bigeminy] beat). VPBs may increase with stimulants (eg, anxiety, stress, alcohol, caffeine, sympathomimetic drugs), hypoxia, or electrolyte abnormalities.
VPBs may be experienced as missed or skipped beats; the VPB itself is not sensed but rather the following augmented sinus beat. When VPBs are very frequent, particularly when they occur at every 2nd heart beat, mild hemodynamic symptoms are possible because the sinus rate has been effectively halved. Existing ejection murmurs may be accentuated because of increased cardiac filling and augmented contractility after the compensatory pause.
Diagnosis of Ventricular Premature Beats
ECG
Diagnosis of ventricular premature beats is by electrocardiography (ECG) showing a wide QRS complex without a preceding P wave, typically followed by a fully compensatory pause.
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Image courtesy of L. Brent Mitchell, MD.
Prognosis for Ventricular Premature Beats
VPBs are not significant in patients without a heart disorder, and no treatment is required beyond avoiding obvious triggers. Beta-blockers or ablation are offered only if symptoms are intolerable or if the VPBs are very frequent and, by inducing interventricular dyssynchrony, induce heart failure. Other antiarrhythmics that suppress VPBs increase risk of more serious arrhythmias.
Treatment of Ventricular Premature Beats
Beta-blockers for patients with symptomatic heart failure and after myocardial infarction
In some cases, ablation
In patients with a structural heart disorder (eg, aortic stenosis), treatment is controversial even though frequent ventricular premature beats (> 10/minute) correlate with increased mortality because no studies have shown that pharmacologic suppression reduces mortality.
In post-myocardial infarction patients, mortality rate is higher with class I antiarrhythmics than with placebo. This finding probably reflects adverse effects of the antiarrhythmics. However, beta-blockers (class II antiarrhythmics) are beneficial in symptomatic heart failure and after myocardial infarction. If VPBs increase during exercise in a patient with coronary artery disease, evaluation for percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery should be considered.
Ablation is offered only if symptoms are intolerable or if the VPBs are very frequent and, by inducing interventricular dyssynchrony, induce heart failure.
