(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.
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.
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.