Premature Ventricular Complexes
A premature ventricular complex is characterized by the premature occurrence of a QRS complex that is bizarre in shape and lasts longer than 120 msec. The T wave is large and usually of opposite polarity to the QRS complex. A premature ventricular complex is usually followed by a full compensatory pause.
The term "ventricular bigeminy" refers to alternating normal sinus and premature ventricular complexes. Three or more successive premature ventricular complexes are arbitrarily defined as ventricular tachycardia.
TABLE 1
Causes of Ventricular Arrhythmias
Cardiac causes
Acute and chronic ischemic heart disease
Cardiomyopathy
Valvular heart disease
Mitral valve prolapse
Noncardiac causes
Stimulants: caffeine, cocaine, alcohol
Metabolic abnormalities: acidosis, hypoxemia, hyperkalemia, hypokalemia, hypomagnesemia
Drugs: digoxin (Lanoxin), theophylline, antipsychotics, tricyclic antidepressants, antiarrhythmics with proarrhythmic potential (e.g., flecainide [Tambocor], dofetilide [Tikosyn], sotalol [Betapace], quinidine)
Premature ventricular complexes become more prevalent with increasing age and occur in association with a variety of stimuli (Table 1). It is important to determine whether underlying structural heart disease is present and left ventricular function is impaired. Other common causes include electrolyte abnormalities, stimulants, and some medications.
Attempts have been made to estimate the risk of chronic premature ventricular complexes based on their frequency and waveforms. Several studies1,2 have demonstrated an increased risk for life-threatening arrhythmias with 10 or more ectopic impulses per hour or the presence of impulse salvos (i.e., three to five consecutive impulses). However, structural heart disease and poor left ventricular function are the key factors in determining whether treatment is warranted and what the prognosis may be.
MANAGEMENT
Patients Without Heart Disease. In the absence of heart disease, premature ventricular complexes are associated with little or no increased risk of developing a dangerous arrhythmia. In this situation, the risk-to-benefit ratio of antiarrhythmic drug therapy does not support routine treatment.3 It is important to review medications, determine if stimulants are being used, and correct electrolyte abnormalities. If no underlying cause is found, the optimal approach is patient reassurance.
Patients should be made aware of the potential dangers of antiarrhythmic drug therapy as determined in the Cardiac Arrhythmia Suppression Trials (CAST and CAST II).4,5 CAST showed that the risk of dying increased, rather than decreased, with successful long-term suppression of premature ventricular complexes after myocardial infarction in older patients. At best, CAST II showed no impact on long-term survival from drug treatment that successfully suppressed premature ventricular complexes.
If patients with multiple premature ventricular complexes have severe, disabling symptoms, beta blockers are the safest initial choice. Referral to a cardiologist is indicated if beta-blocker therapy is not effective. In this situation, the next agents to be tried would be class I antiarrhythmic drugs, such as flecainide (Tambocor) and amiodarone (Cordarone), although radiofrequency ablation of an ectopic focus may also be an appropriate treatment.
Patients with Structural Heart Disease. The occurrence of premature ventricular complexes in patients with structural heart disease has been shown to significantly increase the risk of subsequent morbidity and mortality. Coronary heart disease, cardiomyopathy, and congestive heart failure are the major cardiac diseases associated with unfavorable outcomes in patients with premature ventricular complexes.
from American Academy of Family Physicians
