Ventricular premature beats are seen commonly and increase in prevalence with age. In the absence of underlying heart disease, they do not adversely affect prognosis, and should not be treated unless the patient has intolerable symptoms. In the setting of underlying heart disease, particularly when the ejection fraction is less than forty percent, the presence of complex ventricular ectopy, particularly non-sustained ventricular tachycardia, is associated with an increased risk of sudden cardiac death due to sustained ventricular tachycardia or fibrillation. However, the patients at highest risk are those with a left ventricular ejection fraction of 35% or below. Patients with only moderate left ventricular dysfunction (ejection fraction above 35%) may benefit from electrophysiologic testing, though several studies have suggested that EP testing is not as predictive as was once thought in patients with a low ejection fraction. Patients with near normal ejection fractions generally have a favorable prognosis (in the absence of symptoms such as syncope or presyncope) and treatment of ventricular ectopy should be limited to beta blocker therapy. Empiric antiarrhythmic therapy for ventricular arrhythmias in patients with underlying heart disease has been associated with increased mortality, presumedly due to pro-arrhythmic effects of these potent drugs. As the risk to benefit ratio of empiric antiarrhythmic drugs is unfavorable, it should not be recommended. Amiodarone does not appear to be pro-arrhythmic, but there is a significant risk of organ toxicity and the benefit is marginal if not insignificant in most patient populations.
Ventricular tachycardia (VT) is defined as a ventricular tachyarrhythmia with a rate above one hundred beats per minute. Sustained ventricular tachycardia is defined as lasting over thirty seconds or being hemodynamically unstable such that intervention before thirty seconds is necessary. Ventricular tachycardia may be monomorphic (all QRS complexes look alike) or polymorphic (QRS complex morphology varies). One specific type of polymorphic ventricular tachycardia is known as Torsades de Pointes, which most commonly occurs in the setting of the acquired (drug-induced) long QT syndrome. Sustained monomorphic ventricular tachycardia usually occurs in the setting of underlying heart disease such as an old myocardial infarction or in cardiomyopathy, but rare cases of “idiopathic” ventricular tachycardia may arise in patients with normal hearts. Sustained ventricular tachycardia should be considered a potentially malignant arrhythmia, usually representing reentry within the ventricular myocardium. The acute treatment of unstable (pulseless) sustained ventricular tachycardia is immediate electrical cardioversion. If the patient is relatively stable, antiarrhythmic therapy using intravenous lidocaine, amiodarone, or procainamide can be used to terminate the VT. Acute ischemia is only a rare cause of sustained monomorphic ventricular tachycardia. Although revascularization should be performed if deemed appropriate, revascularization does not eliminate the myocardial substrate that gives rise to monomorphic VT. Therefore, treatment is indicated in all patients with sustained monomorphic ventricular tachycardia that does not occur within the first forty-eight hours of an acute myocardial infarction. In the early hours after acute MI, sustained VT may not necessarily predict future risk of sudden death. Polymorphic ventricular tachycardia (non-Torsades) should be considered secondary to ischemia or metabolic disturbances until proven otherwise.
Distinguishing ventricular tachycardia from other wide-QRS complex arrhythmias such as supraventricular tachycardia with aberrant conduction is usually possible, based on the twelve lead morphology, the presence of AV dissociation, and most importantly, the clinical history. In patients over the age of forty, particularly those with a history of cardiac disease, any wide QRS tachycardia should be assumed to be ventricular in origin and should be treated as such until proven otherwise. Electrophysiologic testing should be performed when the mechanism of the tachycardia is in question. Goals of EP testing are to identify the mechanism and site of origin of the tachycardia, to determine its inducibility and termination characteristics, mainly to determine how best to treat the problem. In patients with documented sustained ventricular tachycardia in the setting of coronary artery disease, the inducibility rate in the electrophysiologic laboratory is approximately ninety percent. Thus, ten percent of patients will have arrhythmias that cannot be reproduced in the lab. In patients with documented ventricular tachycardia and non-ischemic cardiomyopathy, the inducibility rate is only fifty percent. Nevertheless, these patients are at high risk of recurrent arrhythmia and sudden cardiac death and must be treated aggressively regardless of the ability to reproduce the arrhythmia. Currently, the gold standard in treatment of sustained ventricular arrhythmias is the implantable cardioverter-defibrillator (ICD). The risk of implantation is relatively low (the complication rate is approximately 2-5%) and these devices are very effective to terminate recurrent ventricular arrhythmias. In many large randomized studies, ICD therapy has been found to be superior to medical therapy in high-risk patients (ejection fractions less than 35%), even when used as “primary prevention” in patients without a history of spontaneous ventricular arrhythmias. These studies demonstrated improved survival in patients with LV dysfunction who received an ICD.