Nonsustained ventricular tachycardia was defined in different manners over the years, as 3 to 5 consecutive ventricular premature contractions (whose pacemaker is located below the atrioventricular node), lasting for less than 30 seconds or as more than 16 consecutive ventricular extrasystoles, causing a heart rate above 120 or 125 beats/minute. This poorly reproducible arrhythmia is an overall mortality predictor, especially in patients with structural heart disease.
Nonsustained ventricular tachycardia is usually asymptomatic because of its short duration, but some patients complain about palpitations. It can be recorded at rest in asymptomatic individuals [1] and it can be a part of the “athlete's heart syndrome” [2]. In trained athletes with no structural heart disease, genetic channelopathies and early repolarization, it is considered to be benign, as it disappears during deconditioning periods [3]. However, the physician must inquire about the use of potentially proarrhythmic drugs and personal and familial history of heart disease, syncope and sudden death [4].
Longer arrhythmic episodes can cause lightheadedness and anxiety. Syncope, diaphoresis, pallor, hypotension and dyspnea are not usually encountered with nonsustained ventricular tachycardia episodes, but rather with sustained ones. Physical examination may reveal cannon a-waves if atrial fibrillation or flutter is absent and a variation of the first heart sound’s intensity on auscultation. However, these findings are only present during the acute episode, therefore the physician only finds them if he or she examines the patient during those few seconds, so the patient must have already been admitted to a hospital.
Nonsustained ventricular tachycardia patients must undergo a thorough cardiac evaluation. The most frequent causes of the disease in middle-aged individuals are myocardial ischemia, valve diseases and cardiomyopathies, whereas younger people may suffer from long QT syndrome, arrhythmogenic right ventricular cardiomyopathy or Brugada syndrome.
Blood workup should include potassium, calcium, magnesium and phosphate evaluation, as well as measurement of serum digoxin and tricyclic antidepressants levels or toxicology screening where appropriate. Cardiac troponins should also be measured when acute myocardial ischemia is suspected.
A simple electrocardiogram is able to pinpoint the approximate location of the ventricular contractions and to describe the tachycardia as monomorphic or polymorphic. The location of the R/S transition may predict the presence of arrhythmogenic right ventricular cardiomyopathy [5], whereas the duration of the cardiac cycle during the episode is an indicator of concomitant polymorphic ventricular tachycardia [6]. Holter monitoring is usually indicated in symptomatic patients and accurately describes arrhythmic episodes [7]. Further information is added by electrophysiology testing. In patients where arrhythmic episodes can be induced, the mortality risk is higher [8].
Some episodes are exercise-induced and may be caused by ventricular outflow arrhythmias [9]. Right ventricular outflow ectopic loci cause a left bundle branch block pattern, whereas those located in the left ventricle outflow tract appear as right bundle branch block complexes. Structural abnormalities of these areas can be demonstrated by magnetic resonance imaging or myocardial biopsy [10] [11].
Echocardiography is another useful tool, as it is able to describe myocardial scars (visualized as akinetic regions), left ventricular hypertrophy (an indicator of long-term hypertension) and the presence and severity of valvulopathies. Cardiomegaly also predicts nonsustained ventricular tachycardia episodes [12]. If the arrhythmia is detected during the recovery period of an exercise test, it indicates cardiovascular mortality during the next decades [13].