Nonsustained VT in the absence of apparent structural heart disease

INTRODUCTION — Nonsustained ventricular tachycardia (NSVT), defined as three or more consecutive ventricular beats at a rate of greater than 100 beats/min with a duration of less than 30 seconds (waveform 1), is a relatively common clinical problem [1]. It is often asymptomatic and typically diagnosed during cardiac monitoring (eg, ambulatory monitoring or inpatient telemetry) or an exercise test performed for other reasons. It may also be incidentally recorded on a patient's cardiac implantable electronic device. If the patient is asymptomatic, the major clinical challenge is to determine if the NSVT is relatively benign or indicative of an increased risk of sudden cardiac death. A major determinant of prognosis in patients with NSVT is the presence or absence of underlying structural heart disease as diagnosed using other modalities (eg, echocardiography, myocardial perfusion imaging, cardiac computed tomography, or magnetic resonance imaging). The 12 lead electrocardiogram should also be assessed in conjunction with imaging and is particularly important in screening for inherited channelopathies, as those conditions often have no apparent structural heart disease.

This topic will discuss NSVT in patients without apparent structural heart disease. NSVT occurring in patients with different forms of heart disease, as well as sustained VT in patients without apparent structural heart disease, are discussed separately. (See "Ventricular tachycardia in the absence of apparent structural heart disease" and "Catecholaminergic polymorphic ventricular tachycardia".)

INCIDENCE OF NSVT — NSVT, with an incidence ranging from 0 to 4 percent in the general population, is more common with increasing age and more often occurs in men [2]. These incidence figures are drawn from studies using prolonged recordings in relatively small numbers of normal subjects. It is likely, however, that a single 24-hour recording significantly underestimates the true frequency of this often asymptomatic and intermittent arrhythmia.

IDENTIFYING THE ORIGIN OF THE WCT — The initial challenge may be determining if the wide complex tachycardia (WCT) is truly of ventricular origin versus aberrantly conducted supraventricular beats. Aberrancy involves the premature activation of the bundle branches where one bundle conducts normally and the other is still refractory and therefore exhibits a typical bundle branch pattern, usually the right bundle branch block (RBBB). Various morphologic clues favor aberrancy, including:

●Visualization of a premature atrial complex (PAC; also referred to an atrial premature beat,) immediately preceding the WCT

●Typical RBBB or left bundle branch block (LBBB) morphology of the wide complex beats

●An incomplete pause (lack of compensatory pause) following the WCT

●Deceleration of the tachycardia with associated loss of wide complex beats ("peeling back of refractoriness" where the bundle branch block recovers conduction)

●"Ashman phenomenon" or so-called "long-short" initiation of the WCT where a long R-R cycle is followed by the PAC that initiates the WCT

These clues, however, are not absolute rules for aberrancy. In the absence of these findings, the WCT is more likely to represent NSVT. Differentiating VT from SVT with aberrancy is discussed in greater detail separately. (See "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Basic features'.)

SYNDROMES WITH FREQUENT NSVT — There are several syndromes associated with frequent episodes of NSVT in the absence of structural heart disease, including repetitive monomorphic VT, idiopathic left VT, and nonsustained polymorphic VT. These conditions are discussed in detail elsewhere but will be briefly reviewed here. (See "Ventricular tachycardia in the absence of apparent structural heart disease".)

Repetitive monomorphic ventricular tachycardia — Some patients have frequent and repetitive episodes of nonsustained and occasionally sustained VT. The arrhythmias are usually monomorphic, most arise from the right ventricular outflow tract (RVOT), and their frequency and duration can be affected by both exercise and autonomic manipulation. Sixty to 80 percent of patients with idiopathic VT have VT originating from the RVOT, with 30 percent or fewer originating from the left ventricular outflow tract (LVOT) [3]. The prognosis of repetitive monomorphic VT is almost uniformly good, although sudden death can rarely occur. (See "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Repetitive monomorphic VT'.)

Idiopathic left ventricular tachycardia — Patients who have VT with a typical right bundle branch and left anterior fascicular block morphology are said to have idiopathic left VT originating from the LV posterior septum (also known as Belhassen VT or verapamil-responsive VT). This VT is less frequently associated with exercise and also rarely results in sudden cardiac death, although tachycardia-induced cardiomyopathy has been reported in persons with frequent or sustained episodes of VT. (See "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Idiopathic left ventricular tachycardia'.)

Nonsustained polymorphic ventricular tachycardia — Polymorphic VT in the absence of structural heart disease occurs in a few settings which involve inherited channelopathies and associated abnormalities on the 12 lead electrocardiogram (ECG) may be apparent. These include the acquired or inherited long QT syndromes, catecholaminergic polymorphic VT, and Brugada syndrome [4].

In comparison with the generally good prognosis associated with idiopathic monomorphic VT, polymorphic VT is associated with an increased risk of sudden death. (See "Congenital long QT syndrome: Treatment" and "Catecholaminergic polymorphic ventricular tachycardia".)

Arrhythmogenic right ventricular cardiomyopathy — Ventricular arrhythmias, including NSVT, are common in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). While many patients with ARVC have structural cardiac abnormalities that are evident on cardiac imaging, as well as ECG abnormalities, it is also possible to diagnose ARVC by means of genetic testing or endomyocardial biopsy. The clinical manifestations and approach to diagnosing ARVC are discussed in detail separately. (See "Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and clinical manifestations".)

CLINICAL MANIFESTATIONS — Symptoms related to NSVT, as with any tachyarrhythmia, are dependent on the ventricular rate and duration of the arrhythmia as well as the presence or absence of other comorbid conditions (ie, heart failure, obstructive coronary heart disease, cerebrovascular disease). By definition, NSVT is self-limiting, lasting less than 30 seconds. As such, patients with NSVT are less likely to develop symptoms than those with sustained VT, and most patients with NSVT are asymptomatic.

However, patients with NSVT can develop symptoms of palpitations and/or lightheadedness. On rare occasions, syncope may occur if NSVT is very rapid and results in a significant drop in cardiac output. Because of its self-limited duration of less than 30 seconds, NSVT does not usually result in angina or dyspnea, as can sometimes be seen with sustained VT. (See "Evaluation of palpitations in adults".)

EVALUATION — NSVT is typically diagnosed during cardiac monitoring (eg, ambulatory monitoring, inpatient telemetry, or recorded on cardiac implantable electronic device) or an exercise test performed for other reasons. Once NSVT has been identified, it is important to determine the presence or absence of any associated structural heart disease. In asymptomatic patients, the evaluation for prognostically significant structural heart disease should include the following:

●Thorough history, including pertinent family history, and physical examination

●12-lead electrocardiogram

●Transthoracic echocardiography

●Exercise stress testing

In patients who present with syncope felt to be related to ventricular arrhythmia, or those with a strongly positive family history suggesting an inherited cardiomyopathy (eg, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy) or inherited channelopathy, there may be a role for additional testing. This testing may include genetic testing for specific mutations as well as advanced non-invasive imaging with cardiac computed tomography or magnetic resonance imaging. The diagnostic approach in such patients is discussed in detail separately. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation" and "Clinical utility of cardiovascular magnetic resonance imaging".)

Prolonged palpitations, syncope, or presyncope suggest that there may be a coexistent sustained ventricular arrhythmia. Ambulatory event recorders are valuable in this setting. In addition, electrophysiologic studies can be used to provoke sustained arrhythmias that may produce symptoms mimicking the spontaneous arrhythmia. (See "Ambulatory ECG monitoring" and "Invasive diagnostic cardiac electrophysiology studies".)

TREATMENT — For patients with NSVT who are asymptomatic and have no evidence of structural heart disease, we suggest no specific medical therapy. However, drug therapy may be required in patients with disabling symptoms. We generally begin with a beta-blocker unless there is a contraindication (eg, uncontrolled asthma), in which case we will try a calcium channel blocker, usually verapamil or diltiazem. If the arrhythmia persists despite treatment with these drugs, the therapeutic options include more potent antiarrhythmic medications or to perform catheter-based ablative therapy. The management of NSVT, including antiarrhythmic drugs and catheter ablation, is discussed in detail separately. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management".)

Patients with nonsustained polymorphic VT may have a worse prognosis, and management can be quite complex. Such patients should be referred to an electrophysiologist. (See "Catecholaminergic polymorphic ventricular tachycardia".)

PROGNOSIS — The prognosis of NSVT is dependent upon the presence or absence of structural heart disease, with a generally benign prognosis in those without apparent structural heart disease. The prognostic significance of NSVT in the absence of apparent heart disease has been studied by many investigators [5-8]. The results obtained have varied with the rigor with which underlying heart disease was excluded.

●The large, long-term Busselton and Framingham community studies suggested that complex ventricular ectopy and NSVT were associated with an approximately threefold increase in risk of subsequently developing heart disease including angina pectoris, myocardial infarction, and congestive heart failure, but neither study used exercise stress testing to evaluate for coronary artery disease [7,8]. A similar limitation was present in the large Multiple Risk Factor Intervention Trial (MRFIT) [9].

●The results were different in two smaller studies in which exercise testing, echocardiography and, when indicated, coronary arteriography were used to exclude significant structural heart disease [6,10]. These studies followed 118 patients for an average of four years. Only two (1.7 percent) cardiac events were observed, an event rate lower than that in an age-matched population in the United States. The Baltimore Longitudinal Study of Aging, in which patients aged 60 to 85 were screened for cardiovascular disease and followed for 10 years, found that NSVT did not predict a coronary event in this population [11].

●Studies of persons with pacemakers who have incidentally recorded NSVT have not shown worse outcomes [12,13]. A study of 119 pacemaker patients with preserved LVEF and incidentally recorded NSVT had no increased mortality [12]. A large prospective study of 565 pacemaker patients with a mean follow-up of four years found that NSVT was not a predictor of adverse outcomes [13].

These findings suggest that a thorough search for organic heart disease is important and that NSVT in the absence of structural heart disease is generally benign. The prognosis of NSVT in persons with underlying structural heart disease is discussed separately. (See "Incidence of and risk stratification for sudden cardiac death after myocardial infarction".)

●Exercise-induced NSVT – Approximately 1 to 4 percent of subjects without obvious evidence of heart disease develop NSVT during exercise [14-17]. The prognostic significance of this is discussed separately. (See "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Ventricular arrhythmias'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Inherited arrhythmia syndromes" and "Society guideline links: Ventricular arrhythmias" and "Society guideline links: Cardiac implantable electronic devices" and "Society guideline links: Catheter ablation of arrhythmias".)

SUMMARY AND RECOMMENDATIONS

●Background – Nonsustained ventricular tachycardia (NSVT), defined as three or more consecutive ventricular beats at a rate of greater than 100 beats/min with a duration of less than 30 seconds (waveform 1), is a relatively common clinical problem that occurs in up to 4 percent of the population. (See 'Introduction' above and 'Incidence of NSVT' above.)

●Diagnosis – NSVT is typically diagnosed during cardiac monitoring (eg, ambulatory monitoring, inpatient telemetry, via cardiac implantable electronic devices) or during exercise stress testing. The initial challenge may be determining if the wide complex tachycardia is truly of ventricular origin versus aberrantly conducted supraventricular beats, with several clues from the electrocardiogram that can aid in the distinction. (See 'Identifying the origin of the WCT' above.)

●Evaluation for cardiac structural disease – Once NSVT has been diagnosed, it is important to determine the presence or absence of any associated structural heart disease. A thorough history and physical examination, 12-lead electrocardiogram, transthoracic echocardiography, and exercise stress testing is generally sufficient to exclude prognostically significant structural heart disease in asymptomatic patients. (See 'Evaluation' above.)

●NSVT with syncope – In patients who present with syncope felt to be related to NSVT, or those with a strongly positive family history suggesting an inherited cardiomyopathy (eg, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy) or inherited channelopathy, there may be a role for additional testing. This includes genetic testing for specific mutations and advanced noninvasive imaging with cardiac computed tomography or magnetic resonance imaging. (See 'Evaluation' above.)

●Treatment – For patients with NSVT who are asymptomatic and have no evidence of structural heart disease, we suggest no specific medical therapy (Grade 2C).

For patients with bothersome symptoms, we use a beta blocker unless there is a contraindication (eg, uncontrolled asthma). In this case, we use a calcium channel blocker, usually verapamil or diltiazem. If NSVT persists despite treatment with these drugs, therapeutic options include more potent antiarrhythmic medications or catheter-based ablation therapy. (See 'Treatment' above and "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management", section on 'Summary and recommendations'.)

●Prognosis – The prognosis of NSVT is generally benign in those without apparent structural heart disease. (See 'Prognosis' above.)

The prognosis of NSVT occurring in exercise is discussed separately. (See "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Nonsustained ventricular tachycardia'.)