Non-Sustained Ventricular Tachycardia - NSVT

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Ventricular tachycardia that persists for less than 30 seconds is called non-sustained ventricular tachycardia (NSVT). Sustained ventricular tachycardia is by far more dangerous than NSVT, but NSVT is much more common.

What Is NSVT?

NSVT is an episode of ventricular tachycardia with a heart rate of at least 120 beats per minute, lasting for at least three beats and persisting less than 30 seconds.

Most often, NSVT either does not cause any symptoms at all, or will just cause palpitations. Occasionally, however, NSVT can produce lightheadedness, dizziness, or, more rarely, syncope (loss of consciousness).

Because NSVT usually does not produce alarming symptoms, it is typically discovered incidentally, while recording an ECG or during some other form of cardiac monitoring.

Why Is NSVT Important?

There are two reasons NSVT is important. First, it may produce troublesome symptoms. Second and more importantly, it may indicate the presence of previously unknown, significant heart disease.

An obvious question, which is often asked by both patients and doctors, is whether the NSVT itself is dangerous. In other words, is NSVT likely to result in ventricular fibrillation and cardiac arrest?

In general, as long as your heart is otherwise normal, the answer is no.

So what's really important about NSVT is that it is often a clue that serious heart disease is lurking in the background.

How Is NSVT Evaluated?

If you are diagnosed with NSVT, doing an evaluation to look for underlying heart disease becomes Job One.

The kinds of heart disease most commonly associated with NSVT are coronary artery disease (CAD) and heart failure due to dilated cardiomyopathy. NSVT is also seen with hypertrophic cardiomyopathy and heart valve disease (especially aortic stenosis, mitral regurgitation, and mitral valve prolapse).

Your doctor can screen for all of these conditions with an echocardiogram. If you have significant risk factors for CAD, your doctor may also want to perform a stress thallium test to see if CAD is present.

Sometimes, NSVT is caused by cardiac conditions that are not associated with structural heart disease (that is, heart disease that does not alter the anatomy of the heart). The two most common of these conditions are repetitive monomorphic ventricular tachycardia (RMVT) and catecholamine-sensitive polymorphic ventricular tachycardia (CPVT). Both RMVT and CPVT are uncommon congenital disorders involving the heart's electrical system, which produce no structural changes that will be seen on echocardiogram. These disorders are usually diagnosed when doctors notice particular characteristics of the NSVT they produce on the ECG.

What Is the Treatment For a Patient With NSVT?

In most cases, NSVT is significant mainly as an indicator that underlying heart disease may be present. If heart disease is subsequently discovered, treatment should be directed toward that.

If no underlying heart disease is found, in general the NSVT does not measurably increase the risk of cardiac arrest, and from a strictly medical standpoint, no treatment is necessary.

Not infrequently, the underlying heart disease itself poses a significant risk for sudden death from heart arrhythmias. This is especially true for CAD and heart failure. In these conditions, the risk for cardiac arrest is related much more to the left ventricular ejection fraction than it is to the presence or absence of NSVT. To reduce that risk, when the ejection fraction is significantly reduced, an implantable defibrillator should be strongly considered.

In patients with hypertrophic cardiomyopathy, the presence of NSVT indicates a somewhat elevated risk of sudden death. So in these patients, having NSVT would make the cardiologist lean in the direction of an implantable defibrillator, especially if one was being considered based on symptoms and family history.

Having NSVT does not change the prognosis of valvular heart disease, including mitral valve prolapse, and in these conditions should not be a factor in making treatment decisions.

Young people with a lot of NSVT and no structural heart disease should be referred to a cardiac electrophysiologist (a heart rhythm specialist) to be evaluated for RMVT or CPVT. These two arrhythmias can often be treated with ablation therapy.

What About Treating the NSVT Itself?

In most cases NSVT is not itself dangerous, and does not require direct treatment. However, treating the NSVT may be desirable if it is producing a lot of symptoms.

If it were easy and/or safe to get rid of NSVT, this would not be a difficult issue. Unfortunately, the antiarrhythmic drugs that can treat NSVT are often not very effective, and tend to produce a lot of very nasty side effects.

If NSVT needs to be treated, most doctors will begin by using beta blockers, and then calcium channel blockers, since these drugs can occasionally reduce the symptoms, and are relatively safe.

If your symptoms remain very disruptive despite such efforts, then your doctor should consider referring you to a cardiac electrophysiologist. In some cases, these doctors can perform ablation procedures that can help to get rid of NSVT.

Alternately, if trials of antiarrhythmic drugs are being contemplated (despite the risks), electrophysiologists, who have a lot of experience using these drugs, can often conduct drug testing in a way that reduces the risk as much as possible.

Just remember that the important thing about NSVT is usually not the NSVT itself, but that it may be a clue to an underlying cardiac problem that needs to be evaluated and treated.


Zipes, DP, Camm, AJ, Borggrefe, M, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death-Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006; 48:1064.

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