Nonsustained ventricular tachycardia (NSVT) is an abnormal heart rhythm originating in the lower chambers of the heart, the ventricles. Tachycardia means a heart rate faster than normal, usually exceeding 100 beats per minute. When this rapid rhythm begins in the ventricles, it signals a disruption in the heart’s normal electrical signaling. NSVT is distinguished by its short duration, which is a key factor in determining its significance and risk.
What Nonsustained Ventricular Tachycardia Is
Nonsustained Ventricular Tachycardia (NSVT) is an arrhythmia defined by its origin, rate, and duration. A diagnosis requires at least three consecutive heartbeats originating from the ventricles at a rate greater than 100 beats per minute. The defining characteristic is that this rapid electrical activity spontaneously terminates in less than 30 seconds. If the rhythm continues for 30 seconds or longer, or causes immediate collapse, it is classified as sustained ventricular tachycardia, a far more serious condition.
The electrical mechanism often involves re-entry, the most common cause of ventricular arrhythmias. This occurs when an electrical impulse loops back and continuously re-excites a region of heart muscle, typically around scar tissue. Another mechanism is enhanced automaticity, where a group of ventricular cells begins to fire impulses at an abnormally fast rate, overriding the heart’s natural pacemaker.
Because the ventricles beat quickly, they do not have sufficient time to fill with blood between contractions. This rapid, uncoordinated pumping temporarily reduces the heart’s ability to move blood effectively, resulting in reduced cardiac output. Since NSVT episodes are brief, the body usually tolerates this temporary reduction without severe consequences. NSVT is considered a self-terminating event, meaning the heart’s normal rhythm restores itself without intervention.
Conditions That Lead to NSVT
NSVT is often a manifestation of an underlying heart issue, not a primary disease itself. The most common cause is ischemic heart disease. Scar tissue from a previous heart attack (myocardial infarction) creates the substrate for the electrical re-entry circuits that cause NSVT. Structural heart diseases, such as cardiomyopathy and heart failure, are also strongly associated with NSVT development.
Other conditions not directly related to the heart’s structure can also trigger NSVT episodes. Imbalances in electrolytes, such as low potassium or magnesium, disrupt the electrical stability of the heart muscle. Certain medications and drug toxicity can similarly affect electrical signaling. Conditions like an overactive thyroid (hyperthyroidism) or acute lack of blood flow can also increase the heart’s excitability.
NSVT can sometimes occur in individuals whose hearts appear structurally normal, a condition referred to as idiopathic NSVT. This form of arrhythmia generally carries a much lower risk profile. Idiopathic NSVT may be related to genetic channelopathies or an isolated electrical quirk. These cases often present with symptoms during times of emotional stress or physical activity.
How NSVT is Detected
Detecting NSVT can be challenging because episodes are transient and often produce no noticeable symptoms. When symptoms occur, they are typically brief and may include palpitations (a fluttering or racing sensation in the chest). Some people experience dizziness, lightheadedness, or shortness of breath due to the temporary drop in cardiac output. In rare cases, the episode may cause fainting (syncope) or near-fainting (pre-syncope).
Since the arrhythmia is nonsustained, it is frequently missed during a routine 12-lead electrocardiogram (EKG). Physicians rely on extended monitoring devices to capture these fleeting events. A Holter monitor is a portable EKG device worn for 24 to 48 hours that continuously records the heart’s electrical activity. For people who experience symptoms infrequently, an event recorder or a loop recorder may be used. These devices can be worn for weeks or months, or even implanted under the skin, to capture rare events.
Assessing the Risk and Determining Treatment
The clinical significance of NSVT depends highly on the health of the individual’s underlying heart structure. The first step after detection is comprehensive risk stratification to determine if the heart is structurally normal or diseased. This evaluation typically involves an echocardiogram, a non-invasive ultrasound, to assess heart muscle function and look for signs of scarring or enlargement. Stress testing may also be performed to see if the arrhythmia is provoked by physical exertion or lack of blood flow.
For people with NSVT who have a structurally normal heart, the condition is usually considered benign and is not associated with an increased risk of sudden cardiac death. Treatment is primarily aimed at managing symptoms and may involve observation or lifestyle adjustments, such as reducing caffeine and stress. Antiarrhythmic medications are sometimes used to suppress NSVT if symptoms significantly affect quality of life.
Conversely, NSVT occurring with structural heart disease, such as after a heart attack or with severe heart failure, is viewed as a marker of significantly higher risk. In this population, the focus shifts to aggressively treating the underlying heart condition, often involving specialized medications. In the highest-risk cases, particularly those with poor left ventricular function, an Implantable Cardioverter-Defibrillator (ICD) may be considered. The ICD monitors the heart rhythm and delivers an electrical shock to stop potentially fatal sustained ventricular arrhythmias, preventing sudden cardiac death.