Overview
Nonparoxysmal sinus tachycardia (NPST), also known as idiopathic sinus tachycardia (IST), is a hitherto undefined clinical syndrome that is a rare and specific type of sinus tachycardia that occurs in response to excessively accelerated resting heart rate, sinus heart rate >100 beats per minute, when there is no other cause for the tachycardia, during activity or mental stress.
Etiology
1. Abnormal enhancement of autoregulation is possible only on the basis of an abnormality in the sinus node itself, whereas a normal sinus node does not have autoregulatory dysfunction.
2. Non-paroxysmal sinus tachycardia is not sinus rhythm, but ectopic atrial tachycardia in the atria very close to the sinus node. The resulting P-wave pattern on the electrocardiogram can be very similar to the sinus P-wave pattern, but electrophysiologic tests have so far not been able to distinguish between the two.
Symptoms
Nonparoxysmal sinus tachycardia is more common in younger people, mostly between the ages of 20 and 35.
The most common symptom is palpitations, followed by chest tightness, fatigue, and dizziness, and many patients present with symptoms of nervousness that are inconsistent with the severity of the tachycardia. Some patients have intermittent symptoms, while others have long-term persistence, with a duration of 1 to 11 years. Syncope may occur as a result of hypotension induced by beta-blockers. Exercise tolerance tests have been shown to elicit an excessive heart rate response to mild exercise. It has been reported that a few patients in the middle and late stages of the disease may have arrhythmogenic cardiomyopathy and intractable heart failure due to prolonged tachycardia, and the corresponding acute pulmonary edema, heart failure, cardiogenic shock and other critical symptoms. In addition, the corresponding adverse reactions, such as dizziness and weakness of the limbs, occur due to long-term administration of larger doses of drugs such as beta-blockers. Sinus tachycardia is the most important clinical manifestation of this disease, which is mainly characterized by the following features:
1. heart rate greater than 100 beats/minute at rest or during light activity
2. 24-hour ambulatory electrocardiogram shows a significant increase in the average heart rate, which is abnormally high during the day and relatively low at night, and may fall to the normal range in some patients.
3. A disproportionate increase in heart rate occurs during short periods of exercise (5-minute walk or plank exercise test), with an average heart rate of up to 140 beats per minute.
4. In the prone position, the heart rate is relatively low, ranging from 60 to 135 beats per minute; in the upright position, the heart rate increases significantly, ranging from 90 to 160 beats per minute.
5. The tachycardia may be intermittent, continuous or persistent.
6. When combined with arrhythmogenic cardiomyopathy heart failure, the heart rate often sustainably increases to 160～220 beats/minute, impairing cardiac function.
7. Poor response to beta-blocker or calcium antagonist therapy.
In addition to sinus tachycardia, most of the patients with this disease have no other primary organic abnormalities of the heart as confirmed by physical examination, echocardiography, X-ray cardiovascular examination, or other diseases such as hyperthyroidism that cause sinus tachycardia, and a small number of patients have organic heart disease, but there is no obvious relationship between the heart rate changes and heart disease. Non-paroxysmal sinus tachycardia has also been reported to occur in some patients after radiofrequency ablation for atrioventricular nodal refractoriness or atrioventricular refractory tachycardia.
Examination
1. Electrocardiography
(1) Heart rate >100 beats per minute.
(2) P-wave pattern of sinus during tachycardia.
2. Electrophysiologic examination
It is generally believed that during the onset of tachycardia, the pacing site of the elevated right atrium or the pacing site close to the suspected pacing point of the sinus node can be measured to determine the point of origin of excitation. However, since the sinus node is a diffuse structure with nonspecific anatomical localization, and there is no clear boundary between it and the atrial tissues, and the response of nonparoxysmal sinus tachycardia and ectopic right atrial tachycardia to external stimuli is very similar, it is difficult to distinguish between the two.
Diagnosis
The diagnostic criteria have not been standardized so far, but the following points can be used as diagnostic conditions:
1. Ventricular rate >100 beats/minute at rest or during light activity.
2. ECG P-wave pattern of sinus during tachycardia.
3. Tachycardia episodes are accompanied by appropriate symptoms.
4. Other causes of significant sinus tachycardia, such as heart failure, hyperthyroidism, anemia, etc., should be excluded.
5. After complete autonomic blockade of the sinus node with atropine or β-blockers, the intrinsic heart rate of the sinus node is measured, and different doses of isoproterenol are used to evaluate the effect on the heart rate and the response of the heart rate after exercise. Increased intrinsic heart rate and abnormally increased sensitivity to isoprenaline in many patients with nonparoxysmal sinus tachycardia aid in the diagnosis.
Differential Diagnosis
1. Sinus tachycardia
The usual sinus tachycardia has a heart rate of 100 to 150 beats per minute, and the ventricular rate usually does not exceed 100 beats per minute at rest or during light activity. It responds well to beta-blocker therapy.
2. Atrial foldback tachycardia
The heart rate is between 140 and 250 beats per minute, the P-wave morphology is different from that of sinus P-wave, and there may be timely atrial precontractions to induce or terminate episodes, and program-controlled stimulation may induce and terminate episodes.
3. Sinus atrial tachycardia
The heart rate is between 100 and 140 beats per minute, mostly around 120 beats per minute, and the P′ wave morphology is the same or similar to the sinus P wave, which is a paroxysmal attack with sudden onset and end, and the duration of the attack is relatively short, and the atrial precontractions can induce and terminate the tachycardia. Program-controlled stimulation can induce and terminate tachycardia.
4. Autonomic atrial tachycardia
It is difficult to distinguish atrial tachycardia from nonparoxysmal sinus tachycardia. At the onset of atrial tachycardia, the frequency gradually accelerates, and after 3 to 5 cardiac cycles, the heart rate gradually accelerates and stabilizes at a certain level (heart rate fixation), and then gradually decelerates before termination. There is a long compensatory interval at termination. In contrast, in nonparoxysmal sinus tachycardia, the heart rate gradually increases during sympathetic excitation and decreases during vagal excitation, and the ambulatory electrocardiogram shows a fast heart rate with large diurnal variation.
Complications
A small number of patients in the middle and late stages may have arrhythmogenic cardiomyopathy and intractable heart failure due to prolonged tachycardia.
Treatment
1. Drug treatment
The first choice of β-blockers, such as metoprolol (betalactam), atenolol (amylol), propranolol (cardioplegia), etc., whose pharmacological mechanism is to affect the autoregulation of the sinus node and/or autoregulatory tension. However, most patients respond poorly to treatment and often require increasing doses. Too high a dose of beta-blockers or calcium antagonists can cause fatigue, headache and other systemic symptoms and make the patient can not tolerate. In addition, can also make the blood pressure drop sympathetic nerve excitation directly affect the control of non-paroxysmal sinus tachycardia. Calcium ion antagonists also have some efficacy. If the above treatment is ineffective, amiodarone or propafenone can be used to reduce the heart rate, and its adverse effects should be noted when taking it for a long time.
2. Radiofrequency ablation is effective.
If the sinus heart rate decreases steadily by 20% to 40% during the operation, it can be considered that the ablation modification is successful. Although the efficacy is obvious, there are still 30% of patients who have recurrence after the operation.
Prognosis
The prognosis is usually good. If non-paroxysmal sinus tachycardia is caused by sympathetic excitation, beta-blocker therapy can be effective; if it is caused by vagal hypotonia, drug therapy is more difficult, and a small number of patients with prolonged tachycardia, especially interminable sinus tachycardia, can cause arrhythmogenic cardiomyopathy, which impairs the cardiac function and leads to cardiac failure, shock, etc. The prognosis is serious. In daily life, avoid mental stress, quit smoking and drinking, reduce the triggering factors of this disease, live and work regularly, eat and drink appropriately, don’t overwork, exercise appropriately, and prevent colds.