Inappropriate sinus tachycardia | |
---|---|
Other names | IST |
ECG of 33-year-old female showing sinus tachycardia at 132 bpm | |
Specialty | Cardiology |
Symptoms | Palpitations, Chest pain, Fatigue, shortness of breath, Lightheadedness, and syncope.[1] |
Causes | Increased sympathetic or decreased parasympathetic drive, increased intrinsic heart rate, dysfunctional neurohormonal modulation, ectopic sinus node activity, and beta-adrenergic receptor autoantibodies. |
Diagnostic method | Persistent or recurrent sinus tachycardia on a 12-lead electrogram or long-term monitoring that is not explained by other means |
Differential diagnosis | Metabolic myopathies, Postural orthostatic tachycardia syndrome, Sinus node reentry, and Vasovagal syncope. |
Treatment | Medications, lifestyle modifications, surgical sinus node exclusion, and sinus or AV node radiofrequency catheter ablation. |
Medication | Ivabradine and beta-blockers. |
Frequency | 1.16% in the general population |
Inappropriate sinus tachycardia (IST) is defined as sinus tachycardia that is not caused by identifiable medical ailments, a physiological reaction, or pharmaceuticals (a diagnosis of exclusion) and is accompanied by symptoms, frequently invalidating and affecting quality of life.[2] IST symptoms include palpitations, chest discomfort, exhaustion, shortness of breath, presyncope, and syncope.[1]
While sinus tachycardia is very common and is the most common type of tachycardia, it is rare to be diagnosed with inappropriate sinus tachycardia as an independent symptom that is not part of a larger condition. Although somewhat rarely diagnosed, IST is viewed by most to be a benign condition in the long-term. Symptoms of IST, however, may be distracting and warrant treatment. The heart is a strong muscle and typically can sustain the higher-than-normal heart rhythm, though monitoring the condition is generally recommended.[3] The mechanism and primary etiology of inappropriate sinus tachycardia has not been fully elucidated. An autoimmune mechanism has been suggested, as several studies have detected autoantibodies that activate beta adrenoreceptors in some patients.[4][5] The mechanism of the arrhythmia primarily involves the sinus node and peri-nodal tissue[6] and does not require the AV node for maintenance. Treatments in the form of pharmacological therapy or catheter ablation are available, but the condition is currently difficult to treat successfully.