Clinical manifestations of supraventricular tachycardias
Supraventricular tachycardia (SVT) can cause serious symptoms, such as syncopal or presynopal conditions (especially at the onset of an attack), marked palpitations, angina pectoris (even in the absence of coronary artery disease), shortness of breath, feeling of fatigue and polyuria due to the release of atrial natriuretic peptide.
Other patients may simply feel the arrhythmia without experiencing a pronounced heartbeat, or not feel any symptoms at all.
Patients may experience discomfort not only from symptoms caused by tachycardia, but also from the unpredictability of arrhythmias. Some people live in fear of waiting for the next attack and are afraid to travel or even leave the house for fear of a repetition of tachycardia.
In many patients, organic heart disease is absent, however, they fear that the arrhythmia may be a precursor of a severe heart attack or other serious cardiac catastrophe. It is necessary to convince these patients that they have “electrical” heart disease, and not circulatory disorders or structural cardiac pathology.
Stable supraventricular arrhythmia, occurring at a high frequency, can lead to the development of heart failure. In such cases, the term “tachycardiomyopathy” is used. At the same time, restoration of a normal rhythm is accompanied by regress of heart failure.
Sometimes in patients without coronary artery disease, tachycardia can lead to pronounced ECG changes characteristic of myocardial ischemia. It is well known that an increase in serum troponin levels is considered as a sign of acute MI.
However, a slight increase in troponin concentration can be observed in patients with a long-existing tachycardia, in whom angiography shows no signs of coronary disease or whose age and degree of coronary risk make the presence of coronary pathology unlikely. A slight increase in troponin levels in patients with supraventricular tachycardia (SVT) should not be considered a sign of MI.