Ventricular early repolarization syndrome

The graphical recording of ventricular repolarization on an ECG includes wave J, ST segment, as well as waves T and U, which dynamically change their appearance depending on various pathophysiological conditions. The transmural voltage gradient in the initial phase of ventricular repolarization during SRGR is manifested by wave J. This gradient is most likely a consequence of the short-term outgoing potassium current (Ito), which causes the appearance of this notch (connection wave) on the descending part of the R wave. ST segment elevation occurs probably due to an abnormal drop in the Ito current in the epicardial layers of the myocardium.

Currently, it is already known that in the ventricular myocardium there are at least three types of cells with different electrophysiological properties: epi, M and endocardial cells. These three types of cells differ in their repolarization characteristics in the first and third phases of PD. Epicardial and M cells mainly have a pronounced 1st phase, which is due to the outgoing current (Ito), sensitive to 4- aminopyridine (4-AP), as a result of which the action potential takes the form of a “peak” and “arch” or notch. This Ito regional difference was detected in ventricular myocytes in dogs, cats, rabbits , rats, and in humans. An experimental study of LV myocardium with short QT syndrome confirmed the hypothesis that an increase in the outgoing repolarizing current can shorten PD predominantly in M ​​cells, thereby increasing cell dispersion and generating a substrate for the re-entry mechanism ( ri-entri ).

In recent years, SRH is believed to be caused by abnormal changes in the nature of the proteins that make up ion channels, in particular potassium channel proteins. According to various data, the prevalence of SRH in the population varies widely - from 1 to 8.2% ^[1] . Most often registered among young people and people involved in sports. It is traditionally regarded as a variant of the norm.

Some authors believe that SRGR has an associative relationship with myocardial hypertrophy . Since ATSA is more common among people who are actively involved in sports, the association between AHSR and a “athletic heart” seems important in terms of predicting possible consequences. Recent studies ^[2] reject the preexisting approach to the assessment of AED "as a variant of the norm."

Characteristic symptoms, except for ECG changes, are not observed with SRGR.

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A test with physical activity on a bicycle ergometer or treadmill in patients with SRC, as a rule, leads to the elimination of this phenomenon on the ECG due to an increase in heart rate. This is associated with increased sympathetic activation, which helps to normalize the passage of the excitation wave. In the case of aggravation of the symptoms of SRS on the ECG (large elevation of point J), an assessment of the response of the cardiovascular system to the load is required in principle (for example, a stepwise or dystonic type of reaction). The specificity of the test is about 40%, information content is 60%.

Samples with isoproterenol or atropine, as a rule, are not used in clinical practice due to possible adverse reactions.

Sample with potassium. When giving potassium ( potassium chloride , rhythmocor , panangin in sufficient doses, at least 2 g), in patients with impaired repolarization, normalization of the final part of the ventricular complex can be noted. With true SRGR, there is an aggravation of the severity of the ECG criteria. The specificity of the test is about 40%, information content is 80%.

• Cardiomyocyte

• Once again to the problem of "sports heart"
• Ventricular early repolarization syndrome