ECG Dispersion Mapping in Preclinical Diagnosis of Cardiovascular Diseases.

The aim of the study was to develop a method for diagnosing pre-nosological changes in the electrophysiological state of the myocardium in patients with somatoform dysfunction of the autonomic nervous system (SDANS) and risk factors for cardiovascular diseases using the ECG dispersion mapping method.

Materials and methods: The study involved 109 male patients, 58 of them with SDANS, and 51 were healthy subjects. The patients with SDANS had the following risk factors for cardiovascular diseases, in decreasing order: stress (71% of cases), low physical activity (59%), smoking (57%), overweight and obesity (43%), anxiety (41%), low consumption of vegetables and fruit (36%), lack of extra aerobic physical activity (36%), excessive alcohol consumption (34%), depression (26%), total cholesterol ≥5 mmol/L (23%), and heart rate ≥80 (9% of the cases). All the subjects underwent clinical examination, laboratory investigation, ECG, ECG dispersion mapping, heart rate variability monitoring.

Results: Using the method of ECG dispersion mapping allowed a way for diagnosing pre-nosological changes in the electrophysiological state of the myocardium in male patients with SDANS, the basis of the pathogenesis of which is formed by the tension of the regulatory systems. Correlation between the total score according to the developed method, the RRNN value after 4 min of staying in orthostasis, and the "Myocardium" integral index has been proved. The diagnostic sensitivity of the proposed method with a threshold score of 8 was 80%, specificity - 70.8%.

Conclusion: The developed method for assessing pre-nosological changes in the electrophysiological state of the myocardium which includes cardiovascular risk factors with a reclassifying potential, proves the development of pre-nosological changes in patients with SDANS in response to daily physical strain. The changes are associated with the tension of the electrophysiological state of the myocardium, an increased activity of the sympathetic division of the ANS being one of its pathogenetic mechanisms.