One of the most important pathophysiological mechanisms of arrhythmia in inflammatory cardiomyopathy (IC) with heart failure (HF) is the imbalance of the sympathetic innervation.

The aim of the work was to establish the relationship of integral indicators in patients with IC with the imbalance of the autonomic nervous system.

The study included 67 patients with IC with frequent runs of ventricular tachycardia (VT) according to the data of ECG Holter monitoring by defining the duration and dispersion of the interval QTc and QTvar and 20 – without VT. The control group consisted of 15 healthy persons.

QTc interval in patients amounted to 0,075±0,0085 and 0,065±0,009 (p <0.05) ms, respectively. The predominance of duration and spatial variability of QTvar and QTc intervals was revealed. Maximum interval QTvar amounted to, in patients with IC, 0,05±0,008 ms, and QTs – 0,04±0,0095 ms more than the indicator of control group. QT and QTvar dispersion increased to 0,04±0,0095 ms and 0,06±0,006 ms compared to the control group. Corrected QTc dispersion tended to increase in patients by 0,0013±0,001 ms, and QTvar by 0,0019±0,0006 ms.

QTc and QTvar dispersions in the runs of VT amounted to 36,8±3,6 ms and 8,9 ± 1,7% respectively, and in the absence of VT, 32,3±2,5 ms and 7,4±0,5% (p> 0,5). Correlation between QTc dispersion was directly dependent on the functional class of HF – r=0,36 (p<0,01). QTc dispersion determined the dilatation of the cavity of left ventricle (LV) – correlation coefficients for LV EDV and ESV were respectively – r=0,41 and r=0,31 ( p <0.01). The correlation was disclosed between the volume overload (V / M ) – r=0,29 ( p <0.05) and negative correlation with the decrease in myocardial contractility r=-0,32 ( p<0.05). At the same time, QTc interval dispersion did not depend on the severity of left ventricular hypertrophy. Similar patterns were evident for QTvar – for EDV – r= 0,39 (p<0,05), ESV – r=0,30 (p<0,01), V/M – r= 0,23 (p<0,05), LVEF – r=0,28 (p<0,05). It should be noted that reliable statistical correlations between the indicators of heart rate variability (HRV) and QTc and QTvar dispersions were not detected.

Thus, reduced HRV was due to the changes in structural and functional state of the myocardium – dilatation and volume overload of LV. There is no correlation between reduced HRV and ventricular arrhythmia. Increase in QTs and QTvar dispersions was due to the myocardial remodeling.