Structural and electrophysiological remodeling interrelation in postinfarction cardiosclerosis and dilated cardiomyopathy
Kazanskij Medicinskij Žurnal
Aim. To study the interrelation of ventricles echocardiographic parameters and signal-averaged electrocardiogram indicators in patients with postinfarction cardiosclerosis and dilated cardiomyopathy.Methods. 28 patients with postinfarction cardiosclerosis (men aged 49 to 71 years) and 29 patients with dilated cardiomyopathy (men aged 24 to 61 years) were examined. All patients underwent echocardiography, by which left ventricle final diastolic and systolic volumes with ejection fraction
... on fraction calculation, right ventricle end diastolic and systolic volumes were determined. According to the signal-averaged electrocardiogram, filtered ventricular complex duration, the ventricular complex with an amplitude of less than 40 mV terminal part duration and signal root-mean-square (rms) amplitude of the ventricular complex last 40 ms were evaluated.Results.. According to the correlation analysis, increase in left ventricle end-diastolic and systolic volumes and decrease in its ejection fraction, as well as an increase in right ventricle end-diastolic and systolic volumes were associated with an increase in the filtered ventricular complex duration and the ventricular complex with an amplitude of less than 40 mV terminal part duration in patients with postinfarction cardiosclerosis. The left ventricle volumes increase and ejection fraction reduction were also associated with the signal rms amplitude of the ventricular complex last 40 ms reduction in patients with postinfarction cardiosclerosis. Similar interrelation was not found in patients with dilated cardiomyopathy.Conclusion. In patients with postinfarction cardiosclerosis cavities dilation and reduced systolic ventricular function are accompanied by the myocardium electrophysiological properties deterioration; in patients with dilated cardiomyopathy interrelation between structural and electrophysiological indicators of myocardial remodeling was not found.