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Effect of ventricular hypertrophy on conduction velocity of activation front in the ventricular myocardium
Insights
Ventricular hypertrophy increases cardiac conduction velocity due to enlarged cells, while heart failure decreases it. This study introduces a new index to assess these changes noninvasively.
Area of Science:
- Cardiology
- Biophysics
- Medical Imaging
Background:
- Ventricular hypertrophy affects cardiac electrical activity.
- Understanding conduction velocity changes is crucial for diagnosing heart conditions.
Purpose of the Study:
- To investigate the impact of ventricular hypertrophy on cardiac activation front conduction velocity.
- To develop a noninvasive method for assessing transmural conduction.
Main Methods:
- Echocardiography and body surface potential mapping were used in 40 patients.
- A transmural conduction index was calculated by dividing septal thickness by conduction time.
- Patients had right bundle branch block without left anterior fascicular block.
Main Results:
- A positive linear correlation was found between septal thickness and the conduction index (r=0.83).
- Conduction velocity increased in hypertrophied ventricles and decreased in failed hearts.
- Serum electrolyte levels did not significantly differ between groups.
Conclusions:
- Ventricular hypertrophy itself appears to increase cardiac conduction velocity.
- Impaired cellular connections in failed hearts reduce conduction velocity.
- The transmural conduction index aids in ECG interpretation and assessing cardiac pathology.
Abstract:
To study the effect of ventricular hypertrophy on conduction velocity of the activation front noninvasively, transmural conduction indexes were obtained from findings of echocardiography and body surface potential mapping performed in 40 patients with right bundle branch block uncomplicated by the left anterior fascicular block. Because in these patients, left ventricular activation proceeds radially without being modified by right ventricular activation, the index was obtained by dividing ventricular septal thickness measured from the echocardiogram by transmural conduction time, which was taken as the time interval from the onset of the QRS complex to the time when the left ventricular epicardial breakthrough minimum appeared on the potential map. The indexes, ranging from 11 to 45 cm/s, has a good positive linear correlation with the septal thickness (Y = 2.37X - 1.33, correlation coefficient [r] = 0.83) and were abnormally small in some failed hearts. Further, both the mean ventricular activation times in lead V5 and the mean value for total duration of left ventricular activation did not differ significantly in patients with and without left ventricular hypertrophy. These findings suggest that conduction velocity was increased in the hypertrophied ventricle and decreased in the failed hearts. Because there were no significant differences in the mean serum sodium and potassium concentrations in the patients with and without left ventricular hypertrophy, it is concluded that hypertrophy itself most likely caused greater conduction velocity. Enlarged cells and multiple intercalated discs abundant in hypertrophied ventricle would have facilitated intercellular current flow and, hence, conduction velocity and impaired cellular connection in the failed heart would have reduced them. Thus, the transmural conduction index is suggested to be an important aid in interpreting electrocardiograms as well as in estimating the pathologic state of the heart.