Effect of Chronically Increased Ventricular Pressure on Electrical Forces of the Heart

Hemodynamic measurements during left and right heart catheterization in 90 patients with aortic or pulmonic stenosis have been correlated with selected vectorcardiographic parameters obtained by the Frank vectorcardiogram. Evidence has been presented that increased left ventricular peak pressure (r=0.85) or pressure time (r=0.78) leads to augmented maximum spatial voltages. The coefficients for similar correlations on the right side of the heart were 0.87, respectively 0.82. When a sum of selected spatial vectors was used the correlation coefficient with left ventricular peak pressure rose to 0.90 (with controls r=0.93) and with right ventricular peak pressure to 0.89, while at the same time the standard error became less. Less significant correlations existed with the log of the valve area (r=–0.69 for the aortic valve and r=–0.66 for the pulmonary valve) and stroke work (r= 0.24 for left and r=0.32 for right ventricular work). These findings provide a further link between the morphology and the physiology of the ventricle producing wall tension and intracavitary pressure. The demonstration of no change in MSV over years of growth, while the heart increases from 20 grams to its mature weight of 300 grams and the remarkable linear increase in MSV once elevated resting pressure is produced, shows that the vectorcardiogram is capable of reflecting accurately the average peak pressure and pressure time delivered by either ventricle. Furthermore, the less significant relationship with stroke work or valve area, in the face of the good correlation with pressure time per minute and peak pressure, in particular, indicates that chronically increased ventricular pressure in obstructive lesions is the chief factor altering MSV. On the basis of Linzbach's histologic studies, it appears that the essential measurement made by the MSV or the SMSV is the number of cells constituting the actively contracting myocardial syncytium required for the maintenance of average resting ventricular systolic pressure.