Right ventricular hypertrophy in the cat—An electrophysiological and anatomical study

In right ventricular hypertrophy induced by pulmonary artery coarctation the transmembrane electrical activity of papillary muscles and trabeculae has been studied and correlated to anatomic and electrocardiographic findings. The results of an experimental group with mild hypertrophy (group B, 25 days of exposure, 10% increase of free wall/body weight ratio) and severe hypertrophy (group C, 35 days of exposure, 23% increase) were compared with those of the control group. The average cell volume increased significantly and width/length ratio was augmented by an expansion of cell diameter. There was no obvious dilatation of the right ventricle and no increase in sarcomere length. Connective tissue increased in the subendocardial muscle layers of the right ventricle. The resting potential was augmented in both groups of hypertrophy; the overshoot of the action potential was unchanged in group B and increased in C. The rate of rise of the action potential was progressively reduced with increasing degree of hypertrophy. This reduction was more marked if action potentials with identical resting potentials were compared in normal and in hypertrophied fibres. The conduction velocity of excitation decreased in group B probably as a result of the reduced rate of rise. Surprisingly, the conduction velocity was again at or above control level in group C despite the further depressed rate of rise. This is probably due to the outstanding increase in cell diameter in group C. The QRS duration of the heart in situ was also prolonged in B and normal or below normal in C. The action potential duration was augmented in both groups of hypertrophy, this was not reflected as a QT prolongation in situ.