Although preoperative cardiopulmonary capacity in adult patients with nonrestrictive ASD was significantly decreased, some improvement was seen at 4 months postoperatively, with complete restitution to normal at 10 years after shunt closure.

Action potentials were measured in hypertropl~ied rat myocardium by means of glass microelectrodes. Left ventricular hypertrophy was induced by experimental chronic coarctation of one renal artery without contralateral nephrectomy. The action potentials of the hypertrophied myocardium exhibit a marked prolongation without any significant changes in the transmembrane resting potential, in the amplitude, or in the maximum upstroke velocity of the action potential. The increase in the half-width of the action potential for the 6-week stage after the surgical procedure is 235%, for the 12-week stage 281%, and for the 24-week stage 314%. The prolongation of the action potentials was more marked when the degree of hypertrophy was more severe.After depression of the fast Na + inward current either by tetrodotoxin, by augmentation of the extracellular K + concentration, or by reduction of the extracellular Na + concentration, action potentials with similar marked broadening were still obtained in hypertrophied myocardium. The results under variation of the extracellular Ca ++ concentration and simultaneous inactivation of the fast Na* channels suggest that the slow transmembrane inward current is primarily carried by Ca ++ ions.The prolongation of the action potentials could be one cause of the significant increase in the time to peak force as well as the augmentation of isometric force found in this model of hypertrophied myocardium.In contrast to numerous available mechanical, biochemical and mor. phological data, few studies on electrical properties of hypertrophied cardiac muscle have been published: Most studies are concerned with electrocardiographic alterations under cardiac hypertrophy and correlate changes in ECG with changes in geometry of the hypertrophied heart without regard for possible alterations in the transmembrane electrical activity of the hypertrophied cardiac cell.

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