SUMMARYTo obtain information conceming the time course and instantaneous distribution of the excitatory process of the normal human healt, studies were made on isolated human hearts from seven individuals who died from various cerebral conditions, but who had no history of cardiac disease. Measurements were made from as many as 870 intramural terminals.In the isolated human hearts three endocardial areas were synchronously excited o to 5 msec after the start of the left ventricular activity potential. These areas increased rapidly in si ze dUl'ing the next 5 to 10 msec and became confluent in 15 to 20 msec. The left ventricular areas Rrst excited were (1) high on the anterior paraseptal wall just below the attachment of the mitral valve; (2) central on the left surface of the interventricular septum and (3) posterior paraseptal about one third of the distance from apex to base. The last part of the left ventricle to be activated usually was the posterobasal area. Endocardial activation of the right ventricle was found to start ne ar the insertion of the anterior papillary muscle 5 to 10 msec af ter onset of the left ventricular cavity potential. Septal activation started in the micldle third of the left side of the interventricular septurn, somewhat anteriorly, and at the lower third at the junction of the septum and posterior wall. The epicardial excitation pattem reflected the movements of the intramural excitation wave. Conduction velo city was determined in one heart by an appropriate stimulation technic. Atrial excitation, explored in two hearts, spread more or less according to concentric isochronic lines. Control studies, carried out on Rve canine hearts, disclosed that the pattem of ventricular excitation did not change af ter isolation and perfusion. However, total excitation was completed earlier in the isolated heart, and conduction velo city increased.Careful mapping illustrations are presented.Additional Indexing W ords:Ventricular excitation Intramural conduction velo city Epicardial excitation Atrial excitation K NOWLEDGE of the time course and instantaneous distribution of the excitatory pro ce ss of the normal human heart would be of value for an understanding of the QRS complex.Studies of this process during surgical intervention for heart disease or pulmonary

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In exposed hearts of anesthetized dogs with total A-V block, a sudden increase or decrease in heart rate changes the duration of refractoriness immediately. A steady state is established only after a few hundred beats. The time course of shortening of the refractory period caused by an increase in driving rate ("on" effect) has the following characteristics. The first beat shortens the refractory period, as determined from strength-interval curves, about 30% of the total shortening; the second beat shortens it 10% more. After the second beat, the rate of change in the duration of the refractory period suddenly becomes slower. Alternation of the refractory period begins with a slightly prolonged refractory period of the third beat and then diminishes rapidly in about the following 10 beats. These changes are in phase throughout the ventricular myocardium.Following sudden transition to a slower rhythm, the time course of lengthening of the refractory period ("off" effect) is opposite to the "on" effect: the alternation that occurs is less marked. Changes in the duration of the functional refractory period near the stimulus site are parallel to those in the threshold curves.These results demonstrate a long persistence of the effect on myocardial refractoriness of a previous cardiac frequency. ADDITIONAL KEY WORDScycle length premature beats cumulative effect functional refractory period A-V block• During the steady state of regularly driven hearts, the duration of the refractory period of cardiac tissue is inversely related to heart rate: a fast rate shortens, a slow rate lengthens this period (1, 2). The question whether the refractory period reaches a steady-state value immediately or gradually after a new frequency is initiated has not been studied extensively. Mendez et al.From the University Department of Cardiology and Clinical Physiology, Wilhelmina Gasthuis, Amsterdam, the Netherlands. This investigation was supported by a grant from the Netherlands Organization for the Advancement of Pure Research (Z.W.O.), the Hague, the Netherlands.Dr. van der Steen was special research assistant by appointment of the Inspector of the Netherlands Military Medical Service, Department of Defense, the Hague, the Netherlands.Received for publication October 1, 1968. Accepted for publication December 1, 1968. measured the refractory period of dog hearts after one premature beat and compared the results with those obtained during regular driving of the heart with the same cycle length as the delay of the premature beat. Usually no differences were found, and they therefore concluded that the refractory period is determined by the length of the immediately preceding cycle. During stimulation of the ventricle there was evidence in some experiments for a cumulative effect of repetitive short cycles on the refractory period. Mendez et al. (3) assumed that in these experiments both myocardium and conduction system had been stimulated and that the conduction system, unlike atrial or ventricular myocardium, exhibits a cum...

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Investigations are reported in which the excitability cycle of the dog's heart was tested successively by unipolar anodal and cathodal square wave shocks as well as by bipolar stimulation. The classical view that excitability decreases smoothly during the relative refractory phase was substantiated. The excitability for anodal stimulation reached its maximum of the cardiac cycle immediately after the absolute refractory period and exceeded cathodal excitability at that moment. Evidence is presented that the dip phenomenon described by Orias, Brooks and their associates is due to their arrangement of driving and testing electrodes. The coincidence of the dip phenomenon with the vulnerable period may be related to simultaneous spreading of two fronts of activation from cathode and anode of bipolar electrodes which would create favorable conditions for reentry.