Variability of Recovery of Excitability in the Normal Canine and the Ischaemic Porcine Heart

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Abstract
Normal hearts:Refractory periods were determined at 12 to 15 intramural sites of the normal canine left ventricle during (1) steady state regularly driven rates, (2) after eachof a series of four early premature beats, and (3) after a long pause following a series of three premature beats. The dispersion in recovery of excitability, defined as the standard deviation of the mean refractory periods, was in absolute terms the same for all three situations. However, since mean refractory periods shortened after premature beats, in relative terms, dispersion of recovery of excitability was greatest after a series of four premature beats. The refractory periods ofthe specialized conducting system determined during the initial beats of a new, faster rate, showed that in subsequent beats, the refractory periods of the bundle branches are alternatively shorter and longer than the refractory period of the ventricular myocardium. An example of ‘concealed bundle branch re-entry’ is shown. It is concluded that normal hearts are well protected from sustained arrhythmias induced by changes in rate and rhythm. Ischaemic hearts:In isolated, Langendorff perfused porcine hearts, regional ischaemia was produced by clamping the left anterior descending coronary artery. The transmembrane potentials then were recorded within a distance of less than I mm from a stimulating electrode in the ischaemic zone. Refractory periods in the central ischaemic zone lengthened, those in the border zone shortened. Recovery of excitability in an ischaemic myocardium cannot be expressed in terms of intervals between stimuli alone: the quality of the premature response must also be taken into account. Typically, responses elicited well after completion of repolarization have markedly reduced amplitudes and upstroke velocities. Thresholds for stimulation increase in an ischaemic myocardium, and the use of strong test stimuli leads to artefactual results: evidence is presented that strong premature stimuli excite less injured cells far away from the stimulus site. Premature stimuli often induced arrhythmias. Presence of local responses in central ischaemic cells suggest regions of unidirectional block, creating circumstances where re-entry may occur. After a long pause, alternation in action potential amplitude and duration became more pronounced: possibly, a premature impulse elicited after a long pause encounters more regions of unidirectional block so that re-entry is facilitated. This could explain findings in ambulatory ECG recording in victims of sudden death, where in nine out of 23 cases the fatal extrasystole that triggered ventricular fibrillation occurred after a postextrasystolic pause.

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