Ventricular refractoriness during acute myocardial ischaemia and its relationship to ventricular fibrillation

Abstract

Studies were made in anaesthetised dog of the effects of repeated acute occlusions of a branch of the anterior descending coronary artery on ventricular refractory periods in adjacent ischaemic and non-ischaemic myocardium. Differences occurred in refractoriness between normal and ischaemic areas in the ventricle. This was greatest 2.5 min after occlusion, and on release of occlusion, ventricular refractory periods reverted to normal within 5 min. Spontaneous ventricular fibrillation was directly and significantly related to the degree of dispersion of refractoriness in a given dog immediately preceding release and following release of occlusion. Infusion of isoprenaline caused significant shortening of refactory period and increased dispersion of refractoriness during ischaemia. Studies of dispersion of refractoriness should prove valuable in assessing the efficiency of metabolic or antiarrhythmic protection against ventricular fibrillation.

Antiarrhythmic Properties of Antidepressant Drugs after Coronary Artery Occlusion and Reperfusion in Rats

“…During the first minutes of the occlusion period, the ectopic activity proba bly results from re-entrant circuits in the ischaemic zone [17] induced by alterations in adrenergic influence, metabolic activities or ionic concentrations or by accumulation of toxic metabolites. Delayed ventricular ar rhythmias occurring 20 min after ligation could also be induced by re-entrant circuits involving pathways at the Purkinje muscle junction [10].…”

Amphipathic metabolites and membrane dysfunction in ischemic myocardium.

“…Interventions that suppress myocardial fatty acid uptake, such as a 2-fold augmentation of plasma glucose, improve conduction and blunt disparities in refractory periods with mild but not severe ischemia (Russell and Oliver, in press). The decrease in action potential duration in ischemic myocardium induced by FFA can be prevented by high concentrations of glucose (Russell et al, 1978a). Some reports indicate that infusion of neutral lipid and heparin in dogs with myocardial ischemia exacerbates arrhythmia (Kurien et al, 1969(Kurien et al, , 1971), but results have been inconsistent (Opie et al, 1971).…”

Electrophysiological changes and ventricular arrhythmias in the early phase of regional myocardial ischemia.

“…Many studies have been performed in which refractory periods were measured by means of extracellular stimulating electrodes, in which extracellular electrograms recorded at varying distances from the stimulating electrodes were used to measure local responses (Brooks et aL, I960; Reynolds et al, 1960;Han and Moe, 1964;Tsuchida, 1965;Kupersmith et al, 1975;Russell and Oliver, 1978). Most of the studies conducted with this technique found a shortening of refractory periods within the ischemic zone, and several studies emphasized the importance of increased dispersion of refractory period duration (Han and Moe, 1964;Levites et al, 1976;Naimi et al, 1977).…”