Key result
Intracoronary heptanol induces uniform VT in 50% of dogs, while high-dose potassium triggers VF.
Agents that affect cellular coupling, such as heptanol, may increase susceptibility to reentrant ventricular tachycardia in normal myocardium, demonstrating different arrhythmogenic consequences compared to agents that primarily alter active membrane properties.
May promote reentrant VT via gap junction uncoupling in normal myocardium; leaves open relevance to human arrhythmogenesis.
Abnormalities in cellular coupling, modulated in part by intracellular gap junctions, have an important role in the genesis of reentrant arrhythmias in the setting of chronic myocardial infarction. The effects of heptanol, which has a relatively selective action on gap junctional resistance at low concentrations, and potassium, which primarily affects active membrane properties, were assessed using a localized intracoronary infusion system in 11 normal dogs in vivo. Both agents caused a dose-related slowing of conduction. Programmed stimulation during potassium infusion resulted in ventricular fibrillation in two of six animals treated with a low dose (5.0-5.5 meq/l) and five of six animals treated with a high dose (7.0-7.5 meq/l). During the infusion of 1.0 mM heptanol, uniform ventricular tachycardia was induced in four of eight animals. Infusion of heptanol, but not potassium, increased the susceptibility to presumably reentrant ventricular tachycardia in normal myocardium. This suggests that agents that affect cellular coupling may have markedly different arrhythmogenic consequences than agents that primarily alter active membrane properties.
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Callans et al. (1992) studied this question. Intracoronary infusion of heptanol induced uniform ventricular tachycardia in 4 of 8 dogs, whereas high-dose potassium induced ventricular fibrillation in 5 of 6 dogs.
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