Characteristics of I_K and its Response to Quinidine in Experimental Healed Myocardial Infarction

Abstract

Cells in noninfarct region remote from the scar are hypertrophied and display altered electrophysiology. Their reduced I(K) responsiveness to quinidine may explain, in part, failure of quinidine to prolong APD in such cells. Moreover, dispersion of repolarization may be decreased by the effect of quinidine on normal cells.

Ion Channels and Cardiac Arrhythmia in Heart Disease

“…I, was decreased in dog Purkinje fibers 2 days after infarction (191) and decreased in rat left ventricular endocaridum and epicardium 3 days after infarction (306), although it was increased in the right ventricle in the same study. I, was also decreased in the cat left ventricular subepicardium 2 months after infarction (310). In canine models of atrial fibrillation, I,, and I,, were separated and unchanged (312).…”

“…In epicardial cells surviving a 5-day-old infarction in a canine model cell capacitance was in-creased in the absence of overt failure (151). In a more chronic 2-month feline infarction model surviving cells close to the infarction were unchanged, but more remote cells had an increased capacitance consistent with hypertrophy (193,310), emphasizing the importance of timing and locus of study. Results of studies for hypertrophy as measured by membrane capacitance are summarized in Figure 19-1.…”

Excessive Increase in QT Interval and Dispersion of Repolarization Predict Recurrent Ventricular Tachyarrhythmia after Amiodarone

“…Why are the max QT interval and both the spatial and transmural dispersions, excessively increased in some patients but not in other patients? Yuan et al reported in cat heart that myocytes in noninfarct regions remote from the scar were hypertrophied and reduced in I Kr density 32 . Under condition of the I Kr dysfunction, the repolarization current might more depend on I Ks , therefore blockade of I Ks by chronic amiodarone is expected to markedly prolong APD and QT interval.…”

Mechanisms of Postinfarction Electrophysiological Abnormality: Sympathetic Neural Remodeling, Electrical Remodeling and Gap Junction Remodeling

“…Myocardial infarction predisposes to the proarrhythmic actions of Na + channel blocking drugs (Cardiac Arrhythmia Suppression Trial (CAST) Investigators, 1989;Ranger & Nattel, 1995) and I Kr blocking agents (Waldo et al, 1996). Responses to I Kr blocking drugs may be reduced in postinfarction cells, perhaps because of I Kr downregulation (Yuan et al, 1999).…”