Key result
Myocytes from the epicardial border zone of infarcted canine hearts exhibited altered intracellular Ca2+ handling and reduced cell shortening compared to normal epicardial myocytes.
Myocytes surviving in the epicardial border zone of infarcted hearts exhibit markedly altered intracellular Ca2+ handling and impaired cell shortening, which may contribute to arrhythmogenesis.
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Altered Ca2+ handling in infarct border-zone myocytes may promote post-MI arrhythmias; leaves open translation to human disease and targeted therapies.
UNLABELLED: Myocytes that survive in the epicardial border zone of the healing canine infarcted heart provide the substrate for inducible reentrant ventricular arrhythmias. These myocytes have been shown to have altered Ca2+ currents which could impact on Cai homeostasis in these cells. OBJECTIVE AND METHODS: To directly measure and compare intracellular Ca2+ transients and cell shortening in myocytes dispersed from control noninfarcted hearts with those from epicardial border zone of 5 day infarcted canine hearts using the Ca2+ sensitive indicator fura-2/AM. Studies were designed to determine and compare the effects of rate and premature stimulation on intracellular Ca2+ in the two cell types. RESULTS: Epicardial cells from noninfarcted hearts (1) exhibited an increase in amplitude of the fura-2 ratio with decreasing pacing cycle length (CL), while cells from the infarcted heart showed the opposite effect; (2) showed more marked acceleration of relaxation of the Cai transient with decreasing CL than myocytes from the infarcted heart; (3) exhibited little or no post rest potentiation in contrast to cells from the infarcted heart; and (4) showed a more rapid recovery during restitution protocols than cells from the infarcted heart. Cell shortening differences were also observed between cell populations in that most cells from the infarcted zone did not show any degree of cell shortening despite the reasonable intracellular Ca2+ transient. CONCLUSIONS: The handling of intracellular Ca2+ in myocytes that have survived in the epicardial border zone is very different from that of normal epicardial myocytes suggesting that there may exist marked heterogeneity in intracellular Ca2+ handling in cells in the in situ healing infarcted heart. Electrophysiologic implications of these findings are discussed.
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A. Licata (1997) studied Myocardial infarction (canine model). Myocardial infarction (epicardial border zone) vs. Control noninfarcted hearts was evaluated on Intracellular Ca2+ transients and cell shortening. Myocytes from the epicardial border zone of infarcted canine hearts exhibited altered intracellular Ca2+ handling and reduced cell shortening compared to normal epicardial myocytes.
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