Mechano-electric feedback in right atrium after left ventricular infarction in rats

Left ventricular myocardial infarction (MI) can lead to alterations in hemo dynamic load conditions, thereby inducing right atrial hypertrophy and dila tation associated with phenotypic modulation of cardiomyocytes, electrical abnormalities, rhythm disturbances, and atrial fibrillation. However, there is limited information on the electrophysiological basis for these events. We investigated whether atrial stretch in the setting of chronic MI modula tes the electrophysiological properties of cardiomyocytes via "mechano-elec tric feedback", providing a mechanism for atrial arrhythmia after ventricul ar infarction, Five weeks after left ventricular MI (n=37), action potentia ls (AP) were measured in right atrial tissue preparations using a current c lamp scheme, and compared to sham-operated rats (SO. n=10). Contractile act ivity was recorded at a preload of 1 mN, and sustained stretch was applied via a micrometer. In SO, stretch of 1.75 mN shortened repolarization at 50% and prolonged it at 90%. Tn MI, mechanically-induced electrical alteration s were observed at a significantly lower Level of stretch than in SO (0.19 mN). Sustained stretch in MI prolonged AP at 90% repolarization giving rise to stretch-activated depolarizations (SAD) near 90% repolarization (SAD90) . When reaching threshold for premature APs, electrical phenomena similar t o atrial fibrillations were seen in some preparations. Moreover, we observe d APs with prolonged duration at 25%, 50%, and 90% repolarization where str etch induced SAD near 50%. Gadolinium used at a concentration to inhibit st retch-activated channels (40 mu M) suppressed mechanically-induced electric al events. In conclusion, increased susceptibility after MI to mechanical s tretch may predispose atrial cardiomyocytes to arrhythmia. These mechano-el ectrical alterations are sensitive to gadolinium suggesting involvement of stretch-activated ion channels. (C) 2000 Academic Press.