CPAP is an important therapy in OSA patients undergoing PVI that improves arrhythmia free survival. PVI offers limited value to OSA patients not treated with CPAP.

Background-Cardiac memory refers to an altered T-wave morphology induced by ventricular pacing or arrhythmias that persist for variable intervals after resumption of sinus rhythm. Methods and Results-We induced long-term cardiac memory (LTM) in conscious dogs by pacing the ventricles at 120 bpm for 3 weeks. ECGs were recorded daily for 1 hour, during which time pacing was discontinued. At terminal study, the heart was removed and the electrophysiology of left ventricular epicardial myocytes was investigated. Control (C) and LTM ECG did not differ, except for T-wave amplitude, which decreased from 0.12Ϯ0.18 to Ϫ0.34Ϯ0.21 mV (ϮSEM, PϽ0.05), and T-wave vector, which shifted from Ϫ37Ϯ12°to Ϫ143Ϯ4°(PϽ0.05). Epicardial action potentials revealed loss of the notch and lengthening of duration at 20 days (both PϽ0.05). Calcium-insensitive transient outward current (I to ) was investigated by whole-cell patch clamp. No difference in capacitance was seen in C and LTM myocytes. I to activated on membrane depolarization to Ϫ25Ϯ1 mV in C and Ϫ7Ϯ1 mV (PϽ0.05) in LTM myocytes, indicating a positive voltage shift of activation. I to density was reduced in LTM myocytes, and a decreased mRNA level for Kv4.3 was observed. Recovery of I to from inactivation was significantly prolonged: it was 531Ϯ80 ms (nϭ10) in LTM and 27Ϯ6 ms (nϭ9) in C (PϽ0.05) at Ϫ65 mV. Conclusions-I to changes are associated with and can provide at least a partial explanation for action-potential and T-wave changes occurring with LTM. (Circulation. 1999;99:1898-1905.)

CM is a dynamic process for which the final T vector is predicted by the paced QRS vector and which is associated with significant changes in epicardial and endocardial but not midmyocardial cell action potential duration, such that the transmural gradient of repolarization is altered. It is unaccompanied by evidence of altered hemodynamics or flow, requires a change in pathway of activation, and appears to require new protein synthesis.

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Spatially distinct transmural and regional gap junctional remodeling is a consequence of abnormal ventricular activation and is associated with consistent changes in activation that may alter patterns of repolarization and facilitate reentrant arrhythmogenesis.

Thus the reduced rate adaptation of steady-state APD is explained mainly by the loss of a slow phase of APD adaptation in nAF/cAF which is reversed in the presence of ryanodine. Therefore, in both nAF and cAF atria, rate adaptation of MDP as well as APD are reduced, nonsteady state as well as steady state, AP characteristics are markedly altered and these changes are partially explicable by Ca, -dependent processes.

Identification of acute PV reconnection, even when successfully targeted, is a strong predictor of arrhythmia recurrence following PVI.

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