Tachypacing-induced heart failure reduced I(K1) by ~41%, I(to1) by 43-45%, and I(Ks) by 49-58% across ventricular layers, increasing action potential duration and favoring early afterdepolarizations.
Heart failure (HF) produces important alterations in currents underlying cardiac repolarization, but the transmural distribution of such changes is unknown. We therefore recorded action potentials and ionic currents in cells isolated from the endocardium, midmyocardium, and epicardium of the left ventricle from dogs with and without tachypacing-induced HF. HF greatly increased action potential duration (APD) but attenuated APD heterogeneity in the three regions. Early afterdepolarizations (EADs) were observed in all cell types of failing hearts but not in controls. Inward rectifier K(+) current (I(K1)) was homogeneously reduced by approximately 41% (at -60 mV) in the three cell types. Transient outward K(+) current (I(to1)) was decreased by 43-45% at +30 mV, and the slow component of the delayed rectifier K(+) current (I(Ks)) was significantly downregulated by 57%, 49%, and 58%, respectively, in epicardial, midmyocardial, and endocardial cells, whereas the rapid component of the delayed rectifier K(+) current was not altered. The results indicate that HF remodels electrophysiology in all layers of the left ventricle, and the downregulation of I(K1), I(to1), and I(Ks) increases APD and favors occurrence of EADs.
Li et al. (Sun,) conducted a other in Heart failure. Tachypacing-induced heart failure vs. Controls (without heart failure) was evaluated on Action potential duration and ionic currents. Tachypacing-induced heart failure reduced I(K1) by ~41%, I(to1) by 43-45%, and I(Ks) by 49-58% across ventricular layers, increasing action potential duration and favoring early afterdepolarizations.