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Cardiac alternans is promoted by heart failure (HF)–induced calcium (Ca²⁺) cycling abnormalities. Late sodium current (I_Na,L) is enhanced in HF and promotes Ca²⁺ overload; however, mechanisms underlying an antiarrhythmic effect of I_Na,L blockade in HF remain unclear.

The purpose of this study was to determine whether ranolazine suppresses cardiac alternans in HF by normalizing Ca²⁺ cycling.

Transmural dual optical mapping of Ca²⁺ transients and action potentials was performed in wedge preparations from 8 HF and 8 control (normal) dogs. Susceptibility to action potential duration alternans (APD-ALT) and Ca²⁺ transient alternans (Ca-ALT) was compared at baseline and with ranolazine (5–10 μM).

HF increased APD- and Ca-ALT compared to normal (both P <.05), and ranolazine suppressed APD- and Ca-ALT in both groups (P <.05). The incidence of spatially …