Background-Ranolazine, a piperazine derivative, reduces ischemia via inhibition of the late phase of the inward sodium current (late I Na ) during cardiac repolarization, with a consequent reduction in intracellular sodium and calcium overload. Increased intracellular calcium leads to both mechanical dysfunction and electric instability. Ranolazine reduces proarrhythmic substrate and triggers such as early afterdepolarization in experimental models. However, the potential antiarrhythmic actions of ranolazine have yet to be demonstrated in humans. Methods and Results-The Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Elevation Acute CoronarySyndrome (

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ST-segment elevation of > or =0.1 mV in V4R in inferior AMI patients is associated with larger infarct size and higher 30-day mortality rates. Right ventricular involvement is not an independent predictor of survival. In patients with small ST, cardiac mortality is low, even if ST V4R is > or =0.1 mV.

The benefits of an enoxaparin strategy over UFH were observed in both SK and fibrin-specific-treated STEMI patients. Therefore, an enoxaparin strategy is preferred over UFH to support fibrinolysis for STEMI regardless of lytic agent.