Ranolazine and the myocardial demand-supply balance.

Early studies of ranolazine centered on reductions in myocardial oxygen demand produced by partial inhibition of fatty acid oxidation, particularly as free fatty acid levels increase locally during ischemic episodes. More recent studies report that this mechanism is unlikely to be operative at the plasma levels of ranolazine associated with beneficial clinical effect. A reduction in myocardial oxygen demand has also been questioned, because ranolazine only minimally decreases resting and peak values of systolic pressure and heart rate during exercise.