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Hello I was just wondering why a pharmcodynamic interaction does not come up between these drugs. My way of thinking is that ranolazine stops calcium overload in angina patients by inhibiting late sodium current, increasing the activity of the Na/Ca exchanger to get more calcium out of the cell cutting down on calcium overload. Digoxin will have opposite effects inhibiting the Na/K atpase, leading to more sodium in the cell which will decrease the activity of the Na/Ca exchanger, leading to more calcium in the cell (which is why it has iontrophic effects). Aren't these mechanisms at odds with each other, and shouldn't there be a interaction due to this?
