Calcineurin inhibition in hypertrophy: back from the dead!

Reactive cardiac hypertrophy has long been recognized as a compensatory process that enhances ventricular function through normalization of wall stress in the face of increased hemodynamic load. For almost as long, it has also been appreciated that the natural history of a hypertrophied heart faced with unremitting hemodynamic overload is progression from a state of functional compensation to one of functional decompensation, or heart failure.1 Under these circumstances, the heart dilates and fails because hypertrophy fails, and in this manner, nature’s temporary cure for hemodynamic overload becomes part and parcel of the disease.