The biological basis of modified myocardial function in hypertensive cardiopathy.

We now have a biological explanation for most of the physiological characteristics of the hypertrophied chronically overloaded heart: (i) the slowing of the active relaxation is, at least in part, explained by a diminished density in the Ca2+ ATPase of SR, a majority of the modifications in passive myocardial compliance are due to an enhanced collagen density and the diminution of the atrial contribution to ventricular filling is certainly a consequence of an isomyosin change in this particular tissue. (ii) The systolic dysfunction reflects, in fact, one of the most essential parts of the adaptational process, the slowing of Vmax. In human, this diminution is a consequence of a rather complex change in the expression of various genes coding for proteins responsible for myoplasmic calcium transient. (iii) Arrhythmogenecity, a well-known detrimental property of the hypertrophied heart, reflects the fragility of calcium homeostasis in this type of cell, and this fragility is likely to be a direct consequence of the rearrangement of the membrane proteins.