Origin and mechanisms of heart failure in hypertensive patients: left ventricular remodelling in hypertensive heart disease.

This review-editorial proposes a biological explanation for most of the physiological characteristics of the hypertrophied chronically overloaded heart. Various growth signals, including mechanical, hormonal and paracrine factors, appear now to be involved in the induction of myocyte hypertrophy and/or phenotypic modifications. 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. The systolic dysfunction reflects, in fact, one of the most essential parts of the adaptational process, the slowing of Vmax. In humans, this diminution is a consequence of a rather complex change in the expression of various genes coding for proteins responsible for myoplasmic calcium transient. Arrhythmogenicity, 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 membrane protein rearrangement.