[Remission of left ventricular hypertrophy of hypertensive origin. Experimental data]

Left ventricular hypertrophy is an adaptation of the cardiac fibre to the imposed mechanical overload. This adaptation is quantitative; increased numbers of contractile units with decreased wall stress. Qualitative changes in genomic expression allow the hypertrophied cardiac fibre to develop a normal active tension at the expense of its maximal shortening velocity. These changes are preceded by the temporary expression of proto-oncogenes, of genes of the proteins of thermal shock and by reorganisation of the cytoskeleton, all possible candidates of the regulation of the gene expression in cardiac hypertrophy. In the long-term, the hypertrophy becomes harmful: inadequate subendocardial vascular development; the lowering of the Vmax is beneficial at cellular level but eventually affects cardiac output; ventricular compliance decreases with the development of fibrosis; changes in calcium metabolism are arrhythmogenic. Modifying, prolonging and improving the natural process of adaptation is clearly the first therapeutic objective in order to decrease the hypertension and cause the hypertrophy to regress. Propranolol acts by reducing the cardiac work load. However, betablockers have the disadvantage of increasing the relative density of the subendocardial collagen. Rilmenidine decreases the quantity and density of the collagen. Vasodilators and diuretics induce regression of the myocytic hypertrophy by lowering the threshold of adaptation of these cells, but they have no effect on collagen synthesis. Angiotensin converting enzyme inhibitors which have been shown to be beneficial in controlling hypertension, induce a decrease in the hypertrophy of the myocytes and reduce fibrosis.