Dietary Factors and Hereditary Myocardial Diseases
P. Di Nardo, M. Minieri, F. Carotenuto, R. Fiaccavento, M. Zingarelli, C. Fantini, A. Bertoli, A. Fusco.
Dept Internal Medicine, Università di Roma "Tor Vergata", Roma, Italy
The action mechanism of nutritional factors are usually studied in healthy animals and no information are presently available on the effect of nutritional factors in cardiovascular hereditary diseases. In fact, the presence of specific mutations has always been considered as exhaustive explanation of the pathogenesis of hereditary diseases and the role of other factors, such as diet, of marginal interest. Nevertheless, the different human cardiomyopathic phenotypes of individuals sharing the same mutation indicate that other genetic and/or environmental factors can play a fundamental role in the pathophysiology of the disease. In the present study, we evaluated the effects of different diets in hamsters (CMPH) affected by a hereditary myocardial disease. Similarly to human beings, the disease determines the progressive destruction of the myocardium leading animals to death when aged 7-8 months. The administration of fresh vegetables and sunflower or linen seeds from weaning prevents the animal death and the hamster lifespan is prolonged until two years (i.e. the same that healthy animals). The histopathologic evaluation of the myocardium showed that cardiomyopathic tissue modifications are only minimally represented. In addition, several molecular and biochemical parameters, typically characterizing the myopathic phenotype, are reconverted to normality or substantially improved. In particular, the presence in the diet of fresh vegetables modulate the expression of genes coding for hormones (ANF), receptors (SERCA2), and structural (sarcoglycans, dystroglycans, actin) and contractile proteins (myosin heavy chain, myomesin). The improved quality of the myocardial tissue, restores a normal heart contractile function and hemodynamics and the hamster lifespan lasts approximately two years. Obviously, the diet does not eliminate the mutation that causes the disease, but surely interferes with basic pathophysiologic mechanisms of the disease.