Myocardial fibrosis is a complex phenomenon reflecting the loss of the physiological reciprocal regulation between stimulatory (e.g., angiotensin II, endothelin I, catecholamines, aldosterone, basic fibroblast growth factor, insulin-like growth factor, etc.)and inhibitory factors (prostaglandins, nitric oxide, natriuretic peptides, etc.)acting on the turnover of fibrillar collagen [18]. This evidence concerns the gene FGF2 and Myocardial fibrosis.