Myocardial
fibrosis is commonly observed in left ventricular (LV) hypertrophied heart during Arterial
Hypertension. This pathological change coupled with vascular stiffening with aging and diabetes may reduce the cardiovascular system elasticity contributing to the functional impairment. Both the LV adaptive response to the increasing blood pressure and the oxidative damage contribute to myocardial
fibrosis; in particular,
reactive oxygen species (ROS) induce the formation of reactive electrophilic carbonyl species by reacting with
lipids and
sugars which in turn react with
proteins forming irreversible adducts (AGEs, ALEs and EAGLEs) and cross-links. The vascular wall matrix then becomes less distensible, as the formation of the adducts induces greater capacity in
collagen to resist normal turnover. Therefore, monitoring cardiac
fibrosis and markers of
collagen synthesis, degradation and non-enzymatic cross-linking and the use of drugs that revert
collagen accumulation and/or prevent/repair non-enzymatic cross-linking might represent a novel opportunity to alter the natural history of hypertensive
heart disease. Recent evidences have suggested to target the excess of
collagen cross-links; initial evidence seems to show that
fibrosis is not affected to the same degree by all
anti-hypertensive agents. ACEI and ARBs appear particularly effective. Finally, agents acting as cross-link breakers on AGEs or preventing AGEs formation or affecting the TTG activity are emerging.