Association of genetic polymorphisms of extracellular matrix metalloproteinase 2 with arterial stiffness and left ventricular hypertrophy in resistant hypertension.

Abstract

Resistant hypertension (RH) is characterized by high blood pressure in spite of concurrent use of three antihypertensive agents of different classes, combined at optimal doses and including a diuretic. Indeed, RH includes patients with controlled blood pressure using four or more agents. Resistant hypertensive patients have an unfavorable prognostic and the morbidity and mortality occur in consequence of the high prevalence of target-organ damage in these patients, including left ventricular hypertrophy and arterial stiffness. Metalloproteinases (MMPs) are a family of enzymes that degrade extracellular matrix proteins and are involved in cardiovascular remodeling related to target-organ damage in cardiovascular diseases, including hypertension (HT). Several studies in experimental models and in humans showed increased levels of MMP-2 in HT. However, there is no study in resistant hypertension showing the role of MMP-2 in target-organ damage in this group of patients. The aim of this study is to evaluate the association of the levels and activity of MMP-2 and your inhibitor TIMP-2 (tissue inhibitors of metalloproteinases), and how the polymorphisms in these enzyme (MMP-2 -1575G>A; MMP-2 -1306C>T; MMP-2 -735C>T) affect the left ventricular hypertrophy, arterial stiffness and other phenotypes of the RH and HT diseases.