Cardiac fibrosis occurs before arterial hypertension becomes well defined

Abstract

Target organ damage (TOD) of systemic arterial hypertension (AH) in the heart modifies the cardiomyocyte, Interstice and its arteries. Alterations that occur in AH include cardiomyocyte hypertrophy, connective tissue hyperplasia and neovascularization stimulation, among others.1-3 These alterations depend essentially on the stimulus of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS)1-3 which may not homogeneously impact Kidneys, heart, brain and blood vessels. The response of the connective tissue to AH induces collagen production by fibroblasts and consequently interstitial fibrosis.1-3 Since 2006 with the data published by Das MK et al.,4 we have started to correlate the presence of notches that form the fragmented QRS (fQRS) with non-homogeneous electrical conduction resulting from myocardial fibrosis which can be restorative or reactive. With this information, Eyuboglu e Akdeniz5 proposed to correlate the presence of the fQRS and absense of the nocturnal decline in individuals with prehypertension, considering the existence of evidence of higher chances of TOD of AH in these cases.