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NDT Advance Access originally published online on November 1, 2005
Nephrology Dialysis Transplantation 2006 21(1):20-23; doi:10.1093/ndt/gfi237
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Editorial Comment

Hypertensive myocardial fibrosis

Cesare Cuspidi1,2, Michele Ciulla1,2 and Alberto Zanchetti2,3

1 Istituto di Medicina Cardiovascolare, 2 Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Universita’ di Milano, Ospedale Maggiore Policlinico, IRCCS and 3 Istituto Auxologico Italiano IRCCS, Milano, Italy

Correspondence and offprint requests to: C. Cuspidi, Centro Interuniversitario di Fisiologia Clinica e Ipertensione, via F. Sforza 35, 20122 Milano, Italy. Email: dhipertensione@libero.it

Keywords: fibrosis; hypertension; left ventricular hypertrophy

The first 150 words of the full text of this article appear below.



   Introduction
 
A variety of cardiac structural and functional changes, such as increased left ventricular mass (LVM), left atrial and aortic root enlargement, LV dysfunction, impairment of coronary reserve and prolonged ventricular repolarization, have been described in patients with long-standing arterial hypertension [1,2]. However, subtle modifications in LV structure and geometry may occur also in the early phases of the natural history of essential hypertension [3]. Among these manifestations of target organ damage, most attention has been devoted to LV hypertrophy (LVH), because the prevalence of this phenotype is relatively high and is associated with an increased risk of cardiovascular morbidity and mortality [4,5].



   Pathophysiology of cardiac fibrosis
 
Normal myocardium is composed of cardiac myocytes, tethered to an extracellular matrix of fibrillar collagen; they represent one-third of all cells, with cells other than cardiomyocytes accounting for the remaining two-thirds [6]. A large body of . . . [Full Text of this Article]



   Diagnosis of myocardial fibrosis
 


   Regression of cardiac fibrosis
 


   Conclusions
 

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