2002
DOI: 10.1161/01.cir.0000017264.66561.3d
|View full text |Cite
|
Sign up to set email alerts
|

Losartan-Dependent Regression of Myocardial Fibrosis Is Associated With Reduction of Left Ventricular Chamber Stiffness in Hypertensive Patients

Abstract: Background — This study was designed to investigate whether myocardial collagen content is related to myocardial stiffness in patients with essential hypertension. Methods and Results — The study was performed in 34 patients with hypertensive heart disease. Nineteen of these patients… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

16
285
3
8

Year Published

2004
2004
2017
2017

Publication Types

Select...
7
2

Relationship

0
9

Authors

Journals

citations
Cited by 567 publications
(312 citation statements)
references
References 35 publications
16
285
3
8
Order By: Relevance
“…Neurohormonal modulation of the RAAS is currently the only therapy with some effect on the patho‐physiological mechanisms responsible for the increase in vascular and ventricular stiffness 185 , 186 . ACEIs 187 , 188 , ARBs 189 , and aldosterone receptor antagonists 190 , 191 , independent of their hemodynamic effects, mediate potentially favourable effects of reduced smooth muscle cell growth, prevention of collagen deposition, reduced growth factor expression, and regression of myocardial fibrosis. Spironolactone, an aldosterone antagonist, has also been shown to reduce myocardial fibrosis and thus may aid in the treatment of DD 192 .…”
Section: Possible Therapiesmentioning
confidence: 99%
“…Neurohormonal modulation of the RAAS is currently the only therapy with some effect on the patho‐physiological mechanisms responsible for the increase in vascular and ventricular stiffness 185 , 186 . ACEIs 187 , 188 , ARBs 189 , and aldosterone receptor antagonists 190 , 191 , independent of their hemodynamic effects, mediate potentially favourable effects of reduced smooth muscle cell growth, prevention of collagen deposition, reduced growth factor expression, and regression of myocardial fibrosis. Spironolactone, an aldosterone antagonist, has also been shown to reduce myocardial fibrosis and thus may aid in the treatment of DD 192 .…”
Section: Possible Therapiesmentioning
confidence: 99%
“…[1][2][3] As excessive myocardial fibrosis is assumed to be a critical determinant of the deterioration of LV function 4,5 and the cause of arrhythmias, 6 regulating the proliferation and activation of fibroblasts would be an important therapeutic target in the disorder. The renin-angiotensin II (Ang II) system (RAS) is recognized to stimulate fibrosis, 7 whereas the inhibition of either angiotensin-converting enzyme (ACE) or Ang II type 1 receptor has been shown to regress myocardial fibrosis in patients with hypertensive heart disease.…”
Section: Introductionmentioning
confidence: 99%
“…[11][12][13][14] This excess of myocardial collagen is primarily a result of the uncoupling between increased synthesis and unchanged or decreased degradation of collagen type I fibres. 18 However, patients with coronary heart disease have been excluded from these studies, 11-14 so it is not clear if a different pattern of interstitial remodelling may be present in the first months after AMI in patients with antecedent hypertension.…”
Section: Discussionmentioning
confidence: 99%
“…[11][12][13][14] Accordingly, we serially measured serum products collagen types I and III turnover, which constitute the bulk of cardiac ECCM, 15 and LV volumes and function in a consecutive sample of patients successfully treated with primary percuta-neous coronary intervention (PCI) for a first AMI with LV systolic dysfunction. The purpose of this study was to evaluate if a different pattern of ECCM and LV remodelling is present in patients with antecedent hypertension compared with those without hypertension.…”
Section: Introductionmentioning
confidence: 99%