Valsartan decreases type I collagen synthesis in patients with hypertrophic cardiomyopathy

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Hiroaki Kawano1, Genji Toda, Reiichirou Nakamizo

  • 1Department of Cardiovascular Medicine, Course of Medical and Dental Science, Graduate School of Biomedical Science, Nagasaki University, Japan. hkawano@net.nagasaki-u.ac.jp

Circulation Journal : Official Journal of the Japanese Circulation Society
|October 1, 2005
PubMed

Insights

Valsartan treatment reduced collagen synthesis in hypertrophic cardiomyopathy (HCM) patients. This cardiac fibrosis improvement was linked to decreased aldosterone levels, offering a potential therapeutic benefit.

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Myocardial fibrosis and hypertrophy significantly impact hypertrophic cardiomyopathy (HCM) prognosis.
  • Valsartan, an angiotensin II type 1 receptor blocker, is being investigated for its potential to mitigate myocardial fibrosis in HCM.

Purpose of the Study:

  • To evaluate the effect of valsartan on myocardial fibrosis markers in patients with HCM.
  • To assess changes in procollagen peptides and aldosterone levels following valsartan treatment.

Main Methods:

  • A randomized study involving 23 HCM patients divided into valsartan (V group, n=11) and conventional therapy (C group, n=12) arms.
  • Measurements included plasma procollagen type I (PIP), procollagen type III aminoterminal peptide (PIIINP), aldosterone (ALDO), brain natriuretic peptide (BNP), and troponin T (TnT) at baseline and 12 months.
  • Echocardiography assessed left ventricular wall thickness (LVWT) and ejection fraction (LVEF).

Main Results:

  • Procollagen type I (PIP) significantly decreased in the valsartan group (p<0.05) but remained unchanged in the control group (p=0.22).
  • Aldosterone (ALDO) levels were unchanged in the valsartan group (p=0.27) but increased in the control group (p<0.05).
  • No significant changes were observed in BNP, PIIINP, TnT, LVWT, or LVEF between groups.

Conclusions:

  • Valsartan effectively suppresses type I collagen synthesis in HCM patients.
  • This suppression of collagen synthesis is associated with a blunted increase in aldosterone levels.
Abstract

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