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Relationship between oxidative stress and systolic dysfunction in patients with hypertrophic cardiomyopathy

Kazufumi Nakamura1, Kengo Fukushima Kusano, Hiromi Matsubara

  • 1Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.

Journal of Cardiac Failure
|February 26, 2005
PubMed

Insights

Oxidative stress is elevated in hypertrophic cardiomyopathy (HCM) patients, contributing to heart failure. Elevated levels correlate with left ventricular dilatation and reduced systolic function in HCM.

Area of Science:

  • Cardiology
  • Biochemistry
  • Pathophysiology

Background:

  • Hypertrophic cardiomyopathy (HCM) can progress to left ventricular dilatation and systolic dysfunction.
  • The underlying mechanisms driving this progression remain unclear.
  • This study investigates the role of oxidative stress in HCM progression.

Purpose of the Study:

  • To determine if oxidative stress is elevated in the myocardium of HCM patients.
  • To assess the correlation between oxidative stress levels and left ventricular dilatation and systolic dysfunction in HCM.

Main Methods:

  • Immunohistochemical analysis of endomyocardial biopsy samples from 31 HCM patients and 10 controls.
  • Quantification of 4-hydroxy-2-nonenal (HNE)-modified protein, a marker of lipid peroxidation.
  • Correlation analysis with echocardiographic and ventriculographic measurements.

Main Results:

  • HNE-modified protein expression was significantly increased in HCM patients compared to controls (P = .0005).
  • Expression levels correlated positively with left ventricular end-diastolic diameter (r = 0.483) and end-systolic diameter (r = 0.500).
  • Expression levels showed an inverse correlation with left ventricular ejection fraction (r = -0.640).

Conclusions:

  • Oxidative stress is elevated in the myocardium of HCM patients.
  • Elevated oxidative stress is associated with left ventricular dilatation and systolic dysfunction in HCM.
  • Oxidative stress plays a role in the pathogenesis of heart failure in HCM.
Abstract

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