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Association of hyperhomocysteinemia with left ventricular dilatation and mass in human heart

Peter Alter1, Heinz Rupp, Marga B Rominger

  • 1Internal Medicine-Cardiology, Philipps University, Marburg, Germany. alter@staff.uni-marburg.de

Clinical Chemistry and Laboratory Medicine
|February 13, 2010
PubMed

Insights

High homocysteine levels are linked to enlarged left ventricles (LV) in dilated cardiomyopathy. This suggests hyperhomocysteinemia contributes to LV dilatation and hypertrophy, potentially through oxidative stress.

Area of Science:

  • Cardiology
  • Biochemistry
  • Medical Imaging

Background:

  • Hyperhomocysteinemia is a known risk factor for ischemic heart disease.
  • Mechanisms linking hyperhomocysteinemia to non-ischemic heart failure, specifically dilated cardiomyopathy, are being explored.
  • This study investigates the association between elevated homocysteine levels and left ventricular (LV) changes in dilated cardiomyopathy.

Purpose of the Study:

  • To determine if hyperhomocysteinemia is associated with left ventricular (LV) dilatation and hypertrophy in patients with dilated cardiomyopathy.
  • To explore the relationship between homocysteine levels and cardiac structural and functional parameters.

Main Methods:

  • Homocysteine levels were measured in 66 individuals with suspected cardiomyopathy.
  • Cardiac magnetic resonance imaging (CMR) was utilized to assess LV volume, mass, and wall stress.
  • Patients were categorized based on homocysteine levels and compared for cardiac parameters.

Main Results:

  • Hyperhomocysteinemia ( > 12 micromol/L) was prevalent in 68% of patients.
  • Patients with hyperhomocysteinemia exhibited significantly greater LV mass compared to those with normal homocysteine levels (83 vs. 67 g/m²).
  • Elevated homocysteine correlated with increased LV mass, LV end-diastolic volume (LVEDV), and LV end-systolic volume (LVESV), and LV dilatation was more common in patients with hyperhomocysteinemia.

Conclusions:

  • Hyperhomocysteinemia is implicated in disproportionate LV dilatation in dilated cardiomyopathy.
  • The observed hypertrophy may not adequately compensate for increased wall stress.
  • Increased oxidative stress due to hyperhomocysteinemia could be a mechanism contributing to muscle fiber changes and LV remodeling.
Abstract

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