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

Peter Alter 1 , Heinz Rupp 1 , Marga B. Rominger 2 , Jens H. Figiel 2 , Harald Renz 3 , Klaus J. Klose 2 , and Bernhard Maisch 1
  • 1 Internal Medicine – Cardiology, Philipps University, Marburg, Germany
  • 2 Radiology, Philipps University, Marburg, Germany
  • 3 Clinical Chemistry and Molecular Diagnostics, Philipps University, Marburg, Germany

Abstract

Background: Hyperhomocysteinemia is a risk factor for ischemic heart disease. Several other mechanisms apply also to dilative types of heart failure of various, non-ischemic etiologies. We hypothesized that hyperhomocysteinemia is associated with left ventricular (LV) dilatation and hypertrophy in dilative cardiomyopathy.

Methods: Homocysteine was measured in 66 individuals with suspected cardiomyopathy. Cardiac magnetic resonance imaging was used to assess LV volume, mass, and wall stress.

Results: Hyperhomocysteinemia (>12 μmol/L) was found in 45 patients (68%). LV mass was greater in these patients compared with individuals with normal homocysteine (83±27 vs. 67±19 g/m2; p<0.02). Homocysteine was increased in patients with increased brain natriuretic peptide ≥100 pg/mL (18.3±5.9 vs. 14.9±5.1 μmol/L; p=0.018). LV mass, LV end-diastolic and end-systolic volume (LVEDV, LVESV) were significantly increased in individuals in the upper quartile compared with the lower quartile (90±25 vs. 65±18 g/m2, p=0.021; 114±50 vs. 71±23 mL/m2, p=0.042; 76±51 vs. 36±22 mL/m2, p=0.045). LV dilatation (LVEDV≥90 mL/m2) was more common in hyperhomocysteinemia (>12 μmol/L, p=0.0166). Normalized LV mass was correlated with homocysteine (r=0.346, p=0.065). Homocysteine was not significantly correlated with LVEDV (r=0.229, p=0.065), LV end-diastolic wall stress (r=0.226, p=0.069) and LV ejection fraction.

Conclusions: Hyperhomocysteinemia appears to be, at least in part, involved in a disproportional LV dilatation, where the ensuing hypertrophy is not sufficient to compensate for the increased wall stress. A potential mechanism is the hyperhomocysteinemia associated increase in oxidative stress that favors muscle fiber slippage.

Clin Chem Lab Med 2010;48:555–60.

Purchase article
Get instant unlimited access to the article.
$42.00
Log in
Already have access? Please log in.


or
Log in with your institution

Journal + Issues

Search