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

Association of hyperhomocysteinemia with left ventricular dilatation and mass in human heart 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/m 2 ; 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/m 2 , p=0.021; 114±50 vs. 71±23 mL/m 2 , p=0.042; 76±51 vs. 36±22 mL/m 2 , p=0.045). LV dilatation (LVEDV≥90 mL/m 2 ) 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Chemistry and Laboratory Medicine (CCLM) de Gruyter

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

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References (41)

Publisher
de Gruyter
Copyright
Copyright © 2010 by the
ISSN
1434-6621
eISSN
1437-4331
DOI
10.1515/CCLM.2010.102
pmid
20148720
Publisher site
See Article on Publisher Site

Abstract

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/m 2 ; 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/m 2 , p=0.021; 114±50 vs. 71±23 mL/m 2 , p=0.042; 76±51 vs. 36±22 mL/m 2 , p=0.045). LV dilatation (LVEDV≥90 mL/m 2 ) 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.

Journal

Clinical Chemistry and Laboratory Medicine (CCLM) – de Gruyter

Published: Apr 1, 2010

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