{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T11:16:03Z","timestamp":1785150963875,"version":"3.55.0"},"reference-count":42,"publisher":"Walter de Gruyter GmbH","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Chemistry and Laboratory Medicine"],"published-print":{"date-parts":[[2010,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>\n                  <jats:bold>Background:<\/jats:bold> 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.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Methods:<\/jats:bold> Homocysteine was measured in 66 individuals with suspected cardiomyopathy. Cardiac magnetic resonance imaging was used to assess LV volume, mass, and wall stress.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Results:<\/jats:bold> Hyperhomocysteinemia (&gt;12\u00a0\u03bcmol\/L) was found in 45 patients (68%). LV mass was greater in these patients compared with individuals with normal homocysteine (83\u00b127 vs. 67\u00b119\u00a0g\/m<jats:sup>2<\/jats:sup>; p&lt;0.02). Homocysteine was increased in patients with increased brain natriuretic peptide \u2265100\u00a0pg\/mL (18.3\u00b15.9 vs. 14.9\u00b15.1\u00a0\u03bcmol\/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\u00b125 vs. 65\u00b118\u00a0g\/m<jats:sup>2<\/jats:sup>, p=0.021; 114\u00b150 vs. 71\u00b123\u00a0mL\/m<jats:sup>2<\/jats:sup>, p=0.042; 76\u00b151 vs. 36\u00b122\u00a0mL\/m<jats:sup>2<\/jats:sup>, p=0.045). LV dilatation (LVEDV\u226590\u00a0mL\/m<jats:sup>2<\/jats:sup>) was more common in hyperhomocysteinemia (&gt;12\u00a0\u03bcmol\/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.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Conclusions:<\/jats:bold> 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.<\/jats:p>\n               <jats:p>Clin Chem Lab Med 2010;48:555\u201360.<\/jats:p>","DOI":"10.1515\/cclm.2010.102","type":"journal-article","created":{"date-parts":[[2010,2,12]],"date-time":"2010-02-12T09:58:59Z","timestamp":1265968739000},"page":"555-560","source":"Crossref","is-referenced-by-count":23,"title":["Association of hyperhomocysteinemia with left ventricular dilatation and mass in human heart"],"prefix":"10.1515","volume":"48","author":[{"given":"Peter","family":"Alter","sequence":"first","affiliation":[{"name":"Internal Medicine \u2013 Cardiology, Philipps University, Marburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heinz","family":"Rupp","sequence":"additional","affiliation":[{"name":"Internal Medicine \u2013 Cardiology, Philipps University, Marburg, 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