The association of elevated plasma homocyst(e)ine with progression of symptomatic peripheral arterial disease

Plasma homocyst(e)ine (the sum of free and bound homocysteine, homocystine, and the mixed disulfide homocysteine-cysteine, expressed as homocysteine) levels were determined by high performance liquid chromatography in 214 patients with symptomatic (claudication, rest pain, gangrene, amputation) lowe...

Full description

Saved in:
Bibliographic Details
Published inJournal of vascular surgery Vol. 13; no. 1; pp. 128 - 136
Main Authors Taylor, Lloyd M., DeFrang, Robert D., Harris, E.John, Porter, John M.
Format Journal Article
LanguageEnglish
Published United States Mosby, Inc 01.01.1991
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Plasma homocyst(e)ine (the sum of free and bound homocysteine, homocystine, and the mixed disulfide homocysteine-cysteine, expressed as homocysteine) levels were determined by high performance liquid chromatography in 214 patients with symptomatic (claudication, rest pain, gangrene, amputation) lower extremity arterial occlusive disease and/or symptomatic (stroke, cerebral transient ischemic attacks) cerebral vascular disease and in 103 control persons. Mean plasma homocyst(e)ine was significantly higher in patients than in controls (14.37 ± 6.89 nmol/ml vs 10.10 ± 2.16, p < 0.05). Thirtynine percent of patients (83 of 214) had plasma homocyst(e)ine values greater than control mean + 2 standard deviations. Plasma homocyst(e)ine values were contrasted to age, male sex, diabetes, hypertension, smoking, renal failure, and plasma cholesterol. No difference was found in the incidence and/or level of any of these risk factors when patients with normal plasma homocyst(e)ine were compared to those with elevated plasma homocyst(e)ine, both by univariate and multivariate analysis. Patients with elevated plasma homocyst(e)ine were more likely to demonstrate clinical progression of lower extremity disease and of coronary artery disease, but not of cerebral vascular disease than were patients with normal plasma homocyst(e)ine, and the rate of progression was more rapid (p = 0.002). Progression of lower extremity disease as assessed in the vascular laboratory was also more common in patients with elevated plasma homocyst(e)ine (p = 0.01). We conclude that elevated plasma homocyst(e)ine is an independent risk factor for symptomatic lower extremity disease or cerebral vascular disease or both. Symptomatic patients with lower extremity disease and with elevated plasma homocyst(e)ine also appear to have more rapid progression of disease.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0741-5214
1097-6809
DOI:10.1016/0741-5214(91)90020-U