Hyperhomocyst(e)inemia and hemostatic factors: The atherosclerosis risk in communities study

Pamela J Schreiner, Kenneth K. Wu, M. Rene Malinow, Valarie L. Stinson, Moyses Szklo, F. Javier Nieto, Gerardo Heiss

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


PURPOSE: To determine whether homocyst(e)ine (H(e)) is related to hemostatic factors in a population-based sample without evidence of cardiovascular disease. METHODS: A subsample of 660 participants-67 African-American women, 53 African-American men, 201 white women, and 339 white men-was selected from the Atherosclerosis Risk in Communities Study baseline cohort. This was based on carotid intimal-medial wall thickness above the 90th percentile or below the 75th percentile of the population distribution, assessed by B-mode ultrasonography. Unadjusted and multivariable-adjusted associations between fasting plasma H(e) and the hemostatic factors fibrinogen, factor VII:c, factor VIII:c, protein C antigen, hematocrit, platelet count, β-thromboglobulin (β-TG), tissue plasminogen activator (tPA), PAI-1, D-dimer, and lipoprotein[a] were examined. RESULTS: Mean age-adjusted H(e) was positively, albeit weakly, correlated with β-TG, tPA, hematocrit, D-dimer and PAI-1; inversely correlated with protein C; and was higher in smokers, men and African-Americans. In multivariable regression, β-TG, tPA, and factor VII:c were positively associated with H(e), as well as age, black race, male sex, and current cigarette smoking. CONCLUSIONS: These cross-sectional data for a biracial group of middle-aged individuals suggest that H(e) levels falling below values consistent with homocyst(e)inemia are associated with several prothrombotic factors after adjustment for sociodemographic factors. If H(e) change is antecedent to altered hemostasis, FDA-mandated fortification of grain products with folic acid for prevention of fetal neural tube defects may lead to both reduced plasma H(e) levels and improved hemostatic profiles.

Original languageEnglish (US)
Pages (from-to)228-236
Number of pages9
JournalAnnals of epidemiology
Issue number4
StatePublished - 2002

Bibliographical note

Funding Information:
This research was supported by National Heart, Lung and Blood Institute contract N01-HC-55018. The authors acknowledge the contributions of staff at the following ARIC Study centers: The University of North Carolina, Chapel Hill—Phyllis Johnson, Marilyn Knowles, and Catherine Paton; University of North Carolina, Forsyth County—Jeannette Bensen, Kay Burke, Wilhemenia Cheeks, and Revitha Cook; University of Mississippi Medical Center, Jackson—Virginia Overman, Stephanie Paker, Liza Sullivan, and Cora Walls; University of Minnesota, Minneapolis—Amy Shomshak, LaVonne Sjoberg, Margaret Skelton, and Rita Smith; Johns Hopkins University, Baltimore—Pam Bowers, Joyce Chabot, Carol Christman, and Dorrie Costa; University of Texas Medical School, Houston—Pam Pfile, Hogan Pham, and Teri Trevino; The Methodist Hospital, Atherosclerosis Clinical Laboratory, Houston—Wanda R. Alexander, Doris J. Harper, Charles E. Rhodes, and Selma M. Soyal; Bowman-Gray School of Medicine, Ultrasound Reading Center, Winston-Salem—Nancy Bourne, Charlene Kearney-Cash, Kelli Collins, and Delilah Cook; University of North Carolina, Chapel Hill, Coordinating Center—Steve Hutton, Jean Johnson, Doris Jones, and C. Robert Matherly.


  • Atherosclerosis
  • Hemostasis
  • Homocysteine


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