Homocysteine, fibrinogen and physical activity in human males with coronary artery disease

Elevated homocysteine (Hcy) concentration has been identified as an indepen dent risk factor for premature coronary artery disease (CAD). Associations between Hey concentrations and established cardiovascular risk factors have occasionally, but not consistently, been demonstrated. Plasma fibrinogen a nd total Hey concentrations, along with other risk factors, folate and B-vi tamin supplements and medications, were recorded for 40 males (mean age +/- SD: 65 +/- 9.8 years) with CAD. Physical activity was assessed using the M odifiable Activity Questionnaire (MAQ), a written questionnaire which appra ises leisure and occupational activities by recall for a 12-month period. S ubjects in the upper tertile of physical activity had significantly lower f ibrinogen concentrations than those in the lower tertile (274.7 +/- 38 mg/d l vs. 320.2 +/- 63, respectively, p = 0.04). Univariate analyses revealed t hose subjects on beta-blocker therapy (n = 12) had lower fibrinogen concent rations than those not on these medications (n=28) (277.7 +/- 16.7 vs. 316. 1 +/- 10.9 mg/dl respectively, p = 0.04). There was also a trend for those on beta-blockade to have lower Hey concentrations (8.3 +/- 0.66 vs 9.7 +/- 0.43 mu mol/l, respectively, p = 0.058). Homocysteine concentration was fou nd to be positively associated with age (p = 0.0008). No significant associ ations were established with multivariate analyses among fibrinogen, Hey, p hysical activity, age, BMI, B-vitamin and folate supplements, beta-blocker therapy, total cholesterol, high density lipoprotein (HDL), low density pro tein (LDL), triglycerides, and TC/HDL ratio. These results support the hypo thesis that hyperhomocysteinaemia is independent of other CAD risk factors. Future studies should consider the favourable effects of beta-blockade, wh ich may be a confounding factor, on Hcy and fibrinogen concentrations. Know ledge of associations may contribute towards understanding of the pathogene sis of CAD.