Our data suggest that the hyperhomocysteinemia and/or increased plasma level of lipoprotein Lp(a) are risk factors for coronary heart disease. We investigated 178 patients who underwent complete cardiac examination comprising coronary angiography and biological analysis (CT, HDL-c, LDL-c, TG, and apoAI, apoB, homocystein and Lp(a)). Patients presenting a significant stenosis of the coronary artery (greater than or equal to 50% of the vascular lumen) were considered as cases (113 patients). Those without stenosis or with non-significant stenosis (< 50% of the vascular lumen) were used as controls (65 subjects). Homocysteinemia was significantly higher in cases than in control subjects (8.26 mumol/L (2.34 versus 17.85 (2.34, p < 0.001). A strong association between coronary heart disease and homocystein has been found (Eta<^>2 = 0.76). The OR were 0.16 when homocystein level was lower than 15 mumol/L, and 27.78 when homocystein level was upper than or equal to 15 mumol/L. The RR was 5.16 (95% IC = 3.66-6.66, p < 0.001). Eventhough there was a significant correlation between tabagic impregnation and homocysteinemia (Spermann's rho = 0.37, p < 0.05), there was no interactive effect between these two factors and coronary disease (Wald chi(2) = 0.086, p > 0.05). Therefore, no association was found between homocyteinemia and other coronary heart disease risk factors. The Lp(a) levels were significantly higher in cases than in controls subjects (188 (84 mg/L in control subjects versus 590 (199 in cases, p < 0.001). A stronger relationship was noted between coronary heart disease and Lp(a) (Eta<^>2 = 0.66). The OR were 0.09 when lipoprotein (a) levels were lower than 350 mg/L, and 5,88 when Lp(a) levels were higher than or equal to 350 mg/L. The estimate RR was 6.47 (95% IC = 4.39-8.55, p < 0.001). The level of Lp(a) was positively correlated with the severity of coronary heart disease (Spermann's rho = 0.95, p < 0.001). A weak correlation between Lp(a) and LDL-c was observed (Spermann's rho = 0.12, p = 0.048). But the multivariate analysis didn't show interactive effect between these two factors and coronary disease (chi(2) de Wald = 0.264, p > 0.05). No association was noted between Lp(a) and the others risk factors. Moreover, a positive correlation between the levels of homocystein and those of Lp(a) was found (Spermann's rho = 0.54, p < 0.001). In contrast their effect on coronary heart disease seems to be independant (Wald chi(2) = 2.957, p > 0.05). Thus, these two parameters appear as independant risk factors for coronary heart disease.