Serum fetuin-A in metabolic and inflammatory pathways in patients with myocardial infarction.

BACKGROUND: Although multifunctional glycoprotein α2HS-glycoprotein/human fetuin-A (AHSG) is involved in atherosclerosis, it is not clear whether high or low concentrations are more important. We studied the correlation of serum AHSG with adiponectin, leptin, resistin, C-reactive protein (CRP) and tumour necrosis factor-α (TNF-α) to see whether its metabolic effects or its involvement in subclinical inflammation are dominant in patients with established coronary disease. MATERIALS AND METHODS: In this cross-sectional study, AHSG concentration was determined in sera of 171 patients (age: 62 ± 6 years, mean ± SD) with previous myocardial STEMI infarction and normal renal function and 81 age-matched healthy controls by radial immunodiffusion. Results Patients had increased AHSG levels (673 ± 103 vs. 619 ± 96 mg L(-1), P < 0·001) compared to controls. Obese and diabetic patients had higher AHSG concentration than those with normal BMI or without diabetes but even the latter group had elevated AHSG levels (667 ± 101 mg L(-1), n = 88) compared to controls (P = 0·002). Serum AHSG correlated negatively with adiponectin (r = -0·236, P = 0·006) even after adjusting for BMI (r = -0·177, P = 0·043). AHSG determined adiponectin levels independently from BMI, age and other adipocytokines (P = 0·014). The correlation between leptin and AHSG (r = 0·321, P = 0·021) weakened following adjustment for BMI (r = 0·209, P = 0·072). Serum AHSG did not correlate significantly with CRP, resistin and TNF-α concentrations. BMI and resistin but not AHSG determined TNF-α levels independently. CONCLUSIONS: AHSG is elevated in sera of patients with previous myocardial infarction. Association with adipokines favours the concept that AHSG is involved in atherosclerosis more likely through metabolic pathways (insulin resistance, obesity and adipocyte dysfunction) than by inflammation in patients with post-myocardial infarction.

Myocardial infarction is associated with Spl binding site polymorphism of collagen type 1A1 gene.

OBJECTIVE: Human atherosclerotic lesions contain collagen type I, which plays a pivotal role in atherosclerotic plaque stability. In contrast, the normal coronary arteries do not express this type of collagen. Data have shown that the collagen type 1A1 (COL1A1) gene Sp1 binding site (-1245 G/T) polymorphism is associated with disturbed collagen protein production. METHODS: In our study, COL1A1 gene Sp1 polymorphism was investigated in 136 patients with myocardial infarction (MI) 5 months after the acute phase, and 212 age-matched control subjects in association with any cardiovascular risk factors (such as serum adiponectin levels, hyperinsulinaemic status, hyperlipaemia). RESULTS: The "SS" genotype of the COL1A1 gene was found to occur significantly more frequently in patients surviving a MI, as compared to the control group and the "Ss" and "ss" genotype frequencies (the presence of the s allele) were lower in our patients, than in control group. However, the occurrence of cardiovascular risk factors was significantly higher among the "s" allelic carriers as compared to patients carrying the "S" allele of the COL1A1 gene. CONCLUSION: Our results raise the possibility that COL1A1 gene Sp1 polymorphism might have an impact on the development of MI.