Platelet-derived chemokines, PF-4 and RANTES, are significantly increased in hemodynamically significant degenerative aortic stenosis

Aortic valve stenosis (AoS) is the most common acquired valvular disorder found in developed countries, being present in 2% to 7% of adults over the age of 65 [1], [2] and [3]. Calcified AoS is a chronic progressive disease. The pathomechanisms leading to valve degeneration remain unknown. Valve disease shares many features with atherosclerosis. Platelet activation is an important constituent of the atherosclerotic process [4] and [5]. The study focused on two platelet-derived chemokines, which bridge three important components of atherogenesis: platelet activation, inflammation, and generation of atheroma. The study group was comprised of 124 consecutive patients being considered for aortic valve replacement for symptomatic degenerative trileaflet valvular AoS, and were undergoing cardiac catheterization in the Cardiocentre (Table 1) [6]. The exclusion criterion was the presence of an additional hemodynamically significant valve disease

Platelet glycoprotein GP VI 13254C allele is an independent risk factor of premature myocardial infarction

Aim The purpose of this study was to asses the impact of haemostatic and platelet receptor gene polymorphisms as an inherited risk factor for premature onset of myocardial infarction (MI).<p></p> Methods Polymorphisms of platelet receptors - GP Ia (807C>T, rs1126643), GP VI (13254T>C, rs1613662), GP IIIa (HPA-1, rs5918), PAR -1 (IVS -14A>T; rs168753), P2Y12 (34C>T, rs6785930 and H1/H2 haplotype, rs2046934), and genetic variations of the gene coding for cyclooxygenase-1 (COX-1) ( -842A>G, rs10306114 and 50C>T, rs3842787) were investigated. Mutations in the genes coding for coagulation factor V (Q506R (Leiden) mutation, rs6025) and factor II (prothrombin G20210A, rs1799963) were also determined. The prevalence of gene polymorphisms was investigated in 105 consecutive patients with premature MI. This was compared with the same gene polymorphism prevalence in a group of 132 patients in which coronary artery disease had been excluded. Genotyping was done using PCR, followed by melting curve analysis with specific fluorescent hybridization probes.<p></p> Results A significant association between GP VI 13254C allele carriers and premature MI was found (p = 0.025). No other differences in prevalence of the investigated polymorphisms between the compared patient populations reached statistical significance. In a logistic regression, which took other cardiovascular risk factors into account, the significance of the GP VI 13254C allele and vascular risk was suggested (OR 1.888, 95% C.I. 1.029 to 3.464, p = 0.040). In a binary logistic regression the positive relationship between the GP VI genotype and female gender was observed (0R 3.676; 95% C.I. 1.159 to 11.628; p = 0.027). The frequencies of GP VI and GP Ia gene polymorphisms were independent of one another (p = 0.836).<p></p> Conclusion The presence of the GP VI 13254C allele is an independent predictor of premature MI