Páramo José A, Beloqui Oscar, Rodríguez José A, Diez Javier, Orbe Josune
Area de Ciencias Cardiovasculares, CIMA, Universidad de Navarra, Pamplona, Navarra, Spain.
Rev Esp Cardiol. 2008 Dec;61(12):1267-73. doi: 10.1016/s1885-5857(09)60054-2.
Smoking is an important cardiovascular risk factor whose underlying mechanism is incompletely understood. However, it has been suggested that alterations in the balance between synthesis and degradation of the extracellular matrix (ECM) may play a role. The aim of this study was to determine whether there is an independent association between smoking and the concentration of circulating metalloproteinases (MMPs) in individuals without cardiovascular disease.
Metabolic parameters, the carotid intima-media thickness (IMT), inflammatory markers (fibrinogen, C-reactive protein and interleukin-6), markers of endothelial damage (e.g., von Willebrand factor), and the concentration of MMP-1, -9 and -10 and tissue inhibitor of metalloproteinase-1 (TIMP-1) were assessed in 400 asymptomatic individuals with cardiovascular risk factors. Subjects were divided into non-smokers (n=195), smokers (n=118) and former smokers (n=87). In addition, global cardiovascular risk was determined from PROCAM and REGICOR scores.
Both MMP-1 and MMP-10 concentrations were significantly higher in smokers than non-smokers (P< .05 and P< .001, respectively), though there was no difference in the levels of MMP-9, TIMP-1, IMT and other inflammatory parameters. There were positive correlations between the MMP-10 concentration and PROCAM and REGICOR scores (P< .001). Multivariate analysis showed that there was still an association between smoking and the MMP-10 concentration after adjustment for age, sex and other cardiovascular risk factors (P< .001). Multiple regression analysis showed that smoking accounted for 28% of the variability in the MMP-10 concentration.
There was an independent association between smoking and the MMP-10 concentration in asymptomatic individuals. This relationship between MMP-10 and the ECM may indicate a mechanism through which this MMP contributes to smoking-related atherosclerosis.
吸烟是一种重要的心血管危险因素，但其潜在机制尚未完全明确。然而，有研究表明细胞外基质（ECM）合成与降解平衡的改变可能起了一定作用。本研究旨在确定在无心血管疾病的个体中，吸烟与循环金属蛋白酶（MMPs）浓度之间是否存在独立关联。
对400名有心血管危险因素的无症状个体评估其代谢参数、颈动脉内膜中层厚度（IMT）、炎症标志物（纤维蛋白原、C反应蛋白和白细胞介素-6）、内皮损伤标志物（如血管性血友病因子）以及MMP-1、-9和-10及金属蛋白酶组织抑制剂-1（TIMP-1）的浓度。受试者分为非吸烟者（n = 195）、吸烟者（n = 118）和既往吸烟者（n = 87）。此外，通过PROCAM和REGICOR评分确定总体心血管风险。
吸烟者的MMP-1和MMP-10浓度均显著高于非吸烟者（分别为P <.05和P <.001），而MMP-9、TIMP-1、IMT及其他炎症参数水平无差异。MMP-10浓度与PROCAM和REGICOR评分呈正相关（P <.001）。多变量分析显示，在调整年龄、性别和其他心血管危险因素后，吸烟与MMP-10浓度仍存在关联（P <.001）。多元回归分析表明，吸烟占MMP-10浓度变异性的28%。
在无症状个体中，吸烟与MMP-10浓度之间存在独立关联。MMP-10与ECM之间的这种关系可能表明该MMP促成吸烟相关动脉粥样硬化的一种机制。
