据《美国心脏病学会杂志》最近出版的一文章称，荷兰的科学家研究发现，脂蛋白水平和纤维蛋白原的水平升高与斑块进展和心血管事件的危险升高有相关性。
荷兰Medish Psectrum Twente的研究人员为了评估Lp(a)和纤维蛋白原是否可预测不良心血管事件风险，入选了60例受试，分析其非狭窄冠状动脉的斑块进展情况。
结果发现，Lp(a)和纤维蛋白原的水平与斑块-基质面积呈正相关，有斑块进展的患者Lp(a)水平明显高于没有斑块进展者，两组的纤维蛋白原的水平也有类似结果，但多变量分析表明，只有Lp(a)的对数水平与斑块进展独立相关。
在18个月的随访研究中发现，发生心血管事件患者的Lp(a)水平和纤维蛋白原水平明显高于与没发生事件的患者，其纤维蛋白原水平也高于没有发生不良心血管事件的患者。
研究人员称，该研究提示，Lp(a) 和纤维蛋白原水平与斑块-基质面积的年改变呈正相关，而Lp(a)水平大幅提高可预测心血管危险。
英文原文：
Lp(a) and fibrinogen linked to plaque progression
Dutch scientists have found elevated lipoprotein (Lp)(a) and fibrinogen levels are associated with plaque progression and a higher risk of cardiovascular (CV) events.
March Hartmann (Medish Psectrum Twente, Enschede) and colleagues analyzed plaque progression in the non-stenotic coronary arteries of 60 individuals to test whether Lp(a) and fibrinogen levels could predict the onset of adverse CV events.
Both Lp(a) and fibrinogen levels were positively correlated with plaque-plus-media area. Patients with evidence of plaque progression had significantly higher levels of Lp(a) than those without, at 30 mg/dl versus 14 mg/dl, as well as significantly higher levels of fibrinogen, at 295 mg/dl versus 240 mg/dl.
However, after multivariate analysis, only log levels of Lp(a) were independently associated with plaque progression.
The team found that levels of Lp(a) were significantly higher in the 19 patients who experienced adverse CV events within the 18-months of follow-up than in those who remained free of CV events, at 44 and 16 mg/dl, respectively.
Fibrinogen levels were also higher in these 19 patients who experienced CV events than those who experienced no adverse CV events, at 342 mg/dl versus 248 mg/dl.
Unlike plaque progression, multivariate analysis demonstrated that both log levels of Lp(a) and fibrinogen were independently associated with adverse CV events.
"We found a positive correlation between Lp(a) and fibrinogen levels versus annual changes in plaque-plus-media area," write March Hartmann et al in the Journal of the American College of Cardiology.
"The data suggest in particular a considerable incremental value of Lp(a) in predicting cardiovascular risk."
Lp(a) may be involved in atherosclerosis, they conclude, due to its accumulation in the vessel wall, ability to promote foam cell cholesterol accumulation and smooth muscle cell proliferation, and finally through its inactivation of growth factor-beta transformation.
