血脂水平、ApoE和SLCO1B1基因多态性与晚期支架内再狭窄的相关性研究

目的 对比分析晚期支架内再狭窄(in-stent restenosis, ISR)与无ISR患者的临床特点、血脂水平、载脂蛋白E (apolipoprotein E, ApoE)以及SLCO1B1基因的多态性，探讨影响晚期ISR的临床危险因素。方法 入选2018年1月至2020年12月住院行冠状动脉造影证实晚期ISR的患者共61例，另外入选行冠状动脉造影证实无晚期ISR的患者共119例为对照组。比较两组的临床特点、血脂水平以及ApoE以及SLCO1B1基因的多态性。所有患者根据低密度脂蛋白胆固醇（low-density lipoprotein cholesterol, LDL-C）水平分为＜1.4mmol/l组，1.4~1.8 mmol/L组以及＞1.8 mmol/L组，=比较不同组别晚期ISR的发生率。结果 晚期ISR组与无ISR组患者ApoE、SLCO1B1基因型以及等位基因的频率并无统计学差异（P＞0.05），将不同基因型和等位基因频率分别进行组内两两对比，结果也无统计学差异（P＞0.05）。两组患者总胆固醇(total cholesterol ,TC)、LDL-C、载脂蛋白B(apolipoprotein B, ApoB)、ApoB/ApoA比值以及非高密度脂蛋白胆固醇（non-high-density lipoprotein cholesterol, n-HDL-C）水平均有统计学差异，晚期ISR组上述指标均比对照组偏高（P<0.05）。3. ＜1.4 mmol/L组的ISR发生率为17.9%，1.4~1.8mmol/l组的ISR发生率为31.3%，＞1.8 mmol/L组的ISR发生率为39.4%。不同LDL-C水平的组间总体ISR发生率并无统计学差异（P＞0.05）。进一步行组间两两对比，小于＜1.4mmol/l组的ISR发生率为与＞1.8mmol/l组的ISR发生率有差异（P<0.05）。 结论 冠状动脉支架术后的患者，其ApoE或SLCO1B1的基因多态性与晚期ISR的发生率无明确关系。晚期ISR患者血脂水平较无ISR患者升高明显，将LDL-C降至1.4mmol/l以下可能有助于减少晚期ISR的发生。

Relationships between lipid profiles, polymorphisms of ApoE or SLCO1B1 and late in-stent restenosis

Objective To study the characteristics of clinical presentations, lipid profiles, polymorphisms of ApoE and SLCO1B1 in patients with and without late in-stent restenosis (ISR). To discuss the clinical risk factors for ISR. Method 61 patients with angiographically confirmed late ISR and 119 patients without angiographically late ISR were selected for the study. Basic clinical features, lipid profiles and polymorphisms of ApoE and SLCO1B1 were measured and compared between the two groups. All patients were then divided into three groups according to the levels of low-density lipoprotein cholesterol (LDL-C), the rates of ISR in different group were compared. Results There were no significant differences of polymorphisms and allele frequencies of ApoE and SLCO1B1 between different groups(P>0.05). The lipid profiles of total cholesterol (TC), LDL-C, apolipoprotein B(ApoB), ratios of ApoB/ApoA and non-high-density lipoprotein cholesterol(n-HDL-C) in late ISR group were significantly higher than in control group(P<0.05). There was no significant difference of total late ISR rate between the three groups according to the LDL-C levels; but in LDL-C<1.4mmol/l group the ISR rate (17.9%) was significantly lower than in >1.8mmol/l group (39.4%). (P<0.05). Conclusions There were no relationships between polymorphisms of ApoE or SLCO1B1 and late ISR. The lipid profiles of late ISR group were significantly higher, reduce the LDL-C level to less than 1.4mmol/l might help decreasing the ISR rate.