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目的 :探讨脂蛋白脂酶 (LPL)活性与早发冠心病临床表型的关系。方法 :测定 10 6例早发冠心病患者 (病例组 )肝素化后血浆LPL活性 ,血脂参数和血浆C反应蛋白 (CRP)浓度 ,与 5 4例非冠心病者 (对照组 )进行比较 ;病例组按照患者临床表型分组 ,分析LPL活性特点。结果 :病例组肝素化后血浆LPL活性低于对照组 [(2 6 18±3 90 )mmol·L-1·min-1vs (35 2 7± 5 96 )mmol·L-1·min-1,P <0 0 5 ],急性心肌梗死组LPL活性明显低于不稳定性心绞痛和稳定性心绞痛组。双因素相关分析 ,LPL与CRP呈显著负相关 (r=- 0 2 34,P <0 0 1) ;多因素回归分析 ,低LPL活性可能是早发冠心病独立的危险因子 (OR =6 32 ,95 %CI1 96 - 18 2 4 ,P <0 0 5 )。结论 :低LPL活性是早发冠心病独立的危险因子 ,LPL活性与早发冠心病临床表型相关联。
Objective: To investigate the relationship between the activity of lipoprotein lipase (LPL) and the clinical phenotype of premature coronary heart disease. Methods: Plasma LPL activity, lipid parameters and plasma C-reactive protein (CRP) concentrations were determined in 106 patients with premature coronary heart disease (case group), compared with 54 non-coronary heart disease patients (control group) Groups were grouped according to the patient’s clinical phenotype and analyzed for LPL activity characteristics. Results: The plasma LPL activity of heparinized group was lower than that of the control group [(2 6 18 ± 3 90) mmol·L -1 min -1 vs 35 2 7 ± 5 96 mmol·L -1 min -1, P <0 05], LPL activity was significantly lower in patients with acute myocardial infarction than in patients with unstable angina and stable angina. Two-factor correlation analysis showed that there was a significant negative correlation between LPL and CRP (r = -0.234, P <0.01). Multivariate regression analysis showed that low LPL activity might be an independent risk factor for premature coronary heart disease (OR = 6 32 , 95% CI1 96 - 18 2 4, P <0 0 5). Conclusion: Low LPL activity is an independent risk factor for premature coronary heart disease. LPL activity is associated with the clinical phenotype of premature coronary heart disease.