Abstract：Objective To investigate the changes of serum lipoprotein(a)(Lpa) in patients with coronary heart disease and cerebral infarction, and to provide a basis for the prevention and treatment of cardiovascular and cerebrovascular diseases. Methods The Lp(a) was detected by latex agglutination turbidimetry in coronary heart disease patients and cerebral infarction patients,and the hypertension and diabetes patients of their high-risk groups were also observed. Healthy persons served as control group. Results (1)Compared with control group, Lp(a) abnormal proportions were significantly higher in coronary heart disease and cerebral infarction patients groups, also in the hypertension and diabetes patient groups(P<0.05).In the patient groups, Lp(a) serum levels were also obviously elevated, but only in coronary heart disease,cerebral infarction and diabetes patients were statistically significantly higher (P<0.05). (2)For age group, only in coronary heart disease group, Lp(a) serum level was significantly higher in patients ≥60 age than that in patients <60 age (P<0.05). Conclusions Lipoprotein(a) levels are closely related to the occurrence of coronary heart disease and cerebral infarction. The lipoprotein(a) may be an independent risk factor for cardiovascular and cerebrovascular diseases development.
Greif M, Arnoldt T, Ziegler F V, et al. Lipoprotein(a) is independently correlated with coronary calcification [J]. Eur J Inter Med, 2013, 24(1): 75-79.
[2]
Smolders B, Lemmens R, Thijs V. Comments, Opinions and Reviews on Lipoprotein(a) and Stroke [J]. Stroke, 2007, 38(7): 1959-1966.
[3]
Koschinsky M L. Novel insights into Lp (a) physiology and pathogenicity:more question than answers [J]. Cardiovasc Hematol Disord Drug Targets, 2006, 6(4): 267-278.
[2]
Smolders B, Lemmens R, Thijs V. Comments, Opinions and Reviews on Lipoprotein(a) and Stroke [J]. Stroke, 2007, 38(7): 1959-1966.
[3]
Koschinsky M L. Novel insights into Lp (a) physiology and pathogenicity:more question than answers [J]. Cardiovasc Hematol Disord Drug Targets, 2006, 6(4): 267-278.
[4]
Erqou S, Kaptoge S, Perry P, et al. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality [J]. JAMA, 2009, 302(4): 412-423.
[4]
Erqou S, Kaptoge S, Perry P, et al. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality [J]. JAMA, 2009, 302(4): 412-423.
[5]
Brites F D, Fernandez K M, Verona J, et al. Chronic renal failure in diabetic patients increase lipid risk factors for atherosclerosis[J]. Diabetes Res Clin Pract, 2007, 75(1): 35-34.
[5]
Brites F D, Fernandez K M, Verona J, et al. Chronic renal failure in diabetic patients increase lipid risk factors for atherosclerosis[J]. Diabetes Res Clin Pract, 2007, 75(1): 35-34.
[6]
Carey V J, Bishop L, Laranjo N, et al. Contribution of high plasma triglycerides and low high-density lipoprotein cholesterol to residual risk of coronary heart disease after establishment of low-density lipoprotein cholesterol control [J]. Am J Cardiol, 2010, 106(6): 757-763.
[6]
Carey V J, Bishop L, Laranjo N, et al. Contribution of high plasma triglycerides and low high-density lipoprotein cholesterol to residual risk of coronary heart disease after establishment of low-density lipoprotein cholesterol control [J]. Am J Cardiol, 2010, 106(6): 757-763.
[7]
Vogt A, Kassner U, Hostalek U, et al. Prolonged-release nicotinic acid for the management of dyslipidemia: an update including results from the NAUTILUS sdudy [J]. 2007, 3(4): 467-479.
[7]
Vogt A, Kassner U, Hostalek U, et al. Prolonged-release nicotinic acid for the management of dyslipidemia: an update including results from the NAUTILUS sdudy [J]. 2007, 3(4): 467-479.
2013, Vol. 24 
