Clinical significance of lipoprotein(a) in carotid plaque types and ischemic stroke in the elderly

Abstract

Background: The relationship between lipoprotein(a) (Lp(a)) and ischemic stroke is still controversial in the elderly. The purpose of the present paper was to evaluate the significance of Lp(a) in the development of extracranial carotid lesions and ischemic stroke. Methods: A total of 371 elderly subjects, studied with carotid ultrasonography (US) and brain computed tomography (CT), was stratified into two groups according to serum Lp(a) levels: the normal Lp(a) and high Lp(a) (>40 mg/dL) groups. Carotid plaques were divided into three types based on the US echogenicity: hypoechoic, hyperechoic, and heterogeneous plaques. Low‐density areas (LDA) on brain CT images were classified into three groups depending on their distribution: basal ganglionic, cortical and only leuko‐araiosis types. Results: The incidence of bilateral carotid lesions and the ratios of hypoechoic and heterogeneous plaques were significantly higher in the high Lp(a) group than in the normal Lp(a) group. Both the mean height and length of plaque were also greater in the high Lp(a) group. Mean Lp(a) levels were significantly elevated in cases with hypoechoic and heterogeneous types, compared to the cases without lesions. Higher mean Lp(a) levels were seen in cases with any kind of LDA than in normal subjects on CT, but there was no significant difference in the incidence of each LDA between the two groups. Conclusions These findings indicate that serum Lp(a) is strongly related to carotid lesions, especially hypoechoic and heterogeneous plaque types, in Japanese elderly patients. This suggests that Lp(a) could promote the formation of lipid‐rich atheromatous plaque with intraplaque hemorrhage or superimposed thrombi. Serum Lp(a) also seemed to be a risk for all types of LDA.

Dual inverse effects of lipoprotein(a) on the dementia process in Japanese late‐onset Alzheimer's disease

“…In our study, the high Lp(a) level group (40 mg/dL or more) was separated from the normal group since the frequency of Lp(a) level =40 mg/dL was significantly different between the AD and control groups, and the Lp(a) level of 40 mg/dL was considered to be a threshold. Uniformly accepted standards of Lp(a) levels are lacking, but an apparent threshold for coronary risk is also recognized at Lp(a) levels of 30–40 mg/dL, and such levels were observed in approximately 20% of subjects studied 6,13 . Serum Lp(a) concentration depends on apoprotein(a) size polymorphism and is constant throughout life within an individual 6,7 …”

“…Uniformly accepted standards of Lp(a) levels are lacking, but an apparent threshold for coronary risk is also recognized at Lp(a) levels of 30-40 mg/dL, and such levels were observed in approximately 20% of subjects studied. 6,13 Serum Lp(a) concentration depends on apoprotein(a) size polymorphism and is constant throughout life within an individual. 6,7 A relationship between ApoE and the Lp(a) metabolisms has been described, 16 while a recent study 17 showed no independent effect of ApoE polymorphism on the Lp(a) level.…”

“…1,4,6,7,18 Solfrizzi et al 10 also suggested vascular factors involved in high Lp(a) levels with cerebrovascular disease in the development of cognitive impairment, but cerebrovascular disease was not verified. Since Lp(a) is a risk for cerebrovascular disease, 13 and correlates with the occurrence of VaD, 10 a high Lp(a) level appears to promote white-matter lesions due to ischemia in addition to ischemic cerebrovascular disease, resulting in cognitive decline. In our study, a high frequency of severe periventricular lucency was shown in the AD group with high Lp(a) level, as well as in the VaD group.…”

“…These examinations were performed at a commercial laboratory (SRL Laboratory, Tokyo, Japan), where the comparison of Lp(a) levels between the latex immunoassay and enzyme‐linked immunosorbent assay methods shows an excellent correlation coefficient (r, 0.997; y = 1.01X‐0.14; n, 79). Serum Lp(a) level was divided into two groups on the basis of the level of Japanese healthy controls as 30–40 mg/dL 6,13 . Setting three Lp(a) levels of 30, 35, and 40 mg/dL to determine a cut‐off point (Table 2), Lp(a) levels of 40 mg/dL could discriminate the frequency of high Lp(a) level between the AD and control groups.…”

“…Serum Lp(a) level was divided into two groups on the basis of the level of Japanese healthy controls as 30-40 mg/dL. 6,13 Setting three Lp(a) levels of 30, 35, and 40 mg/dL to determine a cut-off point ( Table 2), Lp(a) levels of 40 mg/dL could discriminate the frequency of high Lp(a) level between the AD and control groups. Therefore, normal Lp(a) was defined as less than 40 mg/dL, while high Lp(a) was defined as 40 mg/dL or more.…”