Affiliations: [a]
Department of Epidemiology and Preventive Medicine, School of Public Health, Sackler Faculty of Medicine, Tel Aviv University, Tel-Aviv, Israel
| [b]
The Israel Center for Disease Control, Israel Ministry of Health, Israel
| [c]
School of Public Health, Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel
| [d]
Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel-Aviv, Israel
Correspondence:
[*]
Correspondence to: Prof. David Tanne, Department of Neurology and Department of Epidemiology and Preventive Medicine, Sackler Faculty of Medicine, Tel-Aviv University, Tet-Aviv. Israel. E-mail: tanne@post.tau.ac.il.
Note: [1] This study was performed in partial fulfilment of the requirements for a Ph.D. degree for Miri Lutski, Sackler Faculty of Medicine, Tel Aviv University, Israel.
Note: [2] These authors contributed equally to this work.
Abstract: Background: Lipid levels are associated with an increased risk of cardiovascular disease. Objective: We investigated the association between plasma lipids, apolipoproteins levels, apolipoprotein B/low-density lipoprotein cholesterol (Apo-B/LDL-C), and Apo-B/Apo-A ratios and rate of cognitive decline two decades later in men with coronary heart disease (CHD). Methods: A subset of 337 men (mean age at baseline 56.6±6.4 years) who previously participated in the Bezafibrate Infarction Prevention (BIP) trial (1990–1997) underwent cognitive evaluations 15±3 years (T1) and 19.9±1 years after baseline (T2) as part of the BIP Neurocognitive study. Lipid and apolipoprotein fractions were measured at baseline. Cognitive function for memory, executive function, visual spatial, attention domains, and composite score were assessed using the NeuroTrax Computerized Battery at T1 and T2 evaluations. Linear mixed models were used to assess change in cognitive function between the two cognitive evaluations. Results: Controlling for confounders, the decline in composite cognitive score (β= –0.161±0.06; p = 0.013) as well as in memory (β= –0.269±0.10; p = 0.009) and visual spatial function (β= –0.304±0.12; p = 0.010) was greater among patients in the upper (≥105 mg/dL) Apo-B tertile as compared to counterparts with < 105 mg/dL. The decline in the composite cognitive score (β= –0.124±0.06; p = 0.043) was also greater among patients in the estimated LDL-C≥160 mg/dL group compared to counterparts with LDL-C<160 mg/dL. Upper tertile of Apo-B/LDL-C ratio (≥0.75) compared to the lower tertiles was significantly associated with change in memory score (β= –0.210±0.10; p = 0.041). Conclusion: Our findings suggest that the plasma concentrations of Apo-B, LDL-C, and Apo-B/LDL-C ratio are potential predictors of accelerated late-life cognitive decline among men with CHD.
