Triacylglycerol-rich lipoproteins and atherosclerosis – where is the link?

2003 ◽  
Vol 31 (5) ◽  
pp. 1080-1084 ◽  
Author(s):  
P. Cullen
Keyword(s):  
Arterial Wall ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Substantial Evidence ◽  
Epidemiological Evidence ◽  
Procam Study

The link between raised levels of LDL (low-density lipoprotein) cholesterol in the blood and atherosclerosis is incontrovertible. The situation with regard to TRLs (triacylglycerol-rich lipoproteins) is not as clear. Nevertheless, there is substantial evidence that TRLs may in some cases be just as atherogenic as triacylglycerol-poor LDL. This review focuses on three aspects of the link between TRLs and atherosclerosis: (i) the epidemiological evidence for an association between raised levels of TRLs and atherosclerosis, with particular reference to the results of the PROCAM study; (ii) the possible pathophysiological contribution of TRL to atherogenesis at the level of the arterial wall; and (iii) the case for specific lowering of triacylglycerol levels to prevent atherosclerosis.

scholarly journals Persistent arterial wall inflammation in patients with elevated lipoprotein(a) despite strong low-density lipoprotein cholesterol reduction by proprotein convertase subtilisin/kexin type 9 antibody treatment

2018 ◽  
Vol 40 (33) ◽  
pp. 2775-2781 ◽  
Author(s):  
Lotte C A Stiekema ◽  
Erik S G Stroes ◽  
Simone L Verweij ◽  
Helina Kassahun ◽  
Lisa Chen ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Arterial Wall ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Controlled Study ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A

AbstractAimsSubjects with lipoprotein(a) [Lp(a)] elevation have increased arterial wall inflammation and cardiovascular risk. In patients at increased cardiovascular risk, arterial wall inflammation is reduced following lipid-lowering therapy by statin treatment or lipoprotein apheresis. However, it is unknown whether lipid-lowering treatment in elevated Lp(a) subjects alters arterial wall inflammation. We evaluated whether evolocumab, which lowers both low-density lipoprotein cholesterol (LDL-C) and Lp(a), attenuates arterial wall inflammation in patients with elevated Lp(a).Methods and resultsIn this multicentre, randomized, double-blind, placebo-controlled study, 129 patients {median [interquartile range (IQR)]: age 60.0 [54.0–67.0] years, Lp(a) 200.0 [155.5–301.5] nmol/L [80.0 (62.5–121.0) mg/dL]; mean [standard deviation (SD)] LDL-C 3.7 [1.0] mmol/L [144.0 (39.7) mg/dL]; National Cholesterol Education Program high risk, 25.6%} were randomized to monthly subcutaneous evolocumab 420 mg or placebo. Compared with placebo, evolocumab reduced LDL-C by 60.7% [95% confidence interval (CI) 65.8–55.5] and Lp(a) by 13.9% (95% CI 19.3–8.5). Among evolocumab-treated patients, the Week 16 mean (SD) LDL-C level was 1.6 (0.7) mmol/L [60.1 (28.1) mg/dL], and the median (IQR) Lp(a) level was 188.0 (140.0–268.0) nmol/L [75.2 (56.0–107.2) mg/dL]. Arterial wall inflammation [most diseased segment target-to-background ratio (MDS TBR)] in the index vessel (left carotid, right carotid, or thoracic aorta) was assessed by 18F-fluoro-deoxyglucose positron-emission tomography/computed tomography. Week 16 index vessel MDS TBR was not significantly altered with evolocumab (−8.3%) vs. placebo (−5.3%) [treatment difference −3.0% (95% CI −7.4% to 1.4%); P = 0.18].ConclusionEvolocumab treatment in patients with median baseline Lp(a) 200.0 nmol/L led to a large reduction in LDL-C and a small reduction in Lp(a), resulting in persistent elevated Lp(a) levels. The latter may have contributed to the unaltered arterial wall inflammation.

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