Poor lipid control is a risk factor for cardiovascular diseases and diabetes complications. Frequently, however, patients with these diseases do not achieve blood lipid levels recommended by current standards of care. A retrospective study of 67,244 members eligible for disease management (DM) was initiated to evaluate the ability of interventions to promote improvement in low-density lipoprote...

Reducing low-density lipoprotein cholesterol (LDL-C) to target ≤1.81 mmol/L is a common therapeutic goal after acute coronary syndrome (ACS). This study aimed to examine the factors associated with reaching or not this LDL-C target after 1 year of optimal statin therapy postpercutaneous coronary intervention (PCI). This was a retrospective study of 633 consecutive prospectively enrolled patient...

The mechanism(s) of inhibition of endothelium-dependent relaxation (EDR) by oxidized low-density lipoprotein (Ox-LDL) was examined in isolated porcine coronary arteries and rabbit aortas. Incubation with Ox-LDL but not native LDL caused the inhibition of thrombin- or acetylcholine-induced EDR, whereas A23187-induced EDR was preserved after incubation with Ox-LDL. Lysophosphatidylcholine (lysoPC...

Antioxidants exert contrasting effect on low density lipoprotein (LDL) oxidation catalysed by metals, acting as pro-oxidants under select in vitro conditions. Through our study on the effect of coffee on LDL oxidation, we identified the parameters governing this phenomenon, contributing to the comprehension of its mechanism and discovering significant implications for correct alimentary recomme...

OBJECTIVES Previous research suggests that LDL particle number (LDL-P) may be a better tool than LDL cholesterol (LDL-C) to guide LDL-lowering therapy. Using real-world data, this study has two objectives: [1] to determine the incidence of CHD across LDL-P thresholds; and [2] to compare CHD/stroke events among patients achieving comparably low LDL-P or LDL-C levels. METHODS A claims analysis ...

Aims Migration of monocytes into the arterial wall contributes to arterial inflammation and atherosclerosis progression. Since elevated low-density lipoprotein cholesterol (LDL-C) levels have been associated with activation of plasma monocytes, intensive LDL-C lowering may reverse these pro-inflammatory changes. Using proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies (...

BACKGROUND Cardiovascular disease (CVD) is the leading cause of death in Europe and increased low-density lipoprotein cholesterol (LDL-C) is a major contributor to CVD risk. Extensive evidence from clinical studies of statins has demonstrated a linear relationship between LDL-C levels and CVD risk. It has been proposed that lower LDL-C levels than those currently recommended may provide additio...

Recent clinical trials in patients with coronary artery disease (CAD) provide evidence that low-density lipoprotein cholesterol (LDL-C) levels should be lowered even further to prevent recurrent CAD. However, despite more aggressive interventions for lowering LDL-C levels, the majority of CAD events go undeterred, perhaps related to the fact that intervention was not started earlier in life or ...

he pivotal role of low-density lipoprotein cholesterol LDL-C) in the pathogenesis of atherosclerosis and its schemic complications are well established. Epidemiologic tudies demonstrate a linear relationship between levels of DL-C and the prospective risk of cardiovascular events 1). In animal models, the administration of cholesterol ncreases levels of LDL-C and promotes the formation of esion...