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Stroke
Published in Charles Theisler, Adjuvant Medical Care, 2023
Reducing LDL helps to lower the risk of recurrent stroke. In a French study, reducing LDL to a mean of 66 mg/dL was associated with a 26% risk reduction for the composite endpoint of ischemic stroke, MI, new symptoms requiring urgent coronary or carotid revascularization, and vascular death.14
Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Total cholesterol is the total amount of cholesterol in the bloodstream. Cholesterol, while required in cell membrane formation, healthy skin, normal digestion, and steroid hormones production, can also be extremely harmful. The “good” form is also called high-density lipoprotein (HDL), and high levels of HDL protects against cardiovascular disorders such as myocardial infarction (MI) and stroke. The HDL type carries cholesterol back to the liver. Ranges of HDL should be 40 mg/dL or higher. The “bad” form is also called low-density lipoprotein, and is related to increased risks for coronary heart disease, peripheral artery disease, and stroke. Excessive LDL in the plasma slowly forms plaques that may block blood flow and form clots. If this occurs in the blood vessels near the heart, it may result in an MI. Ideally, the level of LDL should be 100 mg/dL or lower. Control of LDL in the blood cells is mostly by the liver and intestines.
Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Low density lipoproteins (LDL): These particles are derived from VLDL and IDL particles and they are even further enriched in cholesterol. LDL carries the majority of the cholesterol that is in the circulation. An abundance of LDL particles is seen in association with hypertriglyceridemia, low HDL levels, obesity, type 2 diabetes, and infectious and inflammatory states (112). LDL is also known as ‘bad’ cholesterol because it is associated with progression of atherosclerosis.
Evinacumab for the treatment of homozygous familial hypercholesterolemia
Published in Expert Review of Clinical Pharmacology, 2022
Yanli Gao, Baoqi Zhang, Junyi Yang
NCT02265952 was an open-label, phase 2, proof-of-concept study where nine adult patients with HoFH were enrolled [45–47]. All patients were required to be on stable, aggressive lipid-lowering therapy for at least 4 weeks (including statins, fibrates, ezetimibe, lomitapide, or PCSK9 inhibitors), and to have not undergone lipid apheresis within 4 weeks before the screening visit. The mean baseline LDL-C level was 376.0 mg /dL. Patients received evinacumab 250 mg SC at baseline and then a single dose 15 mg/kg IV 2 weeks later. The primary end point was the mean change in LDL-C level from baseline to week 4. After evinacumab treatment, LDL-C level decreased by 49% at week 4, with an absolute decrease from baseline of 157 mg/dL. In addition, Apo B decreased by 46%, TG by 47%, and HDL-C by 36%. All of the nine patients reported at least one adverse event, but no event led to treatment discontinuation. This preliminary study found that evinacumab reduced LDL-C in patients with HoFH.
The role of PCSK9 in inflammation, immunity, and autoimmune diseases
Published in Expert Review of Clinical Immunology, 2022
Lowering of LDL levels to decrease the risk of CVD and atherosclerosis through medication is widely used and plays a role in the age-matched decrease in CVD that has occurred during the last decades. Statins were a clear step forward, and now several new versions of this drug category are used. PCSK9 inhibition represents another principle to lower LDL and is now mostly complementary, since statins remain the first in line treatment. The history of PCSK9 and its inhibition is very interesting also from a more general point of view, with the combination of elegant genetic studies, with experiments. The presence of different mutations, leading to both high and low LDL levels is striking, and its role from an evolutionary point of view should be studied further. In my opinion, it indicates that LDL is far more than a transporter of cholesterol, for example, it may be of importance in the body´s countermeasures against infections, which historically have been a huge problem and major cause of morbidity and mortality and still is in parts of the world. Genotypes causing high LDL could have been beneficial at some historical stages.
Red wine consumption mitigates the cognitive impairments in low-density lipoprotein receptor knockout (LDLr−/−) mice
Published in Nutritional Neuroscience, 2021
Gabriela Cristina De Paula, Jade de Oliveira, Daiane Fátima Engel, Samantha Cristiane Lopes, Eduardo Luiz Gasnhar Moreira, Claudia Pinto Figueiredo, Rui Daniel Prediger, Andreza Fabro de Bem
Familial hypercholesterolemia is linked to genetic abnormalities that affect low-density lipoprotein receptor (LDLr) function and implies a hypocatabolism of lipoproteins, mainly LDL particles, and leading to high levels of plasma cholesterol since childhood [11]. LDL particles are not able to cross the intact blood–brain barrier (BBB), however some evidence have linked BBB disruption with hypercholesterolemia [12] and other metabolic disorders [13,14]. Thus, one plausible hypothesis to explain the effect of hypercholesterolemia in cognition is the endothelial dysfunction in the neurovascular unit (NVU). NVU is comprised of different cell types, including specialized vascular cells (endothelial cells and pericytes), glia (astrocytes, oligodendrocytes and microglia) and neurons that contribute to neurovascular coupling [15]. Through NVU, the endothelial cells together with the cellular junctions make up the BBB, working as a key homeostatic site of the central nervous system (CNS) [16]. Molecular changes in these cells, such as that caused by hypercholesterolemia, can lead to BBB disruption and to CNS impairment [16]. The neurovascular abnormalities contribute to neurodegeneration and cognitive decline, raising the vascular hypothesis for Alzheimer's disease [17]. According to this hypothesis, loss of BBB integrity leads to an oxidative-inflammatory cycle in the brain vasculature, initiating a neuroinflammation environment that results in disruption of Aβ peptide metabolism and neuronal dysfunction, supporting the onset of Alzheimer's disease [18].