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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.
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein
Published in Juan Carlos Jimenez, Samuel Eric Wilson, 50 Landmark Papers Every Vascular and Endovascular Surgeon Should Know, 2020
Juan Carlos Jimenez, Samuel Eric Wilson
Study Impact The JUPITER trial was one of the first to demonstrate the beneficial effects of statins on decreasing first cardiovascular events independent of lipid-lowering effects. The study was stopped early after only 1.9 years by its Independent Data and Safety Monitoring Board due to the significant improved outcomes noted in the rosuvastatin group. Patients in the treatment group demonstrated a relative risk reduction (RRR) for all vascular events of 44%, 48% RRR for stroke, and a 20% RRR for all-cause mortality. Relative risk for myocardial infarction was decreased by 54% and deep venous thrombosis/pulmonary embolism were reduced by 43%. This occurred in patients who all began the study with LDL levels <130 mg/dL. Important to vascular surgeons, rosuvastatin also resulted in a 46% RRR in arterial revascularization procedures in this trial.
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.
Antihyperlipidemic effect of tyrosol, a phenolic compound in streptozotocin-induced diabetic rats
Published in Toxicology Mechanisms and Methods, 2021
Ramasamy Chandramohan, Leelavinothan Pari
Cholesterol is a hydrophobic compound that is transported in circulation via endogenous transporters known as lipoproteins. Among many lipoprotein particles, LDL, HDL, and VLDL contain the body's highest-circulating cholesterol levels. LDL transports cholesterol from the liver to peripheral tissues and advances macrophages' foaming via uptake within the arterial wall. In particular, many studies have found LDL to be the most dangerous among the plasma lipids, and the oxidation of LDL leads to its increased penetration of arterial walls (Arcari et al. 2011). It is considered a key contributor to the initiation and progression of atherosclerosis development. This study observed tyrosol treatment revealed reduced LDL-C levels in the plasma of STZ-induced diabetic rats. This result could have been due to LDL oxidation inhibitory effects of tyrosol and agree with the results of a previous study by Covas et al. (2000), who reported that tyrosol from olive oil phenol able to bind to LDL in vitro and it was significantly associated with the delay in LDL oxidation.