High- Density Lipoprotein and Cardiovascular Risk. Low serum levels of high- density lipoprotein (HDL) are commonly encountered in patients with coronary artery disease (CAD). An example of this type of patient is a 4. The family history was significant for his father, who died of a myocardial infarction (MI) at age 4. Exercise and High-Density Lipoprotein: The Effects on CHD Risk 13 cells. 18 An elevated CETP level causes a decrease in HDL, but could still be anti-atherogenic by. Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management. The patient underwent percutaneous transluminal angioplasty with stenting but developed in- stent restenosis. He underwent cutting balloon angioplasty and brachytherapy and was asymptomatic for approximately 6 months. The stent then developed a high- grade occlusion with recurrence of angina, and the patient required single- vessel bypass surgery. The patient’s baseline serum lipid profile revealed low- density lipoprotein (LDL) 1. L, HDL 2. 7 mg/d. ![]() ![]() ![]() ![]() 691 Exercise Intensity: Its Effect on the High-Density Lipoprotein Profile Ten-i Spate-Douglas, MHS, RN, Randall E. Keyser, PhD ABSTRACT.L, and triglycerides 9. L. His lipoprotein(a), C- reactive protein, and homocysteine levels were normal. He was not hypertensive, had no impairment of glycemic control, and did not smoke. ![]() With a combination of simvastatin 4. Niaspan; Kos Pharmaceuticals) 1. LDL 7. 8 mg/d. L, HDL 4. L, and triglycerides 6. L. Follow- up stress testing demonstrated normal myocardial perfusion, and the patient has been asymptomatic for 2 years. HDL as an Independent Risk Factor for CADWith few exceptions, low HDL is an independent risk factor for CAD in case- control and prospective observational studies. In contrast, high HDL levels are associated with longevity and are protective against the development of atherosclerotic disease. Abstract—High density lipoprotein (HDL) cholesterol is an important risk factor for coronary heart disease, and HDL exerts various. High-density lipoprotein. High-density lipoproteins (HDL) are one of the five major groups of lipoproteins. Lipoproteins are complex particles composed. PRE-BETA HIGH DENSITY LIPOPROTEIN Kunrtak27 e et al. 92.5 66.2 45.0 31.0 B Figure 3. Extended plasmin digestion of pre-beta- and alpha-migrating high density llpoproteln. High-density lipoprotein eller HDL . High-density lipoprotein (HDL) is a complex mixture of lipoproteins that is associated with many minor proteins and lipids that influence. High-density lipoprotein is one of the five major fat and protein particles (lipoproteins) whose role it is to enable blood fats (lipids), such as cholesterol. In the Framingham Study, risk for CAD increases sharply as HDL levels fall progressively below 4. L. 1 In the Quebec Cardiovascular Study, for every 1. HDL, risk for CAD increased 1. Many clinicians believe that low HDL is associated with increased CAD risk because it is a marker for hypertriglyceridemia and elevated remnant particle concentrations. The Prospective Cardiovascular M. In one study, low HDL occurred in approximately 6. CAD. 5 Low HDL is associated with increased risk for MI, stroke, sudden death, restenosis after angioplasty, and severe premature atherosclerotic disease in the proximal left main coronary artery. In one autopsy series, the average total cholesterol: HDL ratio and HDL level in men who died suddenly during exertion were 8. L, respectively. 1. Antiatherogenic Effects of HDLHDLs are a heterogeneous class of lipoproteins with diverse functions and antiatherogenic effects. The most important antiatherogenic function of HDL is believed to be its ability to drive reverse cholesterol transport, a series of reactions by which HDL is able to interact with cells in the systemic vasculature and deliver excess cholesterol back to the liver for disposal as bile salts. There is considerable controversy about whether one HDL subfraction is more antiatherogenic than others. At the present time, the preponderance of evidence favors increasing total HDL mass, rather than any one subfraction of this lipoprotein. HDL reverses endothelial cell dysfunction, stimulates prostacyclin production (which is both vasodilatory and antithrombotic), inhibits endothelial cell apoptosis, decreases platelet aggregability, and inhibits LDL oxidation, among other functions. The intravenous infusion of HDL in animal models prevents atherogenesis and can stimulate some degree of plaque resorption. In one study, the weekly injection of a bioengineered HDL into patients with CAD resulted in a 4. HDL Targets. The National Cholesterol Education Program (NCEP) defines an HDL level < 4. L as a categorical risk factor for CAD. Virtually all cardiologists can point to patients in their practices whose only risk factor for CAD is a low HDL. Despite this, relatively few physicians target it for therapeutic elevation. There are 3 important reasons for this. First, raising HDL can be challenging and frequently requires multiple medications and significant lifestyle modification to be successful. Second, because there are currently no pharmacological interventions available that specifically raise HDL and leave other lipid levels unchanged, it is unclear to many physicians whether raising HDL reduces risk for cardiovascular morbidity and mortality. Third, although the NCEP clearly articulated goals for LDL and non- HDL cholesterol based on global cardiovascular risk evaluation, similar targets for HDL are as yet undefined. In an effort to address some of this uncertainty, guidance in high- risk groups has been offered. The American Diabetes Association recognizes that an HDL level . Statin Therapy. Statins typically raise HDL 6% to 1. A- I expression and weakly inhibiting cholesteryl ester transfer protein (CETP). The Air Force/Texas Coronary Atherosclerosis Prevention Study was a primary prevention trial that compared lovastatin to placebo in men and women with “average” risk for CAD (mean LDL 1. L; HDL 3. 7 mg/d. L). The patients whose baseline HDL level was < 4. L experienced a 3- fold (4. CAD- related events compared with patients whose HDL level was . This observation may be partly explained by the fact that many of the pleiotropic effects exerted by statins (reversing endothelial cell dysfunction, augmenting nitric oxide and prostacyclin production, decreasing inflammation) are also mediated by HDL. Statins should be the drug of choice in patients with a combination of low HDL and an LDL level above NCEP targets. Fibrate Therapy. Fibric acid derivatives are beneficial to patients with a combination of hypertriglyceridemia and low HDL. Fibrates stimulate HDL biosynthesis 6% to 2. A- I expression and lipoprotein lipase activity. The activation of lipoprotein lipase allows for the catabolism of very- low- density lipoprotein and chylomicra. As these large lipoproteins are hydrolyzed, they release surface coat constituents that can be used to form HDL in serum. Patients with insulin resistance states are particularly prone to low lipoprotein lipase activity. The Helsinki Heart Study. Veterans Affairs High- Density Lipoprotein Intervention Trial (VA- HIT)2. HDL. VA- HIT also demonstrated: (1) a reduction in cardiovascular morbidity and mortality occurred, independent of changes in LDL, and (2) the patients with the lowest HDL derived the greatest benefit. Fibrates should be first- line therapy in patients with hypertriglyceridemia, LDL < 1. L, and low HDL (Figure). These patients should also be evaluated for metabolic syndrome and type 2 diabetes mellitus. Relieving insulin resistance with weight loss, exercise, and thiazolidinedione (pioglitazone or rosiglitazone) therapy help to raise serum HDL. Standard dosing regimens for fibrates include: (1) gemfibrozil 6. Fibrate therapy can be associated with a rise in LDL because these drugs stimulate the conversion of very- low- density lipoprotein to LDL in serum. If the LDL rises above NCEP targets, then the addition of a statin or ezetimibe to the fibrate may be indicated. Gemfibrozil can block the glucuronidation of statins and lead to increased risk for hepatic and skeletal muscle toxicity. Fenofibrate is a safer choice when considering combination therapy because it does not interfere with statin metabolism. No outcome trials using the combination of a fibrate and statin have yet been completed. Fibrates can be used to raise HDL in the absence of hypertriglyceridemia. Treatment scheme for patients with low serum levels of HDL. TZD indicates thiazolidinedione. Niacin. Niacin raises serum HDL up to 3. In the Coronary Drug Project, crystalline niacin (3. CAD reduced the risk for stroke and nonfatal MI by 2. An outcomes- based primary prevention trial with niacin monotherapy is not yet available. The combination of niacin and a statin can markedly decrease CAD event rates and rates of coronary plaque progression. Niacin as adjuvant therapy should be used as tolerated (crystalline niacin up to 3. Niaspan . HDL is modestly increased by smoking cessation (up to 2. L per 3 kg), and aerobic exercise. Moderate alcohol ingestion can significantly raise serum HDL and is associated with reduced risk for acute cardiovascular events. Obese patients with insulin resistance may particularly benefit from weight loss and aerobic exercise when trying to raise HDL. Conclusion. There is clear, clinical trial–based support for treating patients with low HDL, especially in the presence of CAD. In the primary and secondary prevention settings, the statin trials demonstrate significant risk reduction when treating patients with low HDL and average or elevated LDL levels (. The fibrate trials support treating patients with hypertriglyceridemia and low HDL. Patients with low HDL, normal triglycerides, and low LDL (< 1. L) constitute a somewhat equivocal group. There are no clinical trial data to guide clinical decision- making. Additional investigation will have to be done to determine which LDL thresholds constitute high risk for CAD at specific levels of HDL. If the patient has no risk factors other than a low HDL but has a strong family history for premature CAD, then consideration should be given to lifestyle modification and treatment with a statin and niacin as indicated (Figure). In other cases, when a patient presents with low HDL and has other risk factors but no evidence for CAD or a CAD risk equivalent, then calculation of the Framingham risk score is recommended. If the 1. 0- year risk exceeds 2. CAD and should be treated in conjunction with lifestyle modification. Exciting new means of raising HDL and treating CAD in patients with low HDL are in development. CETP inhibitors, a vaccine against CETP, and bioengineered HDLs will be entering clinical trials. These studies will help to further clarify the role of HDL in the treatment and prevention of atherosclerotic disease. In the meantime, the treatment of patients with low HDL with currently available antilipidemic medication provides substantial reductions in risk for, and progression of, cardiovascular disease.
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