Atherosclerosis niacin

In general, niacin reduces LDL cholesterol from 5% to 25%, reduces triglycerides by 20% to 50%, and increases HDL cholesterol by 15% to 35% (Table 9-8). Niacin has been shown to reduce CHD events and total mortality31 as well as the progression of atherosclerosis when combined with a statin.31... 

It is used for pellagra (avitaminosis PP), atherosclerosis, liver disease, stomach and duodenum ulcers, and prolonged, nonhealing wounds and ulcers. Synonyms of this drag are niconacid, pemivit, enzycol, niacin, and others. 

Rare genetic disorders, including Tangier disease and LCAT (lecithin cholesterol acyltransferase) deficiency, are associated with extremely low levels of HDL. Familial hypoalphalipoproteinemia is a more common disorder with levels of HDL cholesterol usually below 35 mg/dL in men and 45 mg/dL in women. These patients tend to have premature atherosclerosis, and the low HDL may be the only identified risk factor. Management should include special attention to avoidance or treatment of other risk factors. Niacin increases HDL in many of these patients. Reductase inhibitors and fibric acid derivatives exert lesser effects. 

Luria MH. Atherosclerosis the importance of HDL cholesterol and prostacyclin a role for niacin therapy. Med Hypotheses 1990 32(l) 21-8. 

Primary increases of VLDL probably reflect a number of genetic determinants and are worsened by factors that increase the rate of VLDL secretion from liver, ie, obesity, alcohol, diabetes, and estrogens. A major indication for treatment is the presence of atherosclerosis in the patient or the patient s family. Treatment includes weight reduction, restriction of all types of dietary fat, and avoidance of alcohol. Fibrates or niacin usually produce further reduction in triglyceride levels if dietary measures are not sufficient. Marine omega fatty acids may also be of value. 

In kindreds with this disorder, individuals may have elevated levels of VLDL, LDL, or both, and the pattern may change with time. Familial combined hyperlipoproteinemia involves an approximate doubling in VLDL secretion. It seems to be transmitted as a semidominant trait. Triglycerides can be increased by the factors noted above. Elevations of cholesterol and triglycerides are generally moderate, and xanthomas are usually absent. Drug treatment is warranted because the risk of coronary atherosclerosis is increased and diet alone does not normalize lipid levels. A reductase inhibitor or ezetimibe in combination with niacin is usually required to treat these patients. 

When used in conjunction with niacin or niceritol, Sikorski (4) determined that the benzyl amine cholesteryl ester transfer protein inhibiting agent, (III), was effective in treating atherosclerosis. 

Capuzzi DM, Morgan JM, Brusco OA Jr., and Intenzo CM (2000) Niacin dosing relationship to benefits and adverse effects. Current Atherosclerosis Report 2, 64-71. 

Nicotinic acid has been estcrified to prolong its hypolipidemic effect. Pentaerythritol tetranicotinate has been more effective experimentally than niacin in reducing chnlesternl levels in rabbits. Sorbitnl and niyo-innsitnl hexanicotinate polyesters have been used in the treatment nf patients with atherosclerosis obliterans. 

Blankenhorn DH, Nessim SA, Johnson RL, Sanmarco ME, Azen SP, Cashin-HemphiU L. Beneficial effects of combined colestipol-niacin therapy on coronary atherosclerosis and coronary venous bypass grafts. JAMA 1987 257 3233-40. 

Vittone F, Chait A, Morse JS, Fish B, Brown BG, Zhao XQ (2007) Niacin plus simvastatin reduces coronary stenosis progression among patients with metabolic syndrome despite a modest increase in insulin resistance a subgroup analysis of the HDL-Atherosclerosis Treatment Study (HATS). J Clin Lipidol 1 203-210... 

All HMGRIs are approved for the treatment of primary hypercholesterolemia and familial combined hyperlipidemia (Fredrickson s type Ha and lib) (Table 30.2) In patients who have not responded to diet, exercise, and other non pharmacological methods (Table 30.6) (15,21). They may be used either alone or In combination with bile acid sequestrants, ezetimibe, or niacin. As previously mentioned, they should be administered at least 1 hour before or 4 to 6 hours after bile acid sequestrants when this combination Is desired. Fluvastatin, lovastatin, pravastatin, and simvastatin have been specifically Indicated to reduce the mortality of CHD and stroke. By reducing plasma LDL levels, these compounds slow the progression of atherosclerosis and reduce the risk of myocardial Infarction and other ramifications of vascular occlusion. Atorvastatin, rosuvastatin, and simvastatin have been shown to be effective In homozygous familial hyperlipidemia and are Indicated for this use. Additionally, atorvastatin, pravastatin, and simvastatin are Indicated for primary dysbetallpoprotelnemla (Fredrickson s type III) (Table 30.2). Finally, atorvastatin, pravastatin, rosuvastatin, and simvastatin are Indicated for the treatment of hypertriglyceridemia. 

Vinson, J.A. et al.. Beneficial effects of a novel IH636 grape seed proanthocyanidin extract and a niacin-bound chromium in a hamster atherosclerosis model. Mol. Cell Biochem., 240, 99, 2002. 

However, as a side-effect of the therapy, his patients suffered from a massive flush syndrome (harmless but mostly unpleasant reddening ofthe skin on the face, neck, chest and upper arm). For a better assessment, Hoffer himself took gram quantities of niacin over several months, and discovered to his surprise that this treatment had healed his serious inflammatory gum disease. Inspired by Rudolf Virchow s hypothesis, that atherosclerosis was an inflammatory process, which was associated with serum cholesterol, Rudolf Altschul (1901-1963), Hoffer s former histology teacher, demonstrated in his hypercholesterolemic rabbit model, that within a few days niacin brought cholesterol levels back to normal. This prompted corresponding studies by Hoffer in the psychiatric patients. 

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