Hypercholesterolemia: Zambon A

Poli A, Marangoni F, Paoletti R, Mannarino E, Lupattelli G, Notarbartolo A, Aureli P, Bernini F, Cicero A, Gaddi A, Catapano A, Cricelli C, Gattone M, Marrocco W, Porrini M, Stella R, Vanotti A, Volpe M, Volpe R, Cannella C, Pinto A, Del Toma E, La Vecchia C, Tavani A, Manzato E, Riccardi G, Sirtori C, Zambon A, Anonymous00119. · Nutrition Foundation of Italy, Italy. · Nutr Metab Cardiovasc Dis. · Pubmed #18258418 No free full text.

Abstract: The importance of non-pharmacological control of plasma cholesterol levels in the population is increasing, along with the number of subjects whose plasma lipid levels are non-optimal, or frankly elevated, according to international guidelines. In this context, a panel of experts, organized and coordinated by the Nutrition Foundation of Italy, has evaluated the nutritional and lifestyle interventions to be adopted in the control of plasma cholesterol levels (and specifically of LDL cholesterol levels). This Consensus document summarizes the view of the panel on this topic, with the aim to provide an updated support to clinicians and other health professionals involved in cardiovascular prevention.

Zambon A, Brown BG, Deeb SS, Brunzell JD. · Department of Medicine, University of Washington, Seattle, WA 98195-6426, USA. · J Intern Med. · Pubmed #16629853 No free full text.

Abstract: Increased low-density lipoprotein (LDL) and decreased high-density lipoprotein cholesterol (HDL-C) predict premature coronary artery disease, as do elevated levels of apolipoprotein B or reduced levels of apolipoprotein AI. Probands were studied of families with common genetic forms of dyslipidaemia to determine if apo B or apo AI define genetic groups and if apo B or apo AI levels relate to premature coronary artery disease risk. Elevated apo B was characteristic of familial hypercholesterolaemia, familial combined hyperlipidaemia (FCHL), and was seen in individuals with elevated Lp(a). Normal apo B levels were seen in familial hypertriglyceridaemia and in 'coronary artery disease with low-HDL cholesterol'. Apo AI levels tended to be low in FCHL and were decreased in 'coronary disease with low-HDL cholesterol'. In familial hypertriglyceraemia, even though HDL-C levels were low, normal apo AI and apo B levels were seen in the absence of premature coronary artery disease. Therefore, in genetic dyslipidaemias elevated apo B levels and reduced apo AI levels (or increased apo B/AI ratio) differ and predict premature coronary artery disease.

Zambon A, Brown BG, Hokanson JE, Motulsky AG, Brunzell JD. · Department of Medicine, University of Washington, Seattle, WA 98195-6426, USA. · J Intern Med. · Pubmed #16594908 No free full text.

Abstract: OBJECTIVE: Lipid-lowering therapy (LL-Rx) reduces coronary artery disease (CAD) but the response varies amongst individuals. We investigated the contribution of three genetic forms of dyslipidaemia characterized by elevated plasma apo B, familial hypercholesterolaemia (FH), familial combined hyperlipidaemia (FCHL), and elevated Lp(a), to the angiographic response with LL-Rx. METHODS AND RESULTS: Fifty-one men, with premature CAD and elevated plasma apo B, were selected in whom a genetic diagnosis was based on lipid phenotypes in relatives. Subjects received conventional (diet +/- colestipol) or intensive LL-Rx (niacin or lovastatin plus colestipol). Clinical parameters and CAD severity were measured before and after 2 years of treatment. Twenty-seven patients had FCHL, 12 FH and 12 elevated Lp(a). Regression of coronary stenosis was dependent on the effect of therapy (P < 0.001), genetic form of dyslipidaemia (P = 0.004) and the interaction between the two variables (P = 0.02). Significant regression of coronary stenosis occurred only in FCHL and Lp(a) (P = 0.03, vs. control groups); CAD progression was only slowed in FH. CONCLUSIONS: Three genetic forms of dyslipidaemia were associated with different angiographic outcomes during intensive LL-Rx. Different forms of dyslipidaemia therefore may require different lipid-lowering strategy. Patients with FH and buoyant LDL require more aggressive reduction of LDL cholesterol whilst those with either FCHL or elevated Lp(a) with dense LDL need LDL cholesterol reduction as well as therapies aimed at reduction of the small, dense LDL particles.