Hypercholesterolemia: Morgan JM

Morgan JM, Capuzzi DM. · Jefferson Medical College, Thomas Jefferson University, Cardiovascular Disease Prevention Center, Jefferson Heart Institute, Philadelphia, USA. · Geriatrics. · Pubmed #12938250 No free full text.

Abstract: Coronary heart disease (CHD) is a significant cause of morbidity and mortality in older patients. Therefore, its treatment and prevention is vital to improving the length and quality of life for the geriatric population at large. Clinical trial data have demonstrated that patients age 65 and older derive the same benefit from blood cholesterol reduction as younger adults. As a result, the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) recommends appropriate therapeutic lifestyle changes and drug therapy for older individuals with established CHD or for those at high risk for CHD. Drug therapy in this population, while safe, requires careful monitoring and dose adjustment due to potentially altered drug metabolism and concomitant medications. These factors lead to use of lower starting doses of lipid-lowering medications in older patients. Prudent individualized evaluation and customized therapy provide optimal cardiovascular outcomes.

Capuzzi DM, Morgan JM, Brusco OA, Intenzo CM. · Cardiovascular Disease Prevention Center, 211 S. 9th Street, Walnut Towers Suite 602, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA. · Curr Atheroscler Rep. · Pubmed #11122726 No free full text.

Abstract: Because of the original observation by Altschul et al., that nicotinic acid (niacin), not nicotinamide, in pharmacologic doses lowered human serum cholesterol levels, an avalanche of reports have been published over the past 45 years on the plasma lipid-regulating properties of this drug and its beneficial cardiovascular effects. A myriad of studies that have examined efficacy, safety, adverse effects, and pharmacologic properties of niacin rendered convincing evidence that niacin, used alone or combined with other agents, has favorable effects on serum lipoprotein regulation and on containment of atherothrombotic cardiovascular diseases. However, because of the unusual side effect profile of niacin and the availability of various formulations of this drug, niacin must be used prudently and with careful instruction and monitoring of patients. This review summarizes the pertinent and recent literature on niacin that impacts its therapeutic use. We also discuss some controversial issues and personal clinical experience and opinions on this topic.

Morgan JM, Capuzzi DM, Baksh RI, Intenzo C, Carey CM, Reese D, Walker K. · Jefferson Heart Institute, First Floor, Cardiovascular Disease Prevention Center, Thomas Jefferson University, 925 Chestnut Street, Philadelphia, PA 19107, USA. · Am J Cardiol. · Pubmed #12804729 No free full text.

Abstract: The efficacy of extended-release niacin (niacin ER) on lipoprotein subclasses was evaluated in patients with primary hypercholesterolemia using a proton nuclear magnetic resonance method. Paired plasma samples collected at baseline and after 12 weeks' treatment with niacin ER 1,000 (n = 21) or 2,000 (n = 20) mg/day or placebo (n = 19) were available for 60 eligible patients from a previous multicenter, randomized, controlled trial. Niacin ER increased high-density lipoprotein (HDL) cholesterol and decreased low-density lipoprotein (LDL) cholesterol and very low-density lipoprotein triglycerides in a dose-dependent manner relative to placebo. Niacin ER increased large HDL particles (H5 and H4, corresponding to the HDL(2ab) fraction) without having a net effect on small HDL particles (H3, H2, and H1, corresponding to the HDL(3abc) fraction). It also decreased smaller, denser LDL particles (L1 and L2) and increased the larger, more buoyant L3 subclass. The inhibitory effect of niacin ER on very low-density lipoprotein was evident on the larger particles (V6, V5, V4, and V3 subclasses) rather than the smaller ones (V2 and V1). The results show that niacin ER produces a beneficial effect on lipoprotein subclasses, specifically decreasing the more atherogenic small, dense LDL particles and enhancing the cardioprotective large HDL particles.

Morgan JM, Horton K, Reese D, Carey C, Walker K, Capuzzi DM. · Department of Medicine, Thomas Jefferson University, Philadelphia, Pa 19107, USA. · Int J Vitam Nutr Res. · Pubmed #12463111 No free full text.

Abstract: Serum components, such as lipoproteins, coagulation factors (factor VII, tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), fibrinogen), and homocysteine have been associated with cardiovascular disease. Dietary intervention with a low-fat, low-cholesterol diet has favorably influenced cardiovascular disease and certain food, specifically the consumption of nuts, has been associated with reduced cardiovascular risks. The effects of walnuts, as part of a low-fat, low-cholesterol diet, on serum cardiovascular risk factors were determined. Sixty-seven (67) outpatients with borderline high total cholesterol following a low-fat, low-cholesterol diet for six weeks before being randomly assigned to continue the diet or have 64 grams/day of walnuts in conjunction with the diet. After six weeks, the patients' diets were switched. Therefore, all patients consumed 64 grams/day of walnuts for six weeks during part of the trial as part of a low-fat, low cholesterol diet. Serum lipids demonstrated a significant reduction in triacyglycerols and favorable trend with decreases in total cholesterol, low-density lipoprotein (LDL) cholesterol, and a slight increase in high-density lipoprotein (HDL) cholesterol. No statistical effects on homocysteine or the coagulation factors were observed. However, there was a slight favorable trend for tPA and PAI-1. This study demonstrated that walnuts, when consumed as part of a low fat, low-cholesterol diet, have a beneficial effect on serum cardiovascular risk factors. However, these changes may not explain all of the beneficial effects that walnut consumption has on cardiovascular disease.

Blair SN, Capuzzi DM, Gottlieb SO, Nguyen T, Morgan JM, Cater NB. · Cooper Institute, Dallas, Texas 75230, USA. · Am J Cardiol. · Pubmed #10867091 No free full text.

Abstract: This study compares the effect of plant stanol ester spread with a placebo spread on cholesterol in patients taking statin therapy, but who still had elevated low-density lipoprotein (LDL) cholesterol. This was a randomized, double-blind, placebo-controlled clinical trial, with 67 women and 100 men with LDL cholesterol >/=130 mg/dl and triglycerides </=350 mg/dl who had been taking a stable dose of a statin drug for at least 90 days before the start of the study. For 8 weeks, participants consumed 3 servings/day of the plant stanol ester spread that provided 5.1 g/day of plant stanol ester or a placebo. The addition of plant stanol ester spread significantly reduced total cholesterol and LDL cholesterol at 2, 4, and 8 weeks when compared with placebo spread. Plant stanol ester spread reduced total cholesterol at 8 weeks by 12% compared with a placebo reduction of 5% (-7% difference; p <0.0001). Plant stanol ester spread reduced LDL cholesterol at 8 weeks by 17% compared with a 7% reduction in the placebo group (-10% difference, p <0.0001). The absolute reduction in LDL cholesterol at 8 weeks was 24 and 10 mg/dl in the stanol ester and placebo groups, respectively. The plant stanol ester spread group also had greater reductions in both serum total cholesterol and LDL cholesterol than the placebo group at 2 and 4 weeks (p <0.001 for all comparisons). Both spreads were well tolerated by study participants, and no significant adverse events were noted. Consumption of spread that provided 5.1 g/day of plant stanol esters effectively reduced elevated total and LDL cholesterol levels in participants on a stable regimen of a statin.