What's New? Guidelines and Goals

2006 ◽  
Vol 19 (2) ◽  
pp. 103-112
Author(s):  
Patricia R. Wigle ◽  
Kim K. Birtcher
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Heart Association ◽  
Lipoprotein Cholesterol ◽  
Risk Category ◽  
Lifestyle Modifications ◽  
Lipid Panel ◽  
Heart Blood ◽  
New Guidelines ◽  
Lung Institute

Several expert panels have written guidelines regarding the treatment of dyslipidemias. The recommendations from the National Cholesterol Education Program (NCEP); American Diabetes Association (ADA); American Heart Association (AHA); National Heart, Blood, and Lung Institute (NHBLI); and National Kidney Foundation (NKF) will be reviewed. The guidelines agree on several points: using the fasting lipid panel as the initial screening tool, targeting low-density lipoprotein cholesterol (LDL-C) initially, and achieving lower LDL-C goals. Some guidelines are more aggressive than those of the NCEP: the ADA and AHA have defined low high-density lipoprotein cholesterol as <50 mg/dL for women; the ADA recommends a need for drug therapy when the patient's total cholesterol, rather than LDL-C, is ≥135 mg/dL for patients who are older than 40 years; the NKF and the AHA have classified patients with chronic kidney disease in the high-risk category; and the AHA has revised the diagnostic criteria for metabolic syndrome to include additional people. More patients are qualifying for lifestyle modifications and medication treatment. A subset of these patients may require combination cholesterol-lowering medications to reach the new goals. Pharmacists will need to keep current with the literature and be knowledgeable about the guidelines to maximize the care given to our patients.

scholarly journals Omega-3 Fatty Acids for the Management of Hypertriglyceridemia: A Science Advisory From the American Heart Association

Circulation ◽  
2019 ◽  
Vol 140 (12) ◽  
Author(s):  
Ann C. Skulas-Ray ◽  
Peter W.F. Wilson ◽  
William S. Harris ◽  
Eliot A. Brinton ◽  
Penny M. Kris-Etherton ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Heart Association ◽  
The United States ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Low Density Lipoprotein Cholesterol ◽  
Very High

Hypertriglyceridemia (triglycerides 200–499 mg/dL) is relatively common in the United States, whereas more severe triglyceride elevations (very high triglycerides, ≥500 mg/dL) are far less frequently observed. Both are becoming increasingly prevalent in the United States and elsewhere, likely driven in large part by growing rates of obesity and diabetes mellitus. In a 2002 American Heart Association scientific statement, the omega-3 fatty acids (n-3 FAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were recommended (at a dose of 2–4 g/d) for reducing triglycerides in patients with elevated triglycerides. Since 2002, prescription agents containing EPA+DHA or EPA alone have been approved by the US Food and Drug Administration for treating very high triglycerides; these agents are also widely used for hypertriglyceridemia. The purpose of this advisory is to summarize the lipid and lipoprotein effects resulting from pharmacological doses of n-3 FAs (>3 g/d total EPA+DHA) on the basis of new scientific data and availability of n-3 FA agents. In treatment of very high triglycerides with 4 g/d, EPA+DHA agents reduce triglycerides by ≥30% with concurrent increases in low-density lipoprotein cholesterol, whereas EPA-only did not raise low-density lipoprotein cholesterol in very high triglycerides. When used to treat hypertriglyceridemia, n-3 FAs with EPA+DHA or with EPA-only appear roughly comparable for triglyceride lowering and do not increase low-density lipoprotein cholesterol when used as monotherapy or in combination with a statin. In the largest trials of 4 g/d prescription n-3 FA, non–high-density lipoprotein cholesterol and apolipoprotein B were modestly decreased, indicating reductions in total atherogenic lipoproteins. The use of n-3 FA (4 g/d) for improving atherosclerotic cardiovascular disease risk in patients with hypertriglyceridemia is supported by a 25% reduction in major adverse cardiovascular events in REDUCE-IT (Reduction of Cardiovascular Events With EPA Intervention Trial), a randomized placebo-controlled trial of EPA-only in high-risk patients treated with a statin. The results of a trial of 4 g/d prescription EPA+DHA in hypertriglyceridemia are anticipated in 2020. We conclude that prescription n-3 FAs (EPA+DHA or EPA-only) at a dose of 4 g/d (>3 g/d total EPA+DHA) are an effective and safe option for reducing triglycerides as monotherapy or as an adjunct to other lipid-lowering agents.

scholarly journals Nutrition Intervention for Reduction of Cardiovascular Risk in African Americans Using the 2019 American College of Cardiology/American Heart Association Primary Prevention Guidelines

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3422
Author(s):  
Kim Allan Williams ◽  
Ibtihaj Fughhi ◽  
Setri Fugar ◽  
Monica Mazur ◽  
Sharon Gates ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Heart Association ◽  
Nutrition Intervention ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Ascvd Risk ◽  
Hs Crp

Introduction: The 2019 American College of Cardiology/American Heart Association (ACC/AHA) Prevention Guidelines emphasize reduction in dietary sodium, cholesterol, refined carbohydrates, saturated fat and sweetened beverages. We hypothesized that implementing this dietary pattern could reduce cardiovascular risk in a cohort of volunteers in an urban African American (AA) community church, during a 5-week ACC/AHA-styled nutrition intervention, assessed by measuring risk markers and adherence, called HEART-LENS (Helping Everyone Assess Risk Today Lenten Nutrition Study). Methods: The study population consisted of 53 volunteers who committed to eat only home-delivered non-dairy vegetarian meals (average daily calories 1155, sodium 1285 mg, cholesterol 0 mg; 58% carbohydrate, 17% protein, 25% fat). Body mass index (BMI) and fasting serum markers of cardiometabolic and risk factors were measured, with collection of any dietary deviation. Results: Of 53 volunteers, 44 (mean age 60.2 years, 37 women) completed the trial (88%); 1 was intolerant of the meals, 1 completed both blood draws but did not eat delivered food, and 7 did not return for the tests. Adherence to the diet was reported at 93% in the remaining 44. Cardiometabolic risk factors improved significantly, highlighted by a marked reduction in serum insulin (−43%, p = 0.000), hemoglobin A1c (6.2% to 6.0%, p = 0.000), weight and BMI (−10.2 lbs, 33 to 31 kg/m2, p = 0.000), but with small reductions of fasting glucose (−6%, p = 0.405) and triglyceride levels (−4%, p = 0.408). Additionally, improved were trimethylamine-N-oxide (5.1 to 2.9 µmol/L, −43%, p = 0.001), small dense low-density lipoprotein cholesterol (LDL) (24.2 to 19.1 mg/dL, −21%, p = 0.000), LDL (121 to 104 mg/dL, −14%, p = 0.000), total cholesterol (TC) (190 to 168 mg/dL, −12%, p = 0.000), and lipoprotein (a) (LP(a)) (56 to 51 mg/dL, −11%, p = 0.000); high sensitivity C-reactive protein (hs-CRP) was widely variable but reduced by 16% (2.5 to 2.1 ng/mL, p = NS) in 40 subjects without inflammatory conditions. Soluble urokinase plasminogen activator (suPAR) levels were not significantly changed. The ACC/AHA pooled cohort atherosclerotic cardiovascular disease (ASCVD) risk scores were calculated for 41 and 36 volunteers, respectively, as the ASCVD risk could not be calculated for 3 subjects with low lipid fractions at baseline and 8 subjects after intervention (p = 0.184). In the remaining subjects, the mean 10-year risk was reduced from 10.8 to 8.7%, a 19.4% decrease (p = 0.006), primarily due to a 14% decrease in low-density lipoprotein cholesterol and a 10 mm Hg (6%) reduction in systolic blood pressure. Conclusions: In this prospective 5-week non-dairy vegetarian nutrition intervention with good adherence consistent with the 2019 ACC/AHA Guidelines in an at-risk AA population, markers of cardiovascular risk, cardiometabolism, and body weight were significantly reduced, including obesity, low-density lipoprotein cholesterol (LDLc) density, LP(a), inflammation, and ingestion of substrates mediating production of trimethylamine-N-oxide (TMAO). Albeit reduced, hs-CRP and suPAR, were not lowered consistently. This induced a significant decrease in the 10-year ASCVD risk in this AA cohort. If widely adopted, this could dramatically reduce and possibly eradicate, the racial disparity in ASCVD events and mortality, if 19% of the 21% increase is eliminated by this lifestyle change.

Abstract P126: Unanticipated Lipid Profiles in Victims of Sudden Unexpected Death: Low Low-density Lipoprotein Cholesterol and an Elevated Triglyceride to High-density Lipoprotein Cholesterol Ratio

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Nisha Hosadurg ◽  
Brittany Bogle ◽  
Golsa Joodi ◽  
Murrium I Sadaf ◽  
Philip M Mendys ◽  
...  
Keyword(s):  
Medical Records ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Sudden Unexpected Death ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Low Density Lipoprotein Cholesterol ◽  
Unexpected Death ◽  
Cholesterol Ratio ◽  
Lipid Panel

Background: Though low-density lipoprotein cholesterol (LDL) is a proven cardiovascular risk factor, substantive data on LDL levels in victims of sudden cardiac or sudden unexpected death is lacking. Additionally, post-mortem studies have shown higher concentrations of remnant-like lipoprotein particles (RLP) in sudden cardiac death victims. Triglyceride to high-density lipoprotein cholesterol ratio (TG/HDL) is associated with RLP concentration, but has not been reported for victims prior to sudden death. Hypothesis: We assessed the hypothesis that out-of-hospital sudden unexpected death (OHSUD) victims would have similar or higher calculated LDL levels and higher TG/HDL ratios when compared with National Health and Nutrition Examination Survey (NHANES) participants. Methods: From 2013-15, all free living adults aged 18-64 who died out-of-hospital as reported by emergency medical services in Wake County, North Carolina (population 974,289) were adjudicated to identify OHSUD victims (n=408). Medical records were requested from area healthcare providers; 138 victims had a lipid panel available at an average of 1.2 years prior to death. To emulate a similar follow-up period, 18-64 year old NHANES (2009-2010) participants with a lipid panel who were alive at the end of 2011 served as a comparison group (n=1316). Covariates were abstracted from medical records for OHSUD victims and self-reported in NHANES participants. Subjects with triglycerides>400 mg/dL were excluded for analysis pertaining to LDL. We used multiple linear regression to assess the difference in lipid measures between OHSUD victims and NHANES participants, adjusting for demographics, prevalent dyslipidemia, diabetes, hypertension, body mass index, and coronary artery disease, use of lipid-lowering medication and clinic visits per year. Results: OHSUD victims had a lower mean LDL than NHANES participants (91.6 mg/dL; 95% CI 84.7, 98.5 vs. 115.8 mg/dL; 95%CI 113.8, 117.7 respectively). After multivariate adjustment, mean LDL of victims was still 22.3 mg/dL lower than NHANES participants (p<0.001). OHSUD victims had a higher unadjusted mean TG/HDL ratio than NHANES participants (4.2; 95% CI 3.2, 5.2 vs. 2.9; 95% CI 2.7, 3.2 respectively); this difference was mildly attenuated on adjustment for age, gender and race and insignificant upon additional adjustment for dyslipidemia and diabetes status. Conclusion: Contrary to expectations, out-of-hospital sudden unexpected death victims had a more favorable LDL cholesterol profile unexplained by differences in demographics, comorbid conditions or use of lipid lowering medication. The elevated TG/HDL ratio in victims, though explained by a higher prevalence of comorbidities, corroborates an evolving hypothesis on the contributory nature of vasoactive, prothrombotic remnant-like lipoprotein particles to sudden unexpected death.

Efficacy and Safety of Cerivastatin 0.8 mg in Patients with Hypercholesterolaemia: The Pivotal Placebo-Controlled Clinical Trial

2000 ◽  
Vol 28 (2) ◽  
pp. 47-68 ◽  
Author(s):  
W Insull ◽  
J Isaacsohn ◽  
P Kwiterovich ◽  
P Ma ◽  
R Brazg ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Heart Association ◽  
Pharmacological Therapy ◽  
Apolipoprotein A1 ◽  
Lipoprotein Cholesterol ◽  
Controlled Clinical Trial ◽  
Efficacy And Safety ◽  
Double Blind ◽  
Primary Hypercholesterolaemia

This pivotal, multicentre, double-blind, parallel-group study evaluated the efficacy and safety of cerivastatin 0.8 mg. Patients with primary hypercholesterolaemia were randomized, after 10 weeks' dietary stabilization on an American Heart Association (AHA) Step I diet, to treatment with cerivastatin 0.8 mg ( n = 776), cerivastatin 0.4 mg ( n = 195) or placebo ( n = 199) once daily for 8 weeks. Cerivastatin 0.8 mg reduced mean low density lipoprotein-cholesterol (LDL-C) by 41.8% compared with cerivastatin 0.4 mg (–35.6%, P < 0.0001) or placebo. In 90% of patients receiving cerivastatin 0.8 mg LDL-C was reduced by 23.9–58.4% (6th–95th percentile). Overall attainment of the National Cholesterol Education Program (NCEP) goal was achieved by 84% of patients receiving cerivastatin 0.8 mg and by 59% of those with coronary heart disease (CHD). In the sub-population meeting the NCEP criteria for pharmacological therapy for LDL-C reduction, 74.6% of patients, including the 59% with CHD, reached the goal with cerivastatin 0.8 mg. Cerivastatin 0.8 mg also reduced mean total cholesterol by 29.9%, apolipoprotein B by 33.2% and median triglycerides by 22.9% (all P < 0.0001). Mean high density lipoprotein-cholesterol (HDL-C) and apolipoprotein A1 were elevated 8.7% ( P < 0.0001) and 4.5% ( P < 0.0001), respectively, by cerivastatin 0.8 mg. Reductions of triglyceride and elevation in HDL-C were dependent upon triglyceride baseline levels; in patients having baseline triglyceride levels 250–400 mg/dl, cerivastatin 0.8 mg reduced median triglycerides by 29.5% and elevated HDL-C by 13.2%. Cerivastatin 0.8 mg was well tolerated. The most commonly reported adverse events included headache, pharyngitis and rhinitis (4–6%). Symptomatic creatine kinase elevations > 10 times upper limit of normal occurred in 0%, 1% and 0.9% of patients receiving placebo, cerivastatin 0.4 mg or cerivastatin 0.8 mg, respectively. Cerivastatin 0.8 mg is an effective and safe treatment for patients with primary hypercholesterolaemia who need aggressive LDL-C lowering in order to achieve NCEP-recommended levels.

Primary Hyperlipidemia in a Pediatric Population: Classification and Effect of Dietary Treatment

PEDIATRICS ◽  
1993 ◽  
Vol 91 (1) ◽  
pp. 92-96
Author(s):  
Sheldon M. Polonsky ◽  
Paul S. Bellet ◽  
Dennis L. Sprecher
Keyword(s):  
Pediatric Population ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Heart Association ◽  
Dietary Treatment ◽  
Significant Degree ◽  
Lipoprotein Cholesterol ◽  
Lipid Clinic ◽  
American Heart Association Step

Patients seen at a pediatric lipid clinic over a 27-month period were reviewed retrospectively to evaluate types of primary lipid disorders and effect of dietary treatment at the first follow-up visit. One hundred eighty-two patients were classified into one of four categories: (1) elevated low-density lipoprotein cholesterol (LDL-C) with LDL-C &gt; 95th percentile (32%); (2) isolated triglyceride (TG)/high-density lipoprotein cholesterol (HDL-C) abnormalities, with TG &gt; 95th percentile and/or HDL-C &lt; 5th percentile (30%); (3) borderline LDL-C, TG, or HDL-C (29%); (4) normal (9%). The American Heart Association Step-One Diet was prescribed for all patients older than 2 years, and they received extensive nutritional and risk-management counseling. Of these patients, 59 (32%) returned for at least one follow-up visit and mean changes in lipid values between initial and first follow-up visits were evaluated. Levels of LDL-C decreased by 24 mg/dL in 22 patients with elevated LDL-C levels. Triglyceride levels decreased by a mean of 22 mg/dL and HDL-C increased by a mean of 4 mg/dL in 21 patients with isolated TG/HDL-C abnormalities. Levels of LDL-C tended to rise in this group, but not to a significant degree. A new finding of this report is that screening for total cholesterol results in the identification of many children with TG or HDL-C abnormalities alone and that the Step-One Diet appears to be effective in improving both TG and HDL-C levels in these patients.

Lipid-Lowering Effects of Fluvastatin in Renal Transplant Patients. A Clinical Observation

1997 ◽  
Vol 20 (1) ◽  
pp. 18-21 ◽  
Author(s):  
S.M. Lal ◽  
N. Gupta ◽  
O. Georgiev ◽  
G. Ross
Keyword(s):  
Renal Transplant ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Heart Association ◽  
Term Treatment ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Short Term Treatment ◽  
Transplant Patients ◽  
Renal Transplant Patients

A Atherosclerosis-related cardiovascular disease remains an important cause of morbidity and mortality in renal transplant patients. We assessed the efficacy and safety of the newer synthetic HMG-CoA reductase inhibitor, fluvastatin, in 12 renal transplant patients who remained hypercholesterolemic, despite having been on the American Heart Association (AHA) Step I diet for 6 weeks. At 8 weeks, compared to the control phase, fluvastatin therapy, 20 mg/day, reduced the total cholesterol (TC) from 321 ± 57 [± SD] to 301 ± 123 mg/dl (p=0.3); low-density lipoprotein cholesterol (LDL-C), from 209 ± 56 to 176 ± 81 mg/dl (p=0.2); and the triglyceride (TG) levels from 343 ± 119 to 277 ± 117 mg/dl (p=0.06); all these changes were statistically insignificant. However, the therapy significantly increased the high-density lipoprotein cholesterol (HDL-C) from 37 ± 11 to 46 ± 13 mg/dl (p=0.006). During this short-term treatment period no adverse biochemical effects were noted with the therapy.

scholarly journals A New Equation Based on the Standard Lipid Panel for Calculating Small Dense Low-Density Lipoprotein-Cholesterol and Its Use as a Risk-Enhancer Test

2021 ◽  
Author(s):  
Maureen Sampson ◽  
Anna Wolska ◽  
Russell Warnick ◽  
Diego Lucero ◽  
Alan T Remaley
Keyword(s):  
Survival Curve ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Atherosclerotic Cardiovascular Disease ◽  
Low Density ◽  
Least Squares Regression ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipid Panel ◽  
Ascvd Risk

Abstract Background Increased small dense low-density lipoprotein-cholesterol (sdLDL-C) is a risk factor for atherosclerotic cardiovascular disease (ASCVD) but typically requires advanced lipid testing. We describe two new equations, first one for calculating large buoyant LDL-C (lbLDL-C), based only upon results from the standard lipid panel, and the second one for sdLDL-C. Methods Equations for sdLDL-C and lbLDL-C were generated with least-squares regression analysis using the direct Denka sdLDL-C assay as reference (n = 20 171). sdLDL-C was assessed as a risk-enhancer test in the National Heart and Nutrition Examination Survey (NHANES), and for its association with ASCVD in the Multi-Ethnic Study of Atherosclerosis (MESA). Results The newly derived equations depend on two terms, namely LDL-C as determined by the Sampson equation, and an interaction term between LDL-C and the natural log of triglycerides (TG). The lbLDL-C equation (lbLDLC=1.43 × LDLC-0.14 ×(ln⁡(TG)× LDLC)- 8.99) was more accurate (R2 = 0.933, slope = 0.94) than the sdLDL-C equation (sdLDLC=LDLC- lbLDLC; R2 = 0.745, slope = 0.73). Using the 80th percentile (46 mg/dL) as a cut-point, sdLDL-C identified in NHANES additional high-risk patients not identified by other risk-enhancer tests based on TG, LDL-C, apolipoprotein B, and nonHDL-C. By univariate survival-curve analysis, estimated sdLDL-C was superior to other risk-enhancer tests in predicting ASCVD events in MESA. After multivariate adjustment for other known ASCVD risk factors, estimated sdLDL-C had the strongest association with ASCVD compared to other lipid parameters, including measured sdLDL-C. Conclusions Estimated sdLDL-C could potentially be calculated on all patients tested with a standard lipid panel to improve ASCVD risk stratification.

Effects of exercise accumulation on plasma lipids and lipoproteins

2015 ◽  
Vol 40 (5) ◽  
pp. 441-447 ◽  
Author(s):  
Jason D. Wagganer ◽  
Charles E. Robison ◽  
Terry A. Ackerman ◽  
Paul G. Davis
Keyword(s):  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Random Order ◽  
Blood Lipid ◽  
Lipoprotein Cholesterol ◽  
Exercise Session ◽  
Significant Treatment ◽  
Lipid Panel ◽  
Lipids And Lipoproteins

Debate exists as to whether improvements in some cardiometabolic risk factors following exercise training result more from the last session of, or from an accumulation of, exercise sessions. This study was designed to compare the effect of a single exercise session with 3 consecutive days of exercise on triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C). Twelve young adult (aged 22.5 ± 2.5 years), overweight (body mass index = 29.7 ± 4 kg·m–2), sedentary, black (n = 5) and white (n = 7) men (n = 6) and women (n = 6) completed, in random order, a single treadmill exercise session at 60% maximal oxygen uptake for 90 min (1EX), accumulated exercise sessions (same as for 1EX) for 3 consecutive days (3EX), and a control protocol (no exercise for 6 days). Plasma samples were collected from baseline through 24, 48, and 72 h postexercise. Significant treatment-by-time interactions (p < 0.05) existed in HDL-C and LDL-C. Postexercise responses of HDL-C differed at 48 h (1EX: –3.6, 3EX: + 3.7 mg·dL−1) and 72 h (1EX: –1.7, 3EX: + 3.2 mg·dL−1). LDL-C responses differed at 48 h (1EX: –16, 3EX: + 6 mg·dL−1). Although not statistically significant, TG concentrations decreased by 29% at 24 h after 3EX, compared with –7% after 1EX. An inverse relationship between baseline and postexercise reduction in TG was present with 3EX (r = –0.655; p < 0.05). In conclusion, 3EX increased HDL-C and decreased TG more than 1EX, while the decrease in LDL-C after 1EX was suppressed. Blood lipid panel changes may be due to more accumulated effects over time rather than just a result of the most recent exercise session.

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