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Articles by Kevin C. Maki
Total Records ( 15 ) for Kevin C. Maki
  Peter P. Toth and Kevin C. Maki
  not available
  Kevin C. Maki , Barry C. Lubin , Matthew S. Reeves , Mary R. Dicklin and William S. Harris
 

Background

Prescription omega-3 acid ethyl esters (P-OM3) plus simvastatin 20 and 40 mg/day improves lipids in subjects with mixed dyslipidemia, but no previous studies have examined P-OM3 with the maximum prescribed dose of simvastatin (80 mg).

Objective

To assess the effects of P-OM3 + simvastatin 80 mg versus P-OM3 + simvastatin 20 mg or placebo + simvastatin 20 mg on non-high-density lipoprotein cholesterol (non-HDL-C) and other lipid concentrations.

Methods

Subjects with mixed dyslipidemia who had completed a 12-week double-blind crossover study of simvastatin 20 mg/day + either placebo or P-OM3 4 g/day were enrolled. An analysis (n = 14) was performed following the first six weeks of the extension, during which all subjects received open-label P-OM3 + open-label simvastatin 80 mg/day.

Results

P-OM3 + simvastatin 80 mg resulted in significantly larger reductions from baseline (P < .05 for all) versus P-OM3 + simvastatin 20 mg and placebo + simvastatin 20 mg, respectively, for non-HDL-C (−51.0%, −40.8%, −34.9%), low-density lipoprotein cholesterol (−48.0%, −35.5%, −38.0%), total cholesterol (TC) (−42.6%, −31.9%, −27.1%), the TC/HDL-C ratio (−52.9%, −44.3%, −36.2%), and apolipoprotein B (−42.6%, −32.6%, −30.5%). P-OM3 + simvastatin (80- and 20-mg doses, respectively) resulted in significantly larger changes from baseline (P < .05 for all) versus placebo in very low-density lipoprotein cholesterol (−50.7%, −47.9%, −23.0%), triglycerides (TG; −58.6%, −54.7%, −32.0%), HDL-C (24.5%, 20.7%, 17.9%), and the TG/HDL-C ratio (−66.5%, −62.3%, −42.5%).

Conclusion

These results suggest non-HDL-C, TG (both 50% to 60%), and HDL-C (∼25%) concentrations can be markedly improved by a combination of P-OM3 (4 g/day) and simvastatin (80 mg/day) in subjects with mixed dyslipidemia.

  Kevin C. Maki , Martyn R. Rubin , Les G. Wong , Jamie F. McManus , Christopher D. Jensen , John W. Marshall and Andrea Lawless
 

Background

Low vitamin D status has been associated with markers of cardiovascular disease risk.

Objective

This cross-sectional study assessed the relationships between serum 25-hydroxyvitamin D [25(OH)D] and selected markers for cardiovascular disease risk, including metabolic syndrome and its components, in adult men and women.

Methods

Fasting blood samples, anthropometric measurements, and blood pressure were assessed in 257 men and women. Dietary intake was assessed with food frequency and dietary supplement questionnaires.

Results

Total vitamin D intake and that from dietary supplements were significantly associated with increasing serum 25(OH)D tertile (both P < .001). Mean±SEM serum high-density lipoprotein cholesterol (HDL-C) increased in a graded fashion (P < .001) from the lowest (48.4±1.8 mg/dL) to the highest (62.3±2.1 mg/dL) 25(OH)D tertile. The relationship between 25(OH)D and HDL-C remained significant (P < .001) after adjustment for established determinants of the HDL-C, with each 10-ng/mL increase in 25(OH)D associated with a 4.2-mg/dL increase in HDL-C concentration. Serum triglycerides (P=.008), waist circumference (P < .001), and body mass index (P < .001) showed graded, inverse relationships with 25(OH)D tertile, and the prevalence of metabolic syndrome decreased significantly from the lowest to the highest 25(OH)D tertile (31%, 14%, and 10%, respectively, P for trend=.001).

Conclusions

Lower serum 25(OH)D is associated with the metabolic syndrome and adverse values for some metabolic syndrome risk factors, particularly the HDL-C concentration. Research is warranted to assess whether increasing vitamin D intake will improve the metabolic cardiovascular risk factor profile.

  Michael H. Davidson , Kevin C. Maki , Harold Bays , Roderick Carter and Christie M. Ballantyne
 

Background

Prescription omega-3-acid ethyl esters (P-OM3) often are used for hypertriglyceridemic patients receiving statin therapy who have residual increases in atherogenic lipoprotein lipid levels. To date, limited information has been published regarding the effects of omega-3 fatty acid consumption on lipoprotein particle concentrations.

Objective

We evaluated the effects of adding P-OM3 4 g/d to an ongoing regimen of simvastatin 40 mg/d on lipoprotein particles (P) in subjects with hypertriglyceridemia.

Methods

Data were analyzed from the multicenter, randomized, double-blind, placebo-controlled Combination of Prescription Omega-3s with Simvastatin (COMBOS) study. After an 8-week simvastatin lead-in, 254 subjects received P-OM3 (n=122) or placebo (n=132) for an additional 8 weeks. Nuclear magnetic resonance spectroscopy was used to assess lipoprotein concentrations and sizes. Remnant-like particle cholesterol, apolipoprotein (Apo) CIII, Apo AI, and lipoprotein-associated phospholipase A2 (Lp-PLA2) levels also were measured.

Results

Compared with placebo, P-OM3 reduced mean very-low-density lipoprotein (VLDL-P) size and increased low-density lipoprotein particle (LDL-P) size (P < .006 for both) without altering high-density lipoprotein particle (HDL-P) size. P-OM3 did not significantly change total VLDL-P or LDL-P concentrations relative to placebo, but large VLDL-P and intermediate-density lipoprotein particle (IDL-P) concentrations were lowered (P < .01 for both), and the large LDL-P concentration was increased (P < .0001). HDL-P concentration was reduced (P < .0001) as the result of a decrease in medium HDL-P. Remnant-like particle cholesterol, Apo CIII, and Lp-PLA2 concentrations were reduced compared with placebo (all P < .003).

Conclusions

P-OM3 induces changes in sizes, concentrations, and compositions of lipoproteins that may have relevance for the atherothrombotic process.

  Kevin C. Maki , Dustie N. Butteiger , Tia M. Rains , Andrea Lawless , Matthew S. Reeves , Chuck Schasteen and Elaine S. Krul
 

Background

Soy protein (SP) and low-fat dairy product consumption have been suggested to have hypocholesterolemic effects, although the responsible mechanisms are poorly understood.

Objective

This randomized, controlled, parallel arm trial evaluated the effects of an insoluble fraction of SP and total milk proteins (TMPs) with high calcium content on the fasting lipid profile. It also assessed the potential contributions of increased excretion of bile acids and neutral sterols to their lipid-altering effects.

Methods

Subjects with hypercholesterolemia (low-density lipoprotein cholesterol [LDL-C] 100−199 mg/dL) followed the Therapeutic Lifestyle Changes diet for 4 weeks, followed by a 2-week lead-in with 3.75 g/d colesevelam HCl. Individuals with LDL-C lowering of ≥5.0% with colesevelam HCl were randomly assigned to one of two groups after a 3-week washout: 1) 25 g/d of an insoluble fraction of partially hydrolyzed SP or 2) 25 g/d TMP.

Results

Both SP and TMP reduced atherogenic lipoproteins, as indicated by changes in total cholesterol (−7.4% and −3.6%), LDL-C (−10.9% and −5.9%), nonhigh-density lipoprotein cholesterol (−10.8% and −3.9%), and apolipoprotein B (−9.7% and −2.4%), respectively (P < .05 for between group differences except LDL-C, P = .085). No significant increases were observed in either group for fecal bile acids or neutral sterols.

Conclusion

These results confirm that SP consumption exerts a hypocholesterolemic effect and indicate that TMP elicits a less pronounced response. However, these findings do not support the hypothesis that increased bile acid excretion is an important contributor to the hypocholesterolemic effects of either protein source.

  Kevin C. Maki , Michael H. Davidson , Mary R. Dicklin , Marjorie Bell , MarySue Witchger and Steven B. Feinstein
 

Background

The rate of carotid intima media thickness (CIMT) progression has been widely used in clinical trials as a surrogate marker for subclinical atherosclerosis.

Objective

The aim of this study was to investigate relationships between coronary heart disease (CHD) risk markers and progression of CIMT in patients at moderate CHD risk.

Methods

Participants included men (45-75 years) and women (55-74 years) in the control arm of a clinical trial. All had at least one major CHD risk factor and baseline posterior wall CIMT 0.7-2.0 mm, without significant stenosis. Posterior (n = 134) and anterior wall (in a subset, n = 72) CIMT were assessed with B-mode ultrasound at baseline and 12 and ∼18 months. Fasting lipoprotein lipid, apolipoprotein (Apo), inflammatory, and oxidative stress markers were evaluated.

Results

Baseline CIMT was inversely associated (P < .001) with CIMT progression. After adjustment for baseline CIMT, significant predictors of anterior wall CIMT progression in linear regression analyses included glucose (P = .044), high-density lipoprotein cholesterol (HDL-C, inverse, P = .006), triglycerides (TG, P = .006), and ratios of total cholesterol (TC)/HDL-C (P = .013), TG/HDL-C (P = .005), and Apo B/HDL-C (P = .021). Posterior wall CIMT progressed on average, whereas anterior wall CIMT regressed (0.0078 vs −0.0164 mm/year, P = .014). Significant baseline CIMT-adjusted predictors of posterior wall CIMT progression included TC (P = .028), low-density lipoprotein-C (P = .035), non-HDL-C (P = .004), TG (P = .016), Apo B (P = .005), and ratios of TC/HDL-C (P < .001), TG/HDL-C (P = .015), Apo B/Apo AI (P = .012) and Apo B/HDL-C (P = .004).

Conclusion

The strongest predictors for CIMT progression in anterior and posterior walls were lower baseline CIMT, increased TG, and elevated ratios, including TC/HDL-C, TG/HDL-C and Apo B/HDL-C.

  Michael H. Davidson , Christie M. Ballantyne , Terry A. Jacobson , Vera A. Bittner , Lynne T. Braun , Alan S. Brown , W. Virgil Brown , William C. Cromwell , Ronald B. Goldberg , James M. McKenney , Alan T. Remaley , Allan D. Sniderman , Peter P. Toth , Sotirios Tsimikas , Paul E. Ziajka , Kevin C. Maki and Mary R. Dicklin
  The National Cholesterol Education Program Adult Treatment Panel guidelines have established low-density lipoprotein cholesterol (LDL-C) treatment goals, and secondary non-high-density lipoprotein (HDL)-C treatment goals for persons with hypertriglyceridemia. The use of lipid-lowering therapies, particularly statins, to achieve these goals has reduced cardiovascular disease (CVD) morbidity and mortality; however, significant residual risk for events remains. This, combined with the rising prevalence of obesity, which has shifted the risk profile of the population toward patients in whom LDL-C is less predictive of CVD events (metabolic syndrome, low HDL-C, elevated triglycerides), has increased interest in the clinical use of inflammatory and lipid biomarker assessments. Furthermore, the cost effectiveness of pharmacological intervention for both the initiation of therapy and the intensification of therapy has been enhanced by the availability of a variety of generic statins. This report describes the consensus view of an expert panel convened by the National Lipid Association to evaluate the use of selected biomarkers [C-reactive protein, lipoprotein-associated phospholipase A2, apolipoprotein B, LDL particle concentration, lipoprotein(a), and LDL and HDL subfractions] to improve risk assessment, or to adjust therapy. These panel recommendations are intended to provide practical advice to clinicians who wrestle with the challenges of identifying the patients who are most likely to benefit from therapy, or intensification of therapy, to provide the optimum protection from CV risk.
  Kevin C. Maki , Harold E. Bays , Mary R. Dicklin , Susan L. Johnson and Mayadah Shabbout
 

Background

Prescription omega-3-acid ethyl esters (POM3) reduce triglycerides (TG) and very low-density lipoprotein cholesterol and increase high-density lipoprotein cholesterol (HDL-C) in patients with hypertriglyceridemia.

Objective

To examine the effects of POM3 plus atorvastatin versus placebo plus atorvastatin on lipoprotein particle concentrations and sizes, apolipoprotein (Apo) CIII, and lipoprotein-associated phospholipase A2 mass in subjects with mixed dyslipidemia.

Methods

After a 4-week diet lead in, men and women with non-HDL-C >160 mg/dL and TG 250-599 mg/dL, while taking no lipid-altering drugs, received double-blind 4 g/d POM3 (n = 118) or placebo (n = 119) with open-label atorvastatin 10 mg/d for 8 weeks, followed by escalation to 20 mg/d atorvastatin for 4 weeks, then 40 mg/d atorvastatin for 4 weeks.

Results

Total low-density lipoprotein particle (LDL-P) concentration decreased significantly from baseline, and the reductions did not differ between the POM3 and placebo groups (−659.7 vs −624.4 nmol/L, P = .181). With POM3, compared with placebo, small LDL-P concentration decreased (P = .026), large LDL-P concentration increased (P < .001), mean LDL-P size increased (P = .001), a larger fraction of subjects switched from LDL subclass pattern B to A, and Apo CIII and lipoprotein-associated phospholipase A2 levels were reduced (P < .001). The incremental effects of POM3 were similar across atorvastatin doses for most variables.

Conclusion

This analysis supports the view that LDL-P concentration is not increased by POM3 plus atorvastatin, relative to atorvastatin monotherapy, and is associated with potentially favorable shifts in LDL-P subfractions, Apo CIII and lipoprotein-associated phospholipase A2 in mixed dyslipidemia.

  Seth J. Baum , Penny M. Kris-Etherton , Walter C. Willett , Alice H. Lichtenstein , Lawrence L. Rudel , Kevin C. Maki , Jay Whelan , Christopher E. Ramsden and Robert C. Block
  Research dating back to the 1950s reported an association between the consumption of saturated fatty acids (SFAs) and risk of coronary heart disease. Recent epidemiological evidence, however, challenges these findings. It is well accepted that the consumption of SFAs increases low-density lipoprotein cholesterol (LDL-C), whereas carbohydrates, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) do not. High-density lipoprotein (HDL)-C increases with SFA intake. Among individuals who are insulin resistant, a low-fat, high-carbohydrate diet typically has an adverse effect on lipid profiles (in addition to decreasing HDL-C, it also increases triglyceride and LDL particle concentrations). Consequently, a moderate fat diet in which unsaturated fatty acids replace SFAs and carbohydrates are not augmented is advised to lower LDL-C; compared with a low-fat diet, a moderate-fat diet will lower triglycerides and increase HDL-C. Now, there is some new evidence that is questioning the health benefits of even MUFAs and PUFAs. In addition, in a few recent studies investigators have also failed to demonstrate expected cardiovascular benefits of marine-derived omega-3 fatty acids. To clarify the clinical pros and cons of dietary fats, the National Lipid Association held a fatty acid symposium at the 2011 National Lipid Association Scientific Sessions. During these sessions, the science regarding the effects of different fatty acid classes on coronary heart disease risk was reviewed.
  Kevin C. Maki , Mary E. Van Elswyk , Dominik D. Alexander , Tia M. Rains , Eugenia L. Sohn and Shalene McNeill
 

Background

Limited consumption of red meat, including beef, is one of many often-suggested strategies to reduce the risk of coronary heart disease (CHD). However, the role that beef consumption specifically plays in promoting adverse changes in the cardiovascular risk factor profile is unclear.

Objective

A meta-analysis of randomized, controlled, clinical trials (RCTs) was conducted to evaluate the effects of beef, independent of other red and processed meats, compared with poultry and/or fish consumption, on lipoprotein lipids.

Methods

RCTs published from 1950 to 2010 were considered for inclusion. Studies were included if they reported fasting lipoprotein lipid changes after beef and poultry/fish consumption by subjects free of chronic disease. A total of 124 RCTs were identified, and 8 studies involving 406 subjects met the prespecified entry criteria and were included in the analysis.

Results

Relative to the baseline diet, mean ± standard error changes (in mg/dL) after beef versus poultry/fish consumption, respectively, were −8.1 ± 2.8 vs. −6.2 ± 3.1 for total cholesterol (P = .630), −8.2 ± 4.2 vs. −8.9 ± 4.4 for low-density lipoprotein cholesterol (P = .905), −2.3 ± 1.0 vs. −1.9 ± 0.8 for high-density lipoprotein cholesterol (P = .762), and −8.1 ± 3.6 vs. −12.9 ± 4.0 mg/dL for triacylglycerols (P = .367).

Conclusion

Changes in the fasting lipid profile were not significantly different with beef consumption compared with those with poultry and/or fish consumption. Inclusion of lean beef in the diet increases the variety of available food choices, which may improve long-term adherence with dietary recommendations for lipid management.

  Kevin C. Maki , Harold E. Bays and Mary R. Dicklin
  A severe elevation in triglycerides (TG; ≥500 mg/dL) increases the risk for pancreatitis. TG levels ≥200 mg/dL are associated with a greater risk of atherosclerotic coronary heart disease (CHD). However, no outcomes trials exist to assess the efficacy of TG lowering for preventing pancreatitis in patients with severe hypertriglyceridemia. Similarly, no completed prospective outcomes trial exists to support or refute a reduction in CHD risk resulting from lipid-altering therapy in patients specifically selected for the presence of hypertriglyceridemia. This review examines the available evidence for the use of statins, omega-3 fatty acids, fibrates, and niacin in the management of hypertriglyceridemic patients. Results from CHD outcomes trials support statins as the first-line lipid-altering drug therapy to reduce CHD in hypercholesterolemic patients, and subgroup analyses suggest statins are efficacious in hypertriglyceridemic patients with fasting TG levels <500 mg/dL. Omega-3 fatty acids and fibrates are reasonable first drug options for patients with TG ≥500 mg/dL and often are used to lower TG levels with the objective of reducing pancreatitis risk, although a statin or niacin may also be reasonable options. Combination lipid drug therapy may be needed to achieve both low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol treatment goals for CHD prevention in patients with elevated TG levels, particularly those with TG ≥500 mg/dL. Additional clinical outcomes data are needed to provide a more evidence-based rationale for clinical lipid management of hypertriglyceridemic patients.
  W. Virgil Brown , Harold E. Bays , Kevin C. Maki and Robert A. Wild
  Not available
  Matthew K. Ito , Kevin C. Maki , Eliot A. Brinton , Jerome D. Cohen and Terry A. Jacobson
 

Background

Drug interactions have been identified as a risk factor for muscle-related side effects in statin users.

Objectives

The aim was to assess whether use of medications that inhibit cytochrome P450 (CYP450) isozymes, organic anion transporting polypeptide 1B1 (OATP1B1), or P-glycoprotein (P-gp) are associated with muscle-related symptoms among current and former statin users.

Methods

Persons (n = 10,138) from the Understanding Statin Use in America and Gaps in Education (USAGE) internet survey were categorized about whether they ever reported new or worsening muscle pain while taking a statin (n = 2935) or ever stopped a statin because of muscle pain (n = 1516). Univariate and multivariate logistic regression models were used to assess associations between use of concomitant therapies that inhibit CYP450 isozymes, OATP1B1, P-gp, or a combination and muscle-related outcomes.

Results

In multivariate analyses, concomitant use of a CYP450 inhibitor was associated with increased odds for new or worse muscle pain (odds ratio [OR] = 1.42; P < .001) or ever having stopped a statin because of muscle pain (OR = 1.28; P = .037). Concomitant use of medication known to inhibit both OATP1B1 and P-gp was also associated with increased odds (OR = 1.80; P = .030) of ever having stopped a statin because of muscle pain.

Conclusions

Concomitant use of medication(s) that inhibit statin metabolism was associated with increased odds of new or worse muscle pain while taking a statin and having previously stopped a statin because of muscle symptoms. These data emphasize the importance of enhancing the capabilities of clinicians and health systems for identifying and reducing statin drug interactions.

  John J.P. Kastelein , Kevin C. Maki , Andrey Susekov , Marat Ezhov , Borge G. Nordestgaard , Ben N. Machielse , Douglas Kling and Michael H. Davidson
 

Background

Omega-3 fatty acids in free fatty acid form have enhanced bioavailability, and plasma levels are less influenced by food than for ethyl ester forms.

Objective

The aim was to evaluate the safety and lipid-altering efficacy in subjects with severe hypertriglyceridemia of an investigational pharmaceutical omega-3 free fatty acid (OM3-FFA) containing eicosapentaenoic acid and docosahexaenoic acid.

Methods

This was a multinational, double-blind, randomized, out-patient study. Men and women with triglycerides (TGs) ≥500 mg/dL, but <2000 mg/dL, took control (olive oil [OO] 4 g/d; n = 99), OM3-FFA 2 g/d (plus OO 2 g/d; n = 100), OM3-FFA 3 g/d (plus OO 1 g/d; n = 101), or OM3-FFA 4 g/d (n = 99) capsules for 12 weeks in combination with the National Cholesterol Education Program Therapeutic Lifestyle Changes diet.

Results

Fasting serum TGs changed from baseline by −25.9% (P < .01 vs OO), −25.5% (P < .01 vs OO), and −30.9% (P < .001 vs OO) with 2, 3, and 4 g/d OM3-FFA, respectively, compared with −4.3% with OO. Non-high-density lipoprotein cholesterol (non-HDL-C), total cholesterol-to-HDL-C ratio, very low-density lipoprotein cholesterol, remnant-like particle cholesterol, apolipoprotein CIII, lipoprotein-associated phospholipase A2, and arachidonic acid were significantly lowered (P < .05 at each OM3-FFA dosage vs OO); and plasma eicosapentaenoic acid and docosahexaenoic acid were significantly elevated (P < .001 at each OM3-FFA dosage vs OO). With OM3-FFA 2 and 4 g/d (but not 3 g/d), low-density lipoprotein cholesterol was significantly increased compared with OO (P < .05 vs OO). High-sensitivity C-reactive protein responses with OM3-FFA did not differ significantly from the OO response at any dosage. Fewer subjects reported any adverse event with OO vs OM3-FFA, but frequencies across dosage groups were similar. Discontinuation due to adverse event, primarily gastrointestinal, ranged from 5% to 7% across OM3-FFA dosage groups vs 0% for OO.

Conclusions

OM3-FFA achieved the primary end point for TG lowering and secondary end point of non-HDL-C lowering at 2, 3, and 4 g/d in persons with severe hypertriglyceridemia. This trial was registered at www.clinicaltrials.gov as NCT01242527.

  Terry A. Jacobson , Matthew K. Ito , Kevin C. Maki , Carl E. Orringer , Harold E. Bays , Peter H. Jones , James M. McKenney , Scott M. Grundy , Edward A. Gill , Robert A. Wild , Don P. Wilson and W. Virgil Brown
  Various organizations and agencies have issued recommendations for the management of dyslipidemia. Although many commonalities exist among them, material differences are present as well. The leadership of the National Lipid Association (NLA) convened an Expert Panel to develop a consensus set of recommendations for patient-centered management of dyslipidemia in clinical medicine. The current Executive Summary highlights the major conclusions in Part 1 of the recommendations report of the NLA Expert Panel and includes: (1) background and conceptual framework for formulation of the NLA Expert Panel recommendations; (2) screening and classification of lipoprotein lipid levels in adults; (3) targets for intervention in dyslipidemia management; (4) atherosclerotic cardiovascular disease risk assessment and treatment goals based on risk category; (5) atherogenic cholesterol-non-high-density lipoprotein cholesterol and low-density lipoprotein cholesterol-as the primary targets of therapy; and (6) lifestyle and drug therapies intended to reduce morbidity and mortality associated with dyslipidemia.
 
 
 
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