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Articles by Peter H. Jones
Total Records ( 11 ) for Peter H. Jones
  Venkat Polsani , Christie M. Ballantyne , Peter H. Jones , Vijay Nambi , Salim S. Virani and Daniele Zoch
  not available
  Peter H. Jones , Susan M. Buttler , Michael H. Davidson , Moti L. Kashyap , Maureen T. Kelly , Carolyn M. Setze , Darryl J. Sleep and James C. Stolzenbach
  not available
  Peter H. Jones , Dawn M. Carlson , Thomas Dayspring , Maureen T. Kelly , Aditya Lele , Carolyn M. Setze and Darryl J. Sleep
  not available
  Harold E. Bays , Peter H. Jones , Syed M. Mohiuddin , Maureen T. Kelly , Hsiaoming Sun , Carolyn M. Setze , Susan M. Buttler , Darryl J. Sleep and James C. Stolzenbach
 

Background

Co-administration of a fibrate and statin is an effective treatment option for patients with multiple lipid abnormalities, yet adequate long-term safety and efficacy data are lacking.

Objective

To evaluate the long-term safety and efficacy of fenofibric acid combined with statins in adults with mixed dyslipidemia.

Methods

Three large, 12-week, phase three, double-blind, randomized, controlled trials evaluated fenofibric acid 135 mg combined with a low- or moderate-dose statin compared to fenofibric acid or statin monotherapy, and a subsequent 52-week open-label extension study evaluated fenofibric acid 135 mg combined with moderate-dose statin (rosuvastatin 20 mg, simvastatin 40 mg, or atorvastatin 40 mg). This prespecified analysis integrated results from these studies to assess the long-term safety and efficacy of combination therapy.

Results

Across the controlled studies and the extension study, 2201 patients received at least one dose of fenofibric acid + statin for a median duration of 364 days. The most common adverse events were headache, upper respiratory tract infection, nasopharyngitis, and back pain, with the incidence of all adverse events being similar across all combination therapy treatment groups. Rhabdomyolysis or treatment-related death was not reported in any group. Combination therapy resulted in sustained improvements in multiple lipid parameters, including triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, total cholesterol, apolipoprotein B, and high-sensitivity C-reactive protein.

Conclusion

Long-term fenofibric acid + statin combination therapy was generally well tolerated and resulted in comprehensive and sustained improvements in multiple lipid parameters in adults with mixed dyslipidemia.

  Peter H. Jones , Michael H. Davidson , Anne C. Goldberg , Carl J. Pepine , Maureen T. Kelly , Susan M. Buttler , Carolyn M. Setze , Aditya Lele , Darryl J. Sleep and James C. Stolzenbach
 

Background

Patients with mixed dyslipidemia often require combination therapy to manage multiple lipid abnormalities.

Objective

To evaluate fenofibric acid in combination with a statin across three studies of patients with mixed dyslipidemia.

Methods

As prospectively planned, data were pooled from three randomized, double-blind, phase 3 studies of patients with low-density lipoprotein cholesterol (LDL-C) ≥130 mg/dL, triglycerides (TG) ≥150 mg/dL, and high-density lipoprotein cholesterol (HDL-C) <40 mg/dL (men) or <50 mg/dL (women). A total of 2715 patients were randomly assigned to 12-week treatment with fenofibric acid 135 mg monotherapy; low-, moderate-, or high-dose statin (rosuvastatin, simvastatin, or atorvastatin, depending on study) monotherapy; or fenofibric acid + low- or moderate-dose statin. The primary efficacy comparisons were mean percent change in HDL-C and TG (combination therapy vs. statin) and LDL-C (combination therapy vs. fenofibric acid).

Results

Fenofibric acid + low-dose statin increased HDL-C (18.1% vs. 7.4%) and reduced TG (−43.9% vs. −16.8%) versus low-dose statin monotherapy and reduced LDL-C (−33.1% vs. −5.1%) versus fenofibric acid monotherapy (P <.001 for all). Fenofibric acid + moderate-dose statin increased HDL-C (17.5% vs. 8.7%) and reduced TG (−42.0% vs. −23.7%) versus moderate-dose statin monotherapy and reduced LDL-C (−34.6% vs. −5.1%) versus fenofibric acid monotherapy (P <.001 for all). Combination therapy was generally well tolerated, and safety profiles were similar to monotherapies. No rhabdomyolysis was reported.

Conclusion

In patients with mixed dyslipidemia, combination therapy simultaneously improved multiple lipid abnormalities more effectively than fenofibric acid or statin monotherapies.

  Venkateshwar R. Polsani , Vijay Nambi , Salim S. Virani , Daniele Zoch , Eric Y. Yang , Peter H. Jones and Christie M. Ballantyne
 

Background

Although there is clinical evidence for the safety and efficacy of single-drug therapy and some two-drug combinations for the treatment of hypertriglyceridemia, information is limited on the use of more than 2 drugs.

Objective

We evaluated the efficacy and safety of multidrug regimens (≥3 agents) in the management of hypertriglyceridemia.

Methods

The study included 40 individuals in an academic lipid referral clinic with mean follow-up of 1.98 years and an average use of 3.5 medications.

Results

During the study, mean body mass index decreased significantly (P=.0127), from 29.2 kg/m2 to 28.7 kg/m2, and mean hemoglobin A1C showed a trend towards decreasing (P=.06), from 7.9% to 7.2% in patients with diabetes (n=17). All lipid parameters decreased significantly: total cholesterol level decreased significantly from (mean±SD) 334.3±282.9 mg/dL to 183.8±54.8 mg/dL (P=.001, mean reduction of 45%), mean (± SD) triglyceride level decreased significantly from 1900.9±4576.8 mg/dL to 300.7±372.2 mg/dL (P=.02), median (range) triglyceride level decreased from 599 (242-28,550) mg/dL to 301 (40-1960) mg/dL (P < .001, mean reduction of 50%), and mean (± SD) non-high-density lipoprotein cholesterol decreased significantly from 189.9±131.6 mg/dL to 138.4±49.1 mg/dL (P=.014, mean reduction of 27%). There were no serious adverse effects (rhabdomyolysis or increased liver function tests >3 times upper limit of normal).

Conclusion

In a 2-year follow-up of 40 individuals on multidrug therapy (average of 3.5 drugs) for severe hypertriglyceridemia, combination therapy was efficacious and well tolerated.

  Smita I. Negi , Lynne Steinberg , Venkateshwar R. Polsani , Saqib A. Gowani , Vijay Nambi , Varinder Kumar , Victor Marinescu , Peter H. Jones , Laura A. Petersen , Christie M. Ballantyne and Salim S. Virani
 

Background

Non-high density lipoprotein cholesterol (non-HDL-C) goal attainment per Adult Treatment Panel III (ATP III) guidelines remains low.

Objective

To understand gaps in knowledge and practices of physicians-in-training (internal medicine, family medicine, cardiology, endocrinology) towards non-HDL-C.

Methods

A survey based on a conceptual model to assess the trainee's knowledge, attitudes, and practice regarding non-HDL-C was developed and administered to physicians-in-training (n = 655) at 26 training programs in the United States. Responses of those in internal medicine and family medicine (residents-in-training; n = 418) were compared with those in cardiology and endocrinology (fellows-in-training; n = 124).

Results

Response rate was 83.7%. Fifty-three percent of residents and 31% of fellows-in-training had not read the ATP III guidelines (P < .001). Thirty-three percent of the residents and 35% fellows-in-training could not calculate non-HDL-C from a standard lipid panel (P = .7). Sixty-seven percent of the residents and 52% of fellows were not aware of treatment goals for non-HDL-C (P = .004 for comparison between residents and fellows). Both residents and fellows reported infrequent calculation of non-HDL-C levels in patients with elevated triglycerides (≥200 mg/dL; 32.5% vs 35.4%, respectively, P = .6). Lack of familiarity with ATP III guidelines, lack of knowledge regarding importance of non-HDL-C, lack of institutional mandate to calculate non-HDL-C, and lack of emphasis on non-HDL-C by teaching staff were reported as barriers to non-HDL-C use in routine clinical practice.

Conclusions

At least one-third of physicians-in-training could not calculate non-HDL-C from a standard lipid panel, and a large number were not aware of ATP III treatment goals pertaining to non-HDL-C. This area represents one for improvement if non-HDL-C is to be retained as a treatment target in the forthcoming ATP-IV guidelines.

  Eli M. Roth , Robert S. Rosenson , Peter H. Jones , Michael H. Davidson , Maureen T. Kelly , Carolyn M. Setze , Aditya Lele and Kamlesh Thakker
 

Background

Goal/desirable lipid levels are underachieved in patients with mixed dyslipidemia. These patients may have substantial residual risk of cardiovascular disease even while receiving optimal LDL-C-lowering therapy and may require additional therapy to improve multiple lipid/lipoprotein levels.

Objective

To evaluate attainment of goal/desirable levels of lipids/lipoproteins after 12-week treatment with combination rosuvastatin + fenofibric acid versus rosuvastatin monotherapy.

Methods

This was a post hoc analysis of patients with mixed dyslipidemia who enrolled in one of two randomized controlled trials, and were treated (N = 2066) with rosuvastatin (5, 10, or 20 mg), fenofibric acid 135 mg, or rosuvastatin + fenofibric acid for 12 weeks. Data were pooled across doses of rosuvastatin as monotherapy and combination therapy.

Results

Compared with rosuvastatin monotherapy, combination therapy had comparable effects in achieving risk-stratified LDL-C goals; however, measures of total atherogenic burden were improved because significantly greater percentages of patients attained non-HDL-C goal in high- (62.9% vs 50.4%, P = .006) and moderate-risk groups (87.6% vs 80.4%, P = .016) and apolipoprotein B (ApoB) <90 mg/dL in high-risk group (59.8% vs 43.8%, P < .001). In the overall population, more patients treated with the combination therapy achieved desirable levels of HDL-C >40/50 mg/dL in men/women (P < .001), triglycerides <150 mg/dL (P < .001), and ApoB <90 mg/dL (P < .001), compared with rosuvastatin monotherapy. Furthermore, combination therapy resulted in significantly greater percentages of patients achieving simultaneous specified levels of LDL-C + non-HDL-C (P < .015); LDL-C + HDL-C + TG (P < .001); and LDL-C + HDL-C + triglycerides + non-HDL-C + ApoB (P < .001), compared with rosuvastatin monotherapy.

Conclusion

Rosuvastatin + fenofibric acid may be more efficacious than rosuvastatin alone in patients with mixed dyslipidemia.

  Smita I. Negi , Ariel Brautbar , Salim S. Virani , Aashish Anand , Eliana Polisecki , Bela F. Asztalos , Christie M. Ballantyne , Ernst J. Schaefer and Peter H. Jones
  Tangier disease is a rare autosomal-recessive disorder caused by mutation in the ATP binding cassette transporter 1 (ABCA1) gene. Typically, Tangier disease manifests with symptoms and signs resulting from the deposition of cholesteryl esters in nonadipose tissues; chiefly, in peripheral nerves leading to neuropathy and in reticulo-endothelial organs, such as liver, spleen, lymph nodes, and tonsils, causing their enlargement and discoloration. An association with early cardiovascular disease can be variable. We describe a patient with a unique phenotype of Tangier disease from a novel splice site mutation in the ABCA1 gene that is associated with a central nervous system presentation resembling multiple sclerosis, and the presence of premature atherosclerosis.
  Madhuri Vasudevan , Urbain Tchoua , Baiba K. Gillard , Peter H. Jones , Christie M. Ballantyne and Henry J. Pownall
 

Background

Obesity-linked metabolic syndrome (MetS) is associated with a dyslipidemic profile that includes hypertriglyceridemia and low plasma high-density lipoprotein (HDL) cholesterol. HDL initiates reverse cholesterol transport via macrophage cholesterol efflux (MCE). Some hypothesize that dyslipidemic patients have impaired reverse cholesterol transport. MCE to patient plasma, a metric of HDL function, inversely correlates with atherosclerotic burden. Paradoxically, MCE to plasma of hypertriglyceridemic subjects is higher than that to normolipidemic (NL) plasma.

Objective

Although weight loss reduces dyslipidemia, its effect on MCE to the plasma of obese patients with MetS is unknown. Thus, we tested the hypothesis that reducing dyslipidemia with weight loss reduces the MCE capacity of MetS plasma to that of NL plasma.

Methods

Cholesterol efflux (MCE) from THP-1 macrophages to plasma from NL controls and to obese patients with MetS before and after weight loss was measured.

Results

MCE to plasma of obese patients with MetS was higher than that of control plasma (P = .006). Weight loss in patients with MetS (mean, -9.77 kg) reduced dyslipidemia, insulin resistance, and systolic blood pressure. HDL cholesterol was unchanged, and apolipoprotein A-I decreased with weight loss. Weight loss in patients with MetS normalized MCE (P < .001) to that of NL subjects. MCE correlated with apolipoprotein B levels (r2 = 0.13-0.38). Chromatography showed that macrophage cholesterol initially associates with HDL but accumulates in apolipoprotein B-containing lipoproteins at later times.

Conclusions

Although the initial acceptor of MCE is HDL, the elevated apolipoprotein B lipoproteins are a cholesterol sink that increases MCE in patients with MetS. Weight loss results in decreased apolipoprotein B lipoproteins and decreased MCE to plasma of patients with MetS.

  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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