High density lipoprotein complete list of trials

Jump to navigation Jump to search

High Density Lipoprotein Microchapters

Home

Patient information

Overview

Historical Perspective

Classification

Physiology

Pathophysiology

Causes

Low HDL
High HDL

Epidemiology and Demographics

Screening

Natural History, Complications and Prognosis

Diagnosis

HDL Laboratory Test

Treatment

Medical Therapy

Prevention

Future or Investigational Therapies

Clinical Trials

Landmark Trials

List of All Trials

Case Studies

Case #1

High density lipoprotein complete list of trials On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of High density lipoprotein complete list of trials

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on High density lipoprotein complete list of trials

CDC on High density lipoprotein complete list of trials

High density lipoprotein complete list of trials in the news

Blogs on High density lipoprotein complete list of trials

Directions to Hospitals Treating High density lipoprotein

Risk calculators and risk factors for High density lipoprotein complete list of trials

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]; Raviteja Guddeti, M.B.B.S. [3]

Landmark Trials

VA-HIT Trial

  • OBJECTIVE: To conclude if changes in plasma lipid levels due to gemfibrozil is the cause for reduction in major cardiovascular events in VA-HIT trial.
  • METHOD: VA-HIT (Veterans Affairs HDL Intervention Trial) trial is a multicentered, randomized, double-blinded, placebo-controlled trial wherein 2531 patients with CAD along with LDL levels ≤140 mg/dL (mean 111 mg/dL) and HDL ≤40 mg/dL (mean 32 mg/dL) were randomly assigned to treatment with gemfibrozil or placebo.
  • RESULTS: At one year the following findings were noted in the group treated with gemfibrozil:
    • Mean HDL-C level was higher by 6%
    • 31% lower mean TG concentration
    • Mean total cholesterol was 4% lower

At five years, the combined primary end point of cardiac death and non-fatal myocardial infarction occurred in 17.3% versus 21.7% in the placebo group. Acute coronary events reduced by 11% with gemfibrozil for every 5 mg/dL rise in HDL-C, but the reduction was independent of changes in LDL-C and triglyceride levels.

  • CONCLUSION: Low HDL-C levels strongly and independently predict the occurrence of coronary events which were reduced by treatment with gemfibrozil.[1][2][3][4]

AIM-HIGH Trial[5]

  • OBJECTIVE: To assess if niacin + simvastatin combination is superior to simvastatin alone in raising low levels of high density lipoprotein (HDL).
  • METHOD: AIM-HIGH is a randomized trial wherein 3414 patients randomly received either extended release niacin (1500 to 2000 md per day) or a matching placebo. All patients received simvastatin 40 to 80 mg daily to maintain an LDL-C level in the range of 40-80 mg/dL. Ezetimibe 10 mg daily was added, if needed, to achieve the LDL goal. The primary end point was the first event of the composite of death from coronary heart disease, nonfatal myocardial infarction, ischemic stroke, hospitalization for an acute coronary syndrome, or symptom-driven coronary or cerebral revascularization.
  • RESULTS: The trial was stopped prematurely for futility after a follow-up of 36 months. At two years compared to placebo, niacin increased HDL-C levels and reduced triglyceride and LDL-C levels but there was no reduction in the rate of primary endpoint or all-cause mortality with niacin. Moreover, there was a trend towards more ischemic strokes in the niacin group. This led to the decision to halt the trial prematurely.
  • CONCLUSION: No incremental clinical benefit was observed from addition of niacin to simvastatin during a 36 month follow-up. Also, elevations in HDL-C levels in the placebo group were higher than expected which may have reduced the competency of the trial to detect a real benefit with niacin therapy.[6][7][8][9][10]

Trial of Simvastatin Plus Niacin

  • OBJECTIVE: To suggest that additional benefits may be observed in patients with low HDL-C by combining a statin with a drug that elevates HDL-C.
  • METHOD: This was a three year randomized trial that enrolled 160 patients with clinical and angiographic evidence of coronary artery disease who had an HDL-C <35 mg/dL and an LDL-C <145 mg/dL. Patients were randomly assigned into 4 groups: simvastatin plus niacin; antioxidants; simvastatin plus niacin plus antioxidants or placebo.
  • RESULTS: Mean serum LDL and HDL levels changed substantially in the simvastatin plus niacin group while levels in the antioxidants and placebo groups remained unaltered. Also, patients receiving simvastatin and niacin sustained lower cardiovascular events and experienced angiographic regression of the most significant coronary artery stenosis compared with patients receiving antioxidants or placebo.
  • CONCLUSION: Addition of a drug that increases HDL-C levels to a statin proves to have additional protection over just statin alone.

ARBITER 2 Trial[11]

  • OBJECTIVE: To assess if treatment with extended release niacin when added to statin monotherapy slows progression of atherosclerosis among individuals with known coronary artery disease (CAD) and moderately low HDL-C.
  • METHOD: ARBITER (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol) 2 was a double blinded randomized placebo controlled study of once daily extended release niacin (1000 mg). 167 patients with known CAD and moderately low HDL-C were enrolled in this study and were assessed for the primary end-point carotid intima-media thickness (CIMT) at the end of one year.
  • RESULTS: At the end of 12 months mean CIMT significantly increased in the placebo group but not in the niacin group. Niacin significantly reduced the rate of IMT progression in patients without insulin resistance. Patients treated with niacin had a significant increase in HDL levels from a mean of 39 mg/dL to 47 mg/dL.
  • CONCLUSION: The addition of extended-release niacin to statin therapy slowed the progression of atherosclerosis among individuals with known coronary heart disease and moderately low HDL-C.

ARBITER 3 Trial[12]

  • OBJECTIVE: To study the effects of long term treatment with extended release niacin (ERN) on HDL levels and carotid intima- media thickness in patients who participated in ARBITER 2.
  • METHODS: 88% (149) of patients enrolled in ARBITER trial participated in ARBITER 3 trial, those who either were continued or crossed over to the placebo group. The long term effects of ERN on HDL cholesterol and carotid intima- media thickness were examined during 12- 24 months of treatment.
  • RESULTS:
    • The ERN group showed an increase in HDL-C levels along with modest reductions in LDL-C and triglycerides.
    • A net regression in CMIT was seen in patients treated with ENC for 12 months.
    • An additional regression was noted in patients treated with ENC for 24 months.
    • Changes in HDL-C were independently associated with regression of CIMT, controlling for changes in LDL and triglycerides.
  • CONCLUSIONS: ERN when added to statin therapy significantly increases HDL levels and induces atherosclerosis regression. Open label design and inability to correlate CIMT effects to clinical outcomes were the limitations of this study.

CLAS Trial[13][14][15][16]

  • OBJECTIVE: To determine whether combined therapy with the lipid lowering agents colestipol hydrochloride plus niacin would produce significant change in coronary, carotid, and femoral artery atherosclerosis and coronary bypass graft lesions as determined by angiography. Also, to determine possible correlations between lesion changes and plasma lipid and lipoprotein cholesterol levels and to explore interrelationships of atherosclerosis change in femoral, coronary, and carotid arteries.
  • METHOD: CLAS (Cholesterol Lowering Atherosclerosis Study) was a randomized, selectively blinded study wherein 188 men, with known previous coronary artery bypass grafts, were randomized to diet plus placebo or diet plus combined lipid lowering therapy consisting of colestipol and niacin and followed up at 2 years and 4 years.
  • RESULTS: The following results were noted:[17]
    • Treatment group had a 37% raise in HDL-C levels and a 43% reduction in LDL-C levels.
    • Regression of atherosclerosis, as measured by angiography, was greater with combined drug treatment at 2 years and at 4 years.
    • Reduction in the percentage of subjects with new atheroma formation in native coronary arteries.
    • Significantly reduced percentage of subjects with new lesions or any adverse change in bypass grafts.
    • Atherosclerosis regression occurred in 16.2% of colestipol-niacin treated vs 2.4% placebo treated
  • CONCLUSION: The benefit of combined nicotinic acid and colestipol therapy was most prominent in patients with baseline plasma cholesterol levels above 240 mg/dL.

FATS Trial[18][19][20][21][22][23][24]

  • OBJECTIVE: To compare the effects of two intensive lipid altering therapies in men with familial combined hyperlipidemia as assessed by arteriography.
  • METHOD: Familial Atherosclerosis Treatment Study (FATS) is a randomized, double blinded, placebo controlled study wherein 146 men with one coronary stenosis of greater than 50 percent or three lesions of greater than 30 percent were enrolled and randomized into three groups. The groups included:
    • Placebo plus low dose colestipol (if needed, to lower LDL)
    • Niacin (1 g QID) plus colestipol (10 g TID)
    • Lovastatin (20 mg BID) plus colestipol (10 g TID)

The primary endpoint was a measure of change in the severity of disease in the proximal coronary arteries as measured by quantitative arteriography.

  • RESULTS: Both the intensive lipid lowering therapies were equally effective. Both reduced the frequency of progression of coronary lesions (21% and 25% versus 46% in the control group), increased the frequency of regression (32% and 39% versus 11%), and reduced the incidence of cardiovascular events in men with coronary artery disease who were at high risk for cardiovascular events.

REGRESS Trial[25][26][27][28]

  • OBJECTIVE: To evaluate the effects of cholesterol lowering therapy, using a hydroxymethyl glutaryl coenzyme A reductase inhibitor (pravastatin) in symptomatic men with coronary artery disease (CAD).
  • METHOD: Regression Growth Evaluation Statin Study (REGRESS) was a multicentred, prospective, double-blinded, randomized, placebo-controlled trial that enrolled 885 men with established coronary artery disease with total cholesterol levels in the range of 155 and 310 mg/dL. The patients were randomized into two groups, treatment and control and followed up for two years. Effect of pravastatin on progression and regression of coronary atherosclerosis was assessed by quantitative coronary arteriography. All the patients received routine antianginal treatment for the duration of the trial.
  • RESULTS: Percent diameter stenosis before angioplasty was 78 +/- 14% (mean +/- SD) in the pravastatin group and 80 +/- 14% in the placebo group (p = 0.46). At follow-up, the percent diameter stenosis was 32 +/- 23% in the pravastatin group and 45 +/- 29% in the placebo group (p < 0.001). Clinical restenosis was significantly lower in the pravastatin group (7%) compared with the placebo group (29%) (p < 0.001).
  • CONCLUSIONS: In symptomatic men with significant coronary artery disease and normal to moderately elevated serum cholesterol, less progression of coronary atherosclerosis and fewer new cardiovascular events were observed in the group of patients treated with pravastatin than in the placebo group.

BECAIT Trial[29][30][31][32]

  • OBJECTIVE: To evaluate if bezafibrate could slow the progression of coronary stenoses in dyslipidemic male survivors of myocardial infarction who were younger than 45 years at the time of the event.
  • METHOD: The Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT) was a randomized, double-blinded, placebo-controlled trial over 5 years to assess the angiographic benefits of bezafibrate retard (400 mg a day) in 92 young (45 yrs), male, post-myocardial infarction (post-MI) patients with dyslipidemia (fasting serum cholesterol concentration above 240 mg/dL and triglyceride concentration above 141 mg/dL).
  • RESULTS:
    • Bezafibrate reduced the levels of LDL-C and triglycerides by 53% and 46% respectively
    • Plasma apolipoprotein (apo) B levels reduced by 9%
    • HDL3 levels rose by 9%
  • CONCLUSION: The effect of bezafibrate on progression of focal coronary atherosclerosis could be at least partly attributed to a rise in HDL3 cholesterol and a decrease in the total number of apo B-containing lipoproteins. Treatment with bezafibrate also significantly reduced the levels of insulin-like growth factor (IGF-1) which is one another factor associated with disease progression.

GAIN Trial[33]

  • This trial studied the effects of atorvastatin on the progression of atherosclerosis, assessed by intra-coronary ultrasound in 131 patients.
  • After a 12 month follow-up period, it was found that atorvastatin reduced the progression of mean plaque volume (1.2 versus 9.6 mm3 for placebo). Also, the drug increased the hyperechogenicity of the plaque which indicates a change in plaque composition from lipid-rich core to fibrotic or calcified. This change in composition of the plaque corresponds to increased plaque stability and a reduced tendency for rupture.

HARP Study[34][35][36][37]

  • OBJECTIVE: The Harvard Atherosclerosis Reversibility Project (HARP) aimed at studying the effect of intensive lipid lowering therapy in normocholesterolemic patients and its effect on angiographic progression of atherosclerosis.
  • METHOD: HAPR was a randomized placebo-controlled trial wherein 91 normocholesterolemic patients, with total serum cholesterol levels less than 250 mg/dL, were selected and treated with a stepwise regimen of diet, pravastatin, nicotinic acid, cholestyramine and gemfibrozil for 2.5 years. Repeat coronary angiograms were performed to assess the progression of coronary atherosclerosis.
  • RESULTS: The study found a significant improvement in total cholesterol, LDL-C and HDL-C levels, however repeat coronary angiograms did not show significant differences in the degree of coronary obstruction, progression of coronary stenosis, regression and clinical cardiac events.
  • CONCLUSION: This study concluded that intensive lipid lowering therapy does not alter the rate of progression of coronary stenoses in normocholesterolemic patients.

SCAT Trial[38][39][40]

  • OBJECTIVE: To assess the effects of cholesterol lowering and angiotensin-converting enzyme inhibition on coronary atherosclerosis in normocholesterolemic patients.
  • METHOD: The Simvastatin/Enalapril Coronary Atherosclerosis Trial (SCAT) was a multicentered, randomized, double blinded, placebo-controlled angiographic trial wherein a total of 460 normocholesterolemic patients were enrolled. 230 received simvastatin, 230 a simvastatin placebo, 229 enalapril and 231 an enalapril placebo. All the patients were followed up for an average time period of 47.8 months.
  • RESULTS and CONCLUSION: Less progression was observed in patients receiving simvastatin compared to those receiving placebo. On quantitative coronary angiography the change in mean diameter, minimum diameter, percentage stenosis and the need for angioplasty was less with simvastatin. No additional benefit was observed with enalapril therapy.

REVERSAL Trial

  • OBJECTIVE: To compare the effects of pravastatin and atorvastatin on coronary artery plaque burden and progression by intensive lipid lowering.
  • METHOD: Reversal of Atherosclerosis with Aggressive Lipid Lowering [REVERSAL] was a multicentered, randomized, double- blinded trial wherein 654 patients received the study drug. IVUS examinations were performed at baseline and after 18 months of treatment in 502 patients. Patients randomly received either 40 mg pravastatin or 80 mg of atorvastatin.
  • RESULTS: The mean LDL-C levels reduced from 150 to 110 mg/dL in the pravastatin group and to 79 mg/dL in the atorvastatin. Percentage change in atheroma volume showed a significantly lower progression rate in the atorvastatin (intensive) group compared to the pravastatin group.
  • CONCLUSIONS: In patients with coronary artery disease, atorvastatin reduced progression of coronary atherosclerosis compared with pravastatin.

ASTEROID Trial

  • OBJECTIVE: To assess if an extensive lipid lowering therapy with statins could regress coronary atherosclerosis as determined by IVUS imaging.
  • METHOD: A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden (ASTEROID) was a prospective open-label blinded end-points trial wherein 507 patients, who had a baseline IVUS examination, received at least 1 dose of the study drug rosuvastatin 40 mg/dL and were followed up for 24 months. At the end of 24 months 349 patients had evaluable serial IVUS examinations.
  • RESULTS: Mean baseline LDL-C reduced by 53.2% and mean HDL-C improved by 14.7%. Also mean atheroma volume for the entire vessel, as assessed by intravascular ultrasound, reduced by 0.98%.
  • CONCLUSION: The study showed that treatment with very high intensity statin therapy using rosuvastatin 40 mg/dL reduced LDL-C and improved HDL-C levels significantly resulting in regression of coronary atherosclerosis as measured by IVUS.

Trials on Investigational Therapies

ERASE Trial[41]

  • OBJECTIVE: To study the effects of reconstituted HDL on atheromatous plaque volume.
  • METHOD: This was a randomized placebo-controlled trial conducted in 17 centers across Canada. An intravascular ultrasound was performed at baseline and at 2 to 3 weeks after the last infusion to assess plaque burden.
  • RESULTS: The group with higher doses of reconstituted HDL (CSL-111) was eliminated from the study because of mild liver function test abnormalities. The results of the study are briefed below:
    • Percentage change in plaque volume: -3.4% with CSL-111 and -1.6% with placebo (P= 0.48 between the groups, P< 0.001 vs baseline for CSL-111)
    • Nominal change in plaque volume: -5.3% with CSL-111 and -2.3% with placebo (P= 0.39 between the groups, P< 0.001 vs baseline for CSL-111)
    • Mean changes in plaque characterization on IVUS: −0.0097 for CSL-111 and 0.0128 with placebo (P = .01)
    • Mean changes in coronary score on quantitative coronary angiography: −0.039 mm for CSL-111 and −0.071 mm with placebo (P= 0.03)
  • CONCLUSIONS: Short term infusions of reconstituted HDL (CSL-111) resulted in:
    • No significant reductions in percentage change and nominal change in plaque volume compared to placebo.
    • Statistically significant improvement in mean changes in plaque characterization on IVUS and coronary score on quantitative coronary angiography, compared to placebo.

Infusion of Apo A-1 Milano[42]

  • OBJECTIVE: To study the effects of Apo A-1 Milano on plaque burden on arteries.
  • METHOD: Apo A-1 was infused in cholesterol fed rabbits and showed a decreased intimal thickness and macrophage content after balloon injury in femoral and iliac arteries. Based on these results, another pilot trial was designed using recombinant Apo A-1 Milano phospholipid complex (ETC-216) in 57 patients within two weeks of the onset of acute coronary syndrome. Subjects were randomly assigned to the ETC 216 infusion group at 15 mg/kg or 45 mg/kg or to placebo group. IVUS was performed at baseline and repeated at the completion of the study.
  • RESULTS: Treatment with ETC-216 (in both doses) resulted in a significant decrease in mean percentage of coronary artery volume occupied by atheroma as well as the total atheroma volume. Whereas the placebo group did not show any significant change.
  • CONCLUSIONS: Although Apo A-1 Milano infusions resulted in decrease in plaque burden, further study is required assess efficacy, safety and cost-effectiveness.

References

  1. ↑ Robins SJ, Collins D, Nelson JJ, Bloomfield HE, Asztalos BF (2008). "Cardiovascular events with increased lipoprotein-associated phospholipase A(2) and low high-density lipoprotein-cholesterol: the Veterans Affairs HDL Intervention Trial". Arterioscler. Thromb. Vasc. Biol. 28 (6): 1172–8. doi:10.1161/ATVBAHA.107.160739. PMID 18356553. Unknown parameter |month= ignored (help)
  2. ↑ Asztalos BF, Collins D, Horvath KV, Bloomfield HE, Robins SJ, Schaefer EJ (2008). "Relation of gemfibrozil treatment and high-density lipoprotein subpopulation profile with cardiovascular events in the Veterans Affairs High-Density Lipoprotein Intervention Trial". Metab. Clin. Exp. 57 (1): 77–83. doi:10.1016/j.metabol.2007.08.009. PMC 2194640. PMID 18078862. Unknown parameter |month= ignored (help)
  3. ↑ Peloso GM, Demissie S, Collins D; et al. (2010). "Common genetic variation in multiple metabolic pathways influences susceptibility to low HDL-cholesterol and coronary heart disease". J. Lipid Res. 51 (12): 3524–32. doi:10.1194/jlr.P008268. PMC 2975725. PMID 20855565. Unknown parameter |month= ignored (help)
  4. ↑ Robins SJ, Collins D, McNamara JR, Bloomfield HE (2008). "Body weight, plasma insulin, and coronary events with gemfibrozil in the Veterans Affairs High-Density Lipoprotein Intervention Trial (VA-HIT)". Atherosclerosis. 196 (2): 849–55. doi:10.1016/j.atherosclerosis.2007.01.029. PMID 17335828. Unknown parameter |month= ignored (help)
  5. ↑ Boden WE, Probstfield JL, Anderson T; et al. (2011). "Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy". N. Engl. J. Med. 365 (24): 2255–67. doi:10.1056/NEJMoa1107579. PMID 22085343. Unknown parameter |month= ignored (help)
  6. ↑ Michos ED, Sibley CT, Baer JT, Blaha MJ, Blumenthal RS (2012). "Niacin and statin combination therapy for atherosclerosis regression and prevention of cardiovascular disease events: reconciling the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome With Low HDL/High Triglycerides: Impact on Global Health Outcomes) trial with previous surrogate endpoint trials". J. Am. Coll. Cardiol. 59 (23): 2058–64. doi:10.1016/j.jacc.2012.01.045. PMID 22520249. Unknown parameter |month= ignored (help)
  7. ↑ Brinton EA (2012). "Search and rescue for hypotheses surviving AIM-HIGH, the niacin therapy earthquake: still problematic after the primary publication". J Clin Lipidol. 6 (4): 312–7. doi:10.1016/j.jacl.2012.03.005. PMID 22836067.
  8. ↑ Nicholls SJ (2012). "The AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome With Low HDL/High Triglycerides: Impact on Global Health Outcomes) trial: to believe or not to believe?". J. Am. Coll. Cardiol. 59 (23): 2065–7. doi:10.1016/j.jacc.2012.02.021. PMID 22520248. Unknown parameter |month= ignored (help)
  9. ↑ Nicholls SJ (2012). "Is niacin ineffective? Or did AIM-HIGH miss its target?". Cleve Clin J Med. 79 (1): 38–43. doi:10.3949/ccjm.79a.11166. PMID 22219232. Unknown parameter |month= ignored (help)
  10. ↑ Sharma M (2011). "Combination therapy for dyslipidemia". Curr. Opin. Cardiol. 26 (5): 420–3. doi:10.1097/HCO.0b013e3283499ef1. PMID 21832894. Unknown parameter |month= ignored (help)
  11. ↑ Taylor AJ, Sullenberger LE, Lee HJ, Lee JK, Grace KA (2004). "Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2: a double-blind, placebo-controlled study of extended-release niacin on atherosclerosis progression in secondary prevention patients treated with statins". Circulation. 110 (23): 3512–7. doi:10.1161/01.CIR.0000148955.19792.8D. PMID 15537681. Unknown parameter |month= ignored (help)
  12. ↑ Taylor AJ, Lee HJ, Sullenberger LE (2006). "The effect of 24 months of combination statin and extended-release niacin on carotid intima-media thickness: ARBITER 3". Current Medical Research and Opinion. 22 (11): 2243–50. doi:10.1185/030079906X148508. PMID 17076985. Unknown parameter |month= ignored (help)
  13. ↑ Cashin-Hemphill L, Mack WJ, Pogoda JM, Sanmarco ME, Azen SP, Blankenhorn DH (1990). "Beneficial effects of colestipol-niacin on coronary atherosclerosis. A 4-year follow-up". JAMA. 264 (23): 3013–7. PMID 2243429. Unknown parameter |month= ignored (help)
  14. ↑ Azen SP, Mack WJ, Cashin-Hemphill L; et al. (1996). "Progression of coronary artery disease predicts clinical coronary events. Long-term follow-up from the Cholesterol Lowering Atherosclerosis Study". Circulation. 93 (1): 34–41. PMID 8616937. Unknown parameter |month= ignored (help)
  15. ↑ Blankenhorn DH, Johnson RL, Nessim SA, Azen SP, Sanmarco ME, Selzer RH (1987). "The Cholesterol Lowering Atherosclerosis Study (CLAS): design, methods, and baseline results". Control Clin Trials. 8 (4): 356–87. PMID 3327654. Unknown parameter |month= ignored (help)
  16. ↑ Blankenhorn DH, Azen SP, Crawford DW; et al. (1991). "Effects of colestipol-niacin therapy on human femoral atherosclerosis". Circulation. 83 (2): 438–47. PMID 1991366. Unknown parameter |month= ignored (help)
  17. ↑ Blankenhorn DH, Nessim SA, Johnson RL, Sanmarco ME, Azen SP, Cashin-Hemphill L (1987). "Beneficial effects of combined colestipol-niacin therapy on coronary atherosclerosis and coronary venous bypass grafts". JAMA. 257 (23): 3233–40. PMID 3295315. Unknown parameter |month= ignored (help)
  18. ↑ Brown G, Albers JJ, Fisher LD; et al. (1990). "Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B". N. Engl. J. Med. 323 (19): 1289–98. doi:10.1056/NEJM199011083231901. PMID 2215615. Unknown parameter |month= ignored (help)
  19. ↑ Zhao XQ, Brown BG, Hillger L; et al. (1993). "Effects of intensive lipid-lowering therapy on the coronary arteries of asymptomatic subjects with elevated apolipoprotein B". Circulation. 88 (6): 2744–53. PMID 8252687. Unknown parameter |month= ignored (help)
  20. ↑ Phan BA, Muñoz L, Shadzi P; et al. (2013). "Effects of niacin on glucose levels, coronary stenosis progression, and clinical events in subjects with normal baseline glucose levels (<100 mg/dl): a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), HDL-Atherosclerosis Treatment Study (HATS), Armed Forces Regression Study (AFREGS), and Carotid Plaque Composition by MRI during lipid-lowering (CPC) study". Am. J. Cardiol. 111 (3): 352–5. doi:10.1016/j.amjcard.2012.09.034. PMID 23168285. Unknown parameter |month= ignored (help)
  21. ↑ Stewart BF, Brown BG, Zhao XQ; et al. (1994). "Benefits of lipid-lowering therapy in men with elevated apolipoprotein B are not confined to those with very high low density lipoprotein cholesterol". J. Am. Coll. Cardiol. 23 (4): 899–906. PMID 8106695. Unknown parameter |month= ignored (help)
  22. ↑ Brown BG, Hillger L, Zhao XQ, Poulin D, Albers JJ (1995). "Types of change in coronary stenosis severity and their relative importance in overall progression and regression of coronary disease. Observations from the FATS Trial. Familial Atherosclerosis Treatment Study". Ann. N. Y. Acad. Sci. 748: 407–17, discussion 417–8. PMID 7695184. Unknown parameter |month= ignored (help)
  23. ↑ Maher VM, Brown BG, Marcovina SM, Hillger LA, Zhao XQ, Albers JJ (1995). "Effects of lowering elevated LDL cholesterol on the cardiovascular risk of lipoprotein(a)". JAMA. 274 (22): 1771–4. PMID 7500507. Unknown parameter |month= ignored (help)
  24. ↑ Zambon A, Hokanson JE, Brown BG, Brunzell JD (1999). "Evidence for a new pathophysiological mechanism for coronary artery disease regression: hepatic lipase-mediated changes in LDL density". Circulation. 99 (15): 1959–64. PMID 10208998. Unknown parameter |month= ignored (help)
  25. ↑ Jukema JW, Bruschke AV, van Boven AJ; et al. (1995). "Effects of lipid lowering by pravastatin on progression and regression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. The Regression Growth Evaluation Statin Study (REGRESS)". Circulation. 91 (10): 2528–40. PMID 7743614. Unknown parameter |month= ignored (help)
  26. ↑ van Boven AJ, Jukema JW, Zwinderman AH, Crijns HJ, Lie KI, Bruschke AV (1996). "Reduction of transient myocardial ischemia with pravastatin in addition to the conventional treatment in patients with angina pectoris. REGRESS Study Group". Circulation. 94 (7): 1503–5. PMID 8840836. Unknown parameter |month= ignored (help)
  27. ↑ Mulder HJ, Bal ET, Jukema JW; et al. (2000). "Pravastatin reduces restenosis two years after percutaneous transluminal coronary angioplasty (REGRESS trial)". Am. J. Cardiol. 86 (7): 742–6. PMID 11018193. Unknown parameter |month= ignored (help)
  28. ↑ Barth JD, Zonjee MM (1992). "Regression growth evaluation statin study (REGRESS): study design and baseline characteristics in 600 patients. The REGRESS Research Group". Can J Cardiol. 8 (9): 925–32. PMID 1486543. Unknown parameter |month= ignored (help)
  29. ↑ Ruotolo G, Ericsson CG, Tettamanti C; et al. (1998). "Treatment effects on serum lipoprotein lipids, apolipoproteins and low density lipoprotein particle size and relationships of lipoprotein variables to progression of coronary artery disease in the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT)". J. Am. Coll. Cardiol. 32 (6): 1648–56. PMID 9822092. Unknown parameter |month= ignored (help)
  30. ↑ de Faire U, Ericsson CG, Hamsten A, Nilsson J (1995). "Design features of a five-year Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT)". Drugs Exp Clin Res. 21 (3): 105–24. PMID 7555614.
  31. ↑ Ericsson CG, Hamsten A, Nilsson J, Grip L, Svane B, de Faire U (1996). "Angiographic assessment of effects of bezafibrate on progression of coronary artery disease in young male postinfarction patients". Lancet. 347 (9005): 849–53. PMID 8622389. Unknown parameter |month= ignored (help)
  32. ↑ Ericsson CG (1998). "Results of the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT) and an update on trials now in progress". Eur. Heart J. 19 Suppl H: H37–41. PMID 9717064. Unknown parameter |month= ignored (help)
  33. ↑ Schartl M, Bocksch W, Koschyk DH; et al. (2001). "Use of intravascular ultrasound to compare effects of different strategies of lipid-lowering therapy on plaque volume and composition in patients with coronary artery disease". Circulation. 104 (4): 387–92. PMID 11468198. Unknown parameter |month= ignored (help)
  34. ↑ Sacks FM, Pasternak RC, Gibson CM, Rosner B, Stone PH (1994). "Effect on coronary atherosclerosis of decrease in plasma cholesterol concentrations in normocholesterolaemic patients. Harvard Atherosclerosis Reversibility Project (HARP) Group". Lancet. 344 (8931): 1182–6. PMID 7934538. Unknown parameter |month= ignored (help)
  35. ↑ Sacks FM, Stone PH, Gibson CM, Silverman DI, Rosner B, Pasternak RC (1995). "Controlled trial of fish oil for regression of human coronary atherosclerosis. HARP Research Group". J. Am. Coll. Cardiol. 25 (7): 1492–8. PMID 7759696. Unknown parameter |month= ignored (help)
  36. ↑ Sacks FM, Gibson CM, Rosner B, Pasternak RC, Stone PH (1995). "The influence of pretreatment low density lipoprotein cholesterol concentrations on the effect of hypocholesterolemic therapy on coronary atherosclerosis in angiographic trials. Harvard Atherosclerosis Reversibility Project Research Group". Am. J. Cardiol. 76 (9): 78C–85C. PMID 7572692. Unknown parameter |month= ignored (help)
  37. ↑ Pasternak RC, Brown LE, Stone PH, Silverman DI, Gibson CM, Sacks FM (1996). "Effect of combination therapy with lipid-reducing drugs in patients with coronary heart disease and "normal" cholesterol levels. A randomized, placebo-controlled trial. Harvard Atherosclerosis Reversibility Project (HARP) Study Group". Ann. Intern. Med. 125 (7): 529–40. PMID 8815751. Unknown parameter |month= ignored (help)
  38. ↑ Teo KK, Burton JR, Buller CE; et al. (2000). "Long-term effects of cholesterol lowering and angiotensin-converting enzyme inhibition on coronary atherosclerosis: The Simvastatin/Enalapril Coronary Atherosclerosis Trial (SCAT)". Circulation. 102 (15): 1748–54. PMID 11023927. Unknown parameter |month= ignored (help)
  39. ↑ Crawford DW, Barndt R, Back LH (1976). "Surface characteristics of normal and atherosclerotic human arteries including observations suggesting interaction between flow and intimal morphology". Lab. Invest. 34 (5): 463–70. PMID 1271748. Unknown parameter |month= ignored (help)
  40. ↑ Teo KK, Burton JR, Buller C, Plante S, Yokoyama S, Montague TJ (1997). "Rationale and design features of a clinical trial examining the effects of cholesterol lowering and angiotensin-converting enzyme inhibition on coronary atherosclerosis: Simvastatin/Enalapril Coronary Atherosclerosis Trial (SCAT). SCAT Investigators". Can J Cardiol. 13 (6): 591–9. PMID 9215232. Unknown parameter |month= ignored (help)
  41. ↑ Tardif JC, Grégoire J, L'Allier PL; et al. (2007). "Effects of reconstituted high-density lipoprotein infusions on coronary atherosclerosis: a randomized controlled trial". JAMA : the Journal of the American Medical Association. 297 (15): 1675–82. doi:10.1001/jama.297.15.jpc70004. PMID 17387133. Unknown parameter |month= ignored (help)
  42. ↑ Nissen SE, Tsunoda T, Tuzcu EM; et al. (2003). "Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial". JAMA : the Journal of the American Medical Association. 290 (17): 2292–300. doi:10.1001/jama.290.17.2292. PMID 14600188. Unknown parameter |month= ignored (help)

Template:WikiDoc Sources

Retrieved from "https://www.wikidoc.org/index.php?title=High_density_lipoprotein_complete_list_of_trials&oldid=872719"