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Matti Narkia

Vitamin B Niacin Offers No Additional Benefit To Statin Therapy In Seniors Already Diag... - 0 views

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    "The routine prescription of extended-release niacin, a B vitamin (1,500 milligrams daily), in combination with traditional cholesterol-lowering therapy offers no extra benefit in correcting arterial narrowing and diminishing plaque buildup in seniors who already have coronary artery disease, a new vascular imaging study from Johns Hopkins experts shows.

    In tests on 145 Baltimore-area men and women with existing atherosclerosis, all over age 65, researchers found that after 18 months of drug therapy, reductions in arterial wall thickness were measurably no different between the half who took dual niacin-statin therapy and the rest who remained on statin therapy alone. "
Matti Narkia

NEJM -- Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reacti... - 0 views

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    Conclusions In this trial of apparently healthy persons without hyperlipidemia but with elevated high-sensitivity C-reactive protein levels, rosuvastatin significantly reduced the incidence of major cardiovascular events. \n\nRosuvastatin to prevent vascular events in men and women with elevated C-reactive protein.\nRidker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ; JUPITER Study Group.\nN Engl J Med. 2008 Nov 20;359(21):2195-207. Epub 2008 Nov 9.\nPMID: 18997196
Matti Narkia

NEJM -- Expanding the Orbit of Primary Prevention -- Moving beyond JUPITER - 0 views

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    Expanding the orbit of primary prevention--moving beyond JUPITER.
    Hlatky MA.
    N Engl J Med. 2008 Nov 20;359(21):2280-2. Epub 2008 Nov 9.
    PMID: 18997195
Matti Narkia

Statins in the Water? Not So Fast - Well Blog - NYTimes.com - 0 views

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    Last week, Harvard researchers reported how healthy 50-year-old men and 60-year-old women could benefit from taking a statin even if they didn't have high cholesterol. The people they studied had high levels of C-reactive protein, or CRP, which is a marker for inflammation. The study showed that risk for major heart problems was cut by about 50 percent among the statin users.\n\nBut like many industry-sponsored drug studies, the results focused on something called "relative risk," which compares differences between study groups. Relative risk has the effect of exaggerating a drug's benefits. What does a 50 percent reduction in heart risk mean? It means that just one out of 120 statin users was helped by the drug.
Matti Narkia

Well - A Call for Caution in the Rush to Statins - NYTimes.com - 0 views

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    Judging by recent headlines, you might think so. Last week heart researchers reported that millions of healthy people could benefit from taking statins even if they don't have high cholesterol.\n\nAlthough many doctors hailed the study as a major breakthrough, a closer look at the research suggests that statins (like Crestor, from AstraZeneca, and Lipitor, from Pfizer) are far from magic pills. While they clearly save lives in people with a previous heart attack or other serious heart problems, for an otherwise healthy person the potential benefit remains small.
Matti Narkia

Cholesterol-Fighting Drugs Show Wider Benefit - New York Times - 0 views

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    CHART: Statins Reduce Risks: A study of 18,000 people with high levels of C-reactive protein, or CRP, found that the risk of a heart attack or stroke was cut in half among those who took a statin. The study was stopped after two years, but some participants were tracked for up to five years. (Sources: Dr. Paul M. Ridker; New England Journal of Medicine) (pg.A21)
    A large new study suggests that millions more people could benefit from taking the cholesterol-lowering drugs known as statins, even if they have low cholesterol, because the drugs can significantly lower their risk of heart attacks, strokes and death.

    The study, involving nearly 18,000 people worldwide, tested statin treatment in men 50 and older and in women 60 and older who did not have high cholesterol or histories of heart disease. What they did have was high levels of a protein called high-sensitivity C-reactive protein, or CRP, which indicates inflammation in the body.
Matti Narkia

NEJM -- Extended-Release Niacin or Ezetimibe and Carotid Intima-Media Thickness - 0 views

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    Extended-release niacin or ezetimibe and carotid intima-media thickness.
    Taylor AJ, Villines TC, Stanek EJ, Devine PJ, Griffen L, Miller M, Weissman NJ, Turco M.
    N Engl J Med. 2009 Nov 26;361(22):2113-22. Epub 2009 Nov 15.
    PMID: 19915217

    Conclusions This comparative-effectiveness trial shows that the use of extended-release niacin causes a significant regression of carotid intima-media thickness when combined with a statin and that niacin is superior to ezetimibe. (ClinicalTrials.gov number, NCT00397657 [ClinicalTrials.gov] .
Matti Narkia

Are statins analogues of vitamin D? : The Lancet - 0 views

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    Are statins analogues of vitamin D?
    Grimes DS.
    Lancet. 2006 Jul 1;368(9529):83-6. Review.
    PMID: 16815382
    doi:10.1016/S0140-6736(06)68971-X

    There are many reasons why the dietary-heart-cholesterol hypothesis should be questioned, and why statins might be acting in some other way to reduce the risk of coronary heart disease. Here, I propose that rather than being cholesterol-lowering drugs per se, statins act as vitamin D analogues, and explain why. This proposition is based on published observations that the unexpected and unexplained clinical benefits produced by statins have also been shown to be properties of vitamin D. It seems likely that statins activate vitamin D receptors.
Matti Narkia

Coenzyme Q10 - Wikipedia, the free encyclopedia - 0 views

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    "Coenzyme Q10 (also known as ubiquinone, ubidecarenone, coenzyme Q, and abbreviated at times to CoQ10 - pronounced like "ko-cue-ten" -, CoQ, Q10, or simply Q) is a 1,4-benzoquinone, where Q refers to the quinone chemical group, and 10 refers to the isoprenyl chemical subunits.

    This oil-soluble vitamin-like substance is present in most eukaryotic cells, primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respiration, generating energy in the form of ATP. Ninety-five percent of the human body's energy is generated this way.[1][2] Therefore, those o
Matti Narkia

Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial in... - 0 views

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    Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction.
    Singh RB, Neki NS, Kartikey K, Pella D, Kumar A, Niaz MA, Thakur AS.
    Mol Cell Biochem. 2003 Apr;246(1-2):75-82.
    PMID: 12841346
Matti Narkia

Japan EPA Lipid Intervention Study (JELIS) - Дискуссионный Клуб Русского Меди... - 0 views

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    "18 645 patients with a total cholesterol of 6·5 mmol/L or greater were recruited from local physicians throughout Japan between 1996 and 1999. Patients were randomly assigned to receive either 1800 mg of EPA daily with statin (EPA group; n=9326) or statin only (controls; n=9319) with a 5-year follow-up. The primary endpoint was any major coronary event, including sudden cardiac death, fatal and non-fatal myocardial infarction, and other non-fatal events including unstable angina pectoris, angioplasty, stenting, or coronary artery bypass grafting. Analysis was by intention-to-treat.
    Findings
    At mean follow-up of 4·6 years, we detected the primary endpoint in 262 (2·8%) patients in the EPA group and 324 (3·5%) in controls-a 19% relative reduction in major coronary events (p=0·011). Post-treatment LDL cholesterol concentrations decreased 25%, from 4·7 mmol/L in both groups. Serum LDL cholesterol was not a significant factor in a reduction of risk for major coronary events. Unstable angina and non-fatal coronary events were also significantly reduced in the EPA group. Sudden cardiac death and coronary death did not differ between groups. In patients with a history of coronary artery disease who were given EPA treatment, major coronary events were reduced by 19% (secondary prevention subgroup: 158 [8·7%] in the EPA group vs 197 [10·7%] in the control group; p=0·048). In patients with no history of coronary artery disease, EPA treatment reduced major coronary events by 18%, but this finding was not significant (104 [1·4%] in the EPA group vs 127 [1·7%] in the control group; p=0·132)."
Matti Narkia

JELIS - Japan Eicosapentaenoic acid (EPA) Lipid Intervention Study - Medscape - 0 views

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    The first large-scale, prospective, randomized trial of combined treatment with a statin and an omega-3 fatty acid originally derived from fish, eicosapentaenoic acid (EPA), has shown that the addition of EPA to statin therapy provides additional benefit in preventing major coronary events, apparently through lipid-independent mechanisms.[1] The Japan eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS) tested the effects of long-term use of EPA 1800 mg/day in addition to a statin in Japanese patients with hypercholesterolemia. The results add support to previous evidence of the beneficial effect of omega-3 fatty acids in patients with known coronary heart disease, and show that that effect can extend the benefit of statins, the JELIS investigators believe
Matti Narkia

JELIS: Adding fish oil to low-dose statin therapy reduces major coronary events - thehe... - 0 views

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    "Nov 14, 2005 | Michael O'Riordan.
    Dallas, TX - The addition of eicosapentaenoic acid (EPA) to low-dose statin therapy significantly reduced the incidence of major coronary events, largely driven by a reduction in unstable angina, when compared with patients taking statins alone. A subgroup analysis of the study, which involved a large number of primary-prevention patients, revealed that statin-treated secondary-prevention patients gained the most benefit from fish-oil supplementation.

    Dr Mitsuhiro Yokoyama
    Presenting the results of the Japan EPA Lipid Intervention Study (JELIS) during the late-breaking clinical-trials session at the American Heart Association Scientific Sessions 2005, Dr Mitsuhiro Yokoyama (Kobe University Graduate School of Medicine, Japan) said that the mechanism of benefit with EPA, a seafood-based, long-chain, n-3 polyunsaturated fatty acid, appears to be unrelated to the effects of cholesterol lowering.

    Commenting on the results of the study for heartwire, Dr Lawrence Appel (Johns Hopkins University School of Medicine, Baltimore, MD) said the findings are impressive given that the benefit of fish oil was observed on top of a regimen of statin therapy. He added that there are still some unknowns about which patient population would benefit most from fish oil."
Matti Narkia

The JELIS Trial - The Heart Scan Blog: - 0 views

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    "The Japan eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS) is a clinical trial that all Track Your Plaquers should know about.

    This enormous trial followed a simple design:

    Japanese men, between 40-75 years, and Japanese postmenopausal women aged <75 years 250 total with mg cholesterol />
Matti Narkia

Incremental effects of eicosapentaenoic acid on cardiovascular events in statin-treated... - 0 views

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    Incremental effects of eicosapentaenoic acid on cardiovascular events in statin-treated patients with coronary artery disease.
    Matsuzaki M, Yokoyama M, Saito Y, Origasa H, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K, Matsuzawa Y; JELIS Investigators.
    Circ J. 2009 Jul;73(7):1283-90. Epub 2009 May 8.
    PMID: 19423946

    Conclusions: EPA is effective for secondary prevention of CAD, especially in individuals with prior MI, and
    should be added to conventional treatment.
Matti Narkia

Effects of Atorvastatin on Vitamin D Levels in Patients With Acute Ischemic Heart Disease - 0 views

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    Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease.
    Pérez-Castrillón JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Dueñas A.
    Am J Cardiol. 2007 Apr 1;99(7):903-5. Epub 2007 Feb 8.
    PMID: 17398180

    In conclusion, atorvastatin increases vitamin D levels. This increase could explain some of the beneficial effects of atorvastatin at the cardiovascular level that are unrelated to cholesterol levels.

    The mechanism by which atorvastatin increases vitamin D levels is related to inhibition of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase. Cholesterol is synthesized from 7-dehydrocholesterol, which is also a precursor of vitamin D3. For this reason, we initially observed a statistically significant relation between total cholesterol and vitamin D. HMG-CoA enzyme reductase is key to the synthesis of cholesterol, whereas ultraviolet radiation causes the formation of 25-hydroxyvitamin D. Inhibition of the enzyme may increase levels of 7-dehydrocholesterol and increase the synthesis of 25-hydroxycholecalciferol, thereby increasing vitamin D levels,10 although we observed no relation between lower cholesterol and increased vitamin D. In addition, 25-hydroxyvitamin D has been shown to inhibit HMG-CoA enzyme reductase activity in in vitro studies.11 A greater concentration of vitamin D could increase enzymatic inhibition, acting in synergy with the statin in decreasing total cholesterol.
Matti Narkia

Statins and Vitamin D - 0 views

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    Statins and vitamin D.
    Aloia JF, Li-Ng M, Pollack S.
    Am J Cardiol. 2007 Oct 15;100(8):1329. Epub 2007 Jul 5. No abstract available.
    PMID: 17920383

    A total of 208 women were randomized to receive vitamin D3 (n=104) or placebo (n=104). 51 women were on statins. At baseline, the subjects on statins had a significantly higher 25-OHD level than the subjects who were not on statins (51.2 ± 20.1 nmol/L versus 43.2 ± 18.0 nmol/L respectively, p=0.008). This was also true when averaging 25-OHD levels across the 3-year study period and looking at active and placebo patients separately. 185 subjects had follow-up 25-OHD levels drawn every 6 months during the study. Higher levels were seen in the statin use subgroup whether they were on placebo or active vitamin D (Figure 1Figure 1). There was no interaction seen between vitamin D use and statin use, i.e. the impacts are additive (p=0.5502). This significant difference is comparable to the increase in 25-OHD levels seen in Pérez-Castrillón's study (41 ± 19 versus 47 ± 19 nmol/L, p=0.003) [1]. Although Pérez-Castrillón et al found a statistically significant relation between total cholesterol and 25-OHD (r=0.277, p=0.002), we did not find a significant relation between total cholesterol and 25-OHD in our study population.
Matti Narkia

The Heart Scan Blog: CRP and Jupiter - 0 views

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    What is C-reactive protein (CRP)?

    It is a blood-borne protein that originates in the liver and serves as an index of the body's inflammatory state. It is triggered by yet another inflammatory signal molecule, interleukin-6.

    What triggers this cascade of inflammatory markers? Any inflammatory stimulus, such as being overweight, lack of exercise, vitamin D deficiency, viral illness no matter how trivial, any inflammatory disease like arthritis, small LDL, high triglycerides, poor diet rich in processed foods, resistance to insulin, any injury, incipient diabetes, hidden cancer, lack of education (no kidding), etc.
Matti Narkia

CoQ10 Improves Endothelial Dysfunction in Statin-Treated Type 2 Diabetics - 0 views

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    NEW YORK (Reuters Health) May 29 - Supplementation with coenzyme Q10 (CoQ10) improves endothelial dysfunction in patients with type 2 diabetes on statin therapy, according to results of a study reported in the May issue of Diabetes Care.

    The vascular benefits of statins might be attenuated by inhibition of CoQ10 synthesis, Dr. Gerald T. Chew and colleagues from University of Western Australia, Perth, note in their report.
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