*-* أخبار تونيزيا سات الطبية باللغة الأنجليزية *-*

الموضوع في 'الأخبار الطبية الحديثة' بواسطة cortex, بتاريخ ‏24 أكتوبر 2008.

  1. cortex

    cortex كبير مراقبي منتدى الأخبار الطبيّة والصحيّة الحديثة طاقم الإدارة

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      24-10-2008 08:56
    Zurich, Switzerland - Rimonbant's rough ride may be nearly over: today, the European Medicines Agency (EMEA) announced that it has recommended suspension of the weight-loss drug, marketed as Acomplia in Europe [1]. According to an EMEA committee, the benefits of the drug "no longer outweigh its risks."

    Its manufacturer, Sanofi-Aventis, has responded, agreeing to what it is calling a "temporary suspension" of the drug [2].

    As previously reported by heartwire, the drug has known neurological and psychiatric side effects, including depression and "suicidal ideation," which are noted in the product labeling in Europe and were enough to persuade an FDA advisory committee in June 2007 that the drug should not be marketed in the US. In Europe, however, the drug has been available since June 2006, although the EMEA reconvened after one year to reassess the safety profile of the drug, ultimately leading to new contraindications for its use.

    In a press statement, Sanofi-Aventis says that the company "remains committed to Acomplia to bring an important therapeutic approach to obese and overweight patients." More than 700 000 patients have been treated with the drug worldwide, the company notes; the drug has been sold in 18 EU countries over the past two years. The press statement also asserts that Sanofi-Aventis will work to provide the EMEA with "additional evidence for the reevaluation of the benefit/risk profile of Acomplia in patients with diabetes and cardiovascular diseases through the ongoing clinical studies."

    Recent study results with rimonabant have been mixed, however. Analyses from the ADAGIO-LIPIDS study, presented earlier this year at the 77th European Atherosclerosis Society Congress, pointed to improvements in lipid parameters and reductions in visceral adipose tissue. But STRADIVARIUS, an intravascular ultrasound study presented at the ACC 2008 meeting, showed no benefit of rimonabant in terms of progression of atherosclerosis.

    Earlier this month, Merck announced that it had halted development of its own cannabinoid-receptor blocker, taranabant, due to its overall safety and efficacy profile.
     
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  2. cortex

    cortex كبير مراقبي منتدى الأخبار الطبيّة والصحيّة الحديثة طاقم الإدارة

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      24-10-2008 09:40
    The US Food and Drug Administration (FDA) needs more time to complete a review of TriLipix, Abbott Laboratories, the maker of the newer, patent-protected fenofibrate, announced Wednesday.

    Abbott applied for FDA approval for use of the drug as monotherapy and in combination with statins. The FDA has not asked more data, according to Abbott, just more time, and the company expects a decision by the end of 2008.

    TriCor, an older fenofibrate that Abbott hopes TriLipix will replace, has been a massive moneymaker for the company, breaking the $1 billion mark in sales in 2007. In the first nine months of 2008, worldwide sales are again nearing the $1 billion range.
     
  3. maraouirezki

    maraouirezki دكتور تونيزيا سات

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      25-10-2008 10:16
    لما لا بعث موضوع موحد للأخبار باللغة الأنجليزية

    خاصة لأعضائنا و زوارنا من المشرق العربي الذين يحبذون هذه اللغة

    شكرا أخي محمد
     
    2 شخص معجب بهذا.
  4. cortex

    cortex كبير مراقبي منتدى الأخبار الطبيّة والصحيّة الحديثة طاقم الإدارة

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      28-10-2008 07:43
    Statin use reduces mortality after hospitalization for pneumonia

    Preadmission statin use among patients admitted to the hospital for pneumonia is associated with lower rates of mortality compared with those not taking the lipid-lowering medications, according to a new study [1]. The reduced mortality risk became evident during the first weeks of hospitalization for pneumonia and persisted for at least 90 days, report investigators.

    "Our study adds to the accumulating evidence that statin use is associated with improved prognosis after severe infections," write lead investigator Dr Reimar Thomsen (Aarhus University, Aalborg, Denmark) and colleagues in the October 27, 2008 issue of the Archives of Internal Medicine. "Given the availability of statins, with their relatively low cost and mild adverse effects, positive results of statin-therapy trials in patients with pneumonia would have substantial clinical and public-health implications."

    Review of patients hospitalized with pneumonia

    Prior studies investigating the benefits of statin therapy in patients with pneumonia have had conflicting results. There are several biological mechanisms, however, including the ability of statins to modify the humoral response, to suggest that the drugs might be beneficial in this setting. Other clinical and experimental studies have shown that the lipid-lowering agents improved outcomes after severe infections.

    In this study, Thomsen and colleagues reviewed data of 29 900 adults hospitalized with pneumonia for the first time between 1997 and 2004 in northern Denmark. Of these patients, 1372 were taking statins when admitted to the hospital.

    Within 30 days, those patients taking statins who were hospitalized with pneumonia had a 31% lower risk of dying compared with patients not taking statins. By 90 days, the reduction in mortality was maintained, with those taking statins having a 25% lower risk of dying compared with those not on statin therapy.

    Association between preadmission statin use and death within 30 and 90 days

    The differences became apparent during the first few weeks of hospitalization, a period associated with a high number of pneumonia-related deaths, and increased minimally between 30 and 90 days after admission. This suggests that statin use is beneficial primarily in the early phase of infection, write Thomsen and colleagues.

    The benefit remained robust in several subgroups, including patients >80 years old and patients with bacteremia, and there was no protective effect observed with aspirin or ACE inhibitors. There was a slight reduction in mortality among those currently taking beta blockers, although the benefit was small and observed only at 30 days.

    The investigators adjusted for several comorbidities, eliminating the bias that might arise from statin users being "healthy users"—that is, younger, healthier, better educated, or more affluent.

    In an editorial accompanying the study, Dr Kasturi Haldar (University of Notre Dame, South Bend, IN) says that the findings are consistent with mechanisms of statin action on reducing G-protein-mediated inflammation and infection [2]. The results also raise the question of whether statins should be used to improve anti-infective therapy.

    He notes that the drugs are not ideal for treating acute infection because it takes days to achieve the desirable concentrations in plasma, and the protective effects of statins are clearly prominent after longer treatment times.

    "However, because statins target the host, drug resistance, a major problem in treating bacterial infections, is not likely to develop," writes Haldar. "Thus, it may be useful to consider clinical research testing of combinations of statins with existing antibiotic agents to evaluate whether it is possible to develop optimized combination therapies effective against both acute and persistent infections."
     
  5. cortex

    cortex كبير مراقبي منتدى الأخبار الطبيّة والصحيّة الحديثة طاقم الإدارة

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      29-10-2008 22:56
    Hypertension
    Reducing heart rate in hypertension is harmful—or is it just atenolol?


    New York, NY - Slowing the heart rate with beta blockers in people with hypertension is associated with an increased risk of cardiovascular events and death, a new systematic review shows [1]. Furthermore, the slower the heart rate, the greater the risk, report Dr Sripal Bangalore (St Luke's Roosevelt Hospital, New York) and colleagues in the October 28, 2008 issue of the Journal of the American College of Cardiology.
    Senior author Dr Franz Messerli (St Luke's Roosevelt Hospital) told heartwire: "Slowing heart rate is known to prolong life expectancy, and with beta blockers post-MI and in heart failure, the slower you can make the heart rate, the better. But this new paper goes against the grain. What we show is that in hypertension, when you slow down the heart rate with a beta blocker, it actually shortens your life expectancy, it causes more heart attacks, more heart failure, and more strokes." Messerli says he and his team believe the likely explanation for this is "that slowing the heart rate with beta blockers increases the central pressure, and obviously the latter is one of the determinants of stroke and heart attack."

    Another hypertension expert sees things slightly differently, however. Dr John Cockcroft (Wales Heart Institute, Cardiff, UK) argues that in this review, the studies included almost exclusively used atenolol—something the authors do point out—and that it is this drug per se that is likely the culprit here.

    What is vitally important to determine in this setting, he adds, "is whether it's atenolol that's bad or whether it's reduction of heart rate that's bad." This is crucial because there are other drugs that aren't beta blockers that lower heart rate, he explained, such as the new agent ivabradine (Procoralan, Servier). "This issue needs resolving because if it's heart-rate reduction [that is the cause], then that's bad news, and we need to know about it."

    Bradycardia not synonymous with cardioprotection in hypertension

    In the new review, Bangalore et al included nine randomized controlled trials evaluating beta blockers for hypertension that also reported heart-rate data, including 34 096 patients taking beta blockers, 30 139 taking other antihypertensives, and 3987 receiving placebo. Of the patients in the beta-blocker arms, 78% received atenolol, 9% took oxprenolol, 1% propranolol, and 12% received atenolol/metoprolol/pindolol or hydrochlorothiazide.

    Paradoxically, a lower heart rate (as attained in the beta-blocker group at study end) was associated with a greater risk for the end points of all-cause mortality (r=-0.51; p<0.0001), cardiovascular mortality (r=-0.61; p<0.0001), MI (r=-0.85; p<0.0001), stroke (r=-0.20; p=0.06), or heart failure (r=-0.64; p<0.0001).

    "In contrast to patients with MI and heart failure, beta-blocker-associated reduction in heart rate increased the risk of cardiovascular events and death for hypertensive patients," the researchers conclude.

    Messerli told heartwire: "In the past, the term cardioprotection was synonymous with bradycardia. The more you had bradycardia, the better the heart was protected. This is not the case in hypertension. This may be okay post-MI and in heart failure, but it's not okay in hypertension."

    In an editorial accompanying the review, Dr Norman M Kaplan (University of Texas Southwestern Medical Center, Dallas) agrees [2]: "With this addition to the evidence, beta blockers will surely remain as indicated for heart failure, for after MI, and for tachyarrhythmias, but no longer for hypertension in the absence of these compelling indications."

    Difficult to extrapolate findings beyond atenolol

    Messerli and his colleagues do state in their discussion, however: "Further studies are needed to establish causation. It should also be noted that the beta blocker used in the studies was mainly atenolol, and hence, any meaningful extrapolation of these results to other beta blockers, including the newer vasodilating beta blockers, should be done with caution."

    Cockcroft contends that because this new review contains studies almost exclusively using atenolol, "this doesn't move the argument forward very much." Atenolol, he says, "has been tried and found guilty, and yet around 40% of prescriptions for beta blockers in the UK and in the US are still for atenolol. Atenolol should not be given to anybody. Nobody disagrees that atenolol is guilty, and yet we are still using it."

    He says that people think lowering heart rate is good, "because it reduces the amount of cyclical stress on the aorta, but if at the same time you are putting the central aortic pressure up, these things may cancel each other out." Atenolol has been compared in this respect with one of the newer vasodilating beta blockers, nebivolol (Bystolic, Forest/Mylan), and it was found that atenolol increases the central aortic pressure but nebivolol does not [3], he notes.

    "The newer vasodilating beta blockers may well not have any of these detrimental effects. Because they are vasodilatory, they may well offset the slowing of heart rate by decreasing wave reflection from the periphery and, in the case of nebivolol, by releasing nitric oxide, an endogenous vasodilator with antiatherogenic activity," he adds.

    To beta block or not, that is the question

    Regarding the role now of beta blockers in hypertension, Messerli commented to heartwire: "Beta blockers in hypertension are not very useful, and you probably should use any other single drug first before you add a beta blocker, and if you want to add a beta blocker, please use a vasodilating one such as carvedilol or nebivolol."
    Cockcroft agrees with much of this, but maintains that beta blockade is still very important. "Beta blockade is vital. A large number of patients with hypertension have angina as well, so they've got to have a beta blocker. Furthermore, there is now evidence that younger subjects with hypertension (<50 years of age) may well be better treated with a beta blocker than older hypertensives, as they have a different hemodynamic form of hypertension. It's what beta blocker you give them that counts, and it shouldn't be atenolol."

    He believes the continued obsession with atenolol is "partly due to cheapness and habit, but also due to the failure of the people with good beta blockers to disseminate information on the deleterious effects of atenolol."

    Most important issue still not resolved; central pressure should be the focus

    Cockcroft says the more vital issue "that still needs resolving is whether it's atenolol that is bad or heart-rate reduction that is bad news. If it's the latter, we need to know about it, because there are other drugs that lower heart rate, such as ivabradine, and if you look at the BEAUTIFUL trial with this new drug, it was very negative."

    He believes a trial directly comparing ivabradine with atenolol in terms of central aortic pressure is needed, "and then you look at the effects on hemodynamics in terms of central pressure."

    Another way of examining this issue could be to give atenolol to people who have pacemakers in to slow their heart rate down and then switch the pacemaker back on and bring the heart rate back up to the baseline level—still with them having atenolol on board—and "if the detrimental hemodynamics go away, then it's all heart rate, and if it doesn't, then atenolol has some effect beyond heart-rate reduction that is bad.

    "These are very, very important mechanistic experiments that need to be done now that we have other drugs that lower heart rate that aren't beta blockers, and we clearly need to be doing these studies," Cockcroft stresses.

    "I personally think that it's the atenolol that is bad and that it has some effects beyond heart-rate reduction that are bad, but we don't know from this Messerli review. If half [the trials they included] had used another beta blocker, then you would know for sure."

    "It's central pressure that the pharmaceutical industry should be focusing on," he adds, "because different drugs, especially beta blockers, have differential effects on central pressure, and we know from the Strong Heart Study that central aortic pressure is a better predictor of outcome than pressure in the arm."
     
  6. cortex

    cortex كبير مراقبي منتدى الأخبار الطبيّة والصحيّة الحديثة طاقم الإدارة

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      31-10-2008 11:26
    Genetically Elevated C-Reactive Protein and Ischemic Vascular Disease

    Background Elevated levels of C-reactive protein (CRP) are associated with increased risks of ischemic heart disease and ischemic cerebrovascular disease. We tested whether this is a causal association.

    Methods We studied 10,276 persons from a general population cohort, including 1786 in whom ischemic heart disease developed and 741 in whom ischemic cerebrovascular disease developed. We examined another 31,992 persons from a cross-sectional general population study, of whom 2521 had ischemic heart disease and 1483 had ischemic cerebrovascular disease. Finally, we compared 2238 patients with ischemic heart disease with 4474 control subjects and 612 patients with ischemic cerebrovascular disease with 1224 control subjects. We measured levels of high-sensitivity CRP and conducted genotyping for four CRP polymorphisms and two apolipoprotein E polymorphisms.

    Results The risk of ischemic heart disease and ischemic cerebrovascular disease was increased by a factor of 1.6 and 1.3, respectively, in persons who had CRP levels above 3 mg per liter, as compared with persons who had CRP levels below 1 mg per liter. Genotype combinations of the four CRP polymorphisms were associated with an increase in CRP levels of up to 64%, resulting in a theoretically predicted increased risk of up to 32% for ischemic heart disease and up to 25% for ischemic cerebrovascular disease. However, these genotype combinations were not associated with an increased risk of ischemic vascular disease. In contrast, apolipoprotein E genotypes were associated with both elevated cholesterol levels and an increased risk of ischemic heart disease.

    Conclusions Polymorphisms in the CRP gene are associated with marked increases in CRP levels and thus with a theoretically predicted increase in the risk of ischemic vascular disease. However, these polymorphisms are not in themselves associated with an increased risk of ischemic vascular disease.


    [​IMG]
     

  7. cortex

    cortex كبير مراقبي منتدى الأخبار الطبيّة والصحيّة الحديثة طاقم الإدارة

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    5.044
      04-11-2008 15:11
    Doctors and lawyers butt heads over statins for primary prevention in women

    The use of statins for primary prevention in women is not supported by clinical-trial data, and any advertising claims made by drugmakers about their benefits in this population are vulnerable to legal action .

    These are the conclusions of Drs Theodore Eisenberg and Martin Wells (Cornell University, Ithaca, NY), a legal scholar and a statistician, in the September 2008 issue of the Journal of Empirical Legal Studies. An analysis of statin studies do not show that the lipid-lowering drugs reduce MI and other cardiovascular events in women, and the presumed benefit of the popular medications should not be extrapolated from data in men, they argue.

    "Meta-analysis of leading randomized clinical drug trials finds no evidence that statins protect women against nonfatal myocardial infarction or fatal coronary heart disease in a primary-prevention context," write Eisenberg and Wells. "Unqualified advertising claims of protection against heart attacks therefore may be misleading. Existing legal doctrine supports the viability of state law claims based on questionable advertising."

    Speaking with heartwire about the conclusions reached by the Cornell researchers, Dr Richard Karas (Tufts University School of Medicine, Boston, MA) said the use of statins for primary prevention in women is clinically controversial.

    "You can slice and dice the statin trials a number of ways, and one of the ways is primary vs secondary prevention," he said. "Another way is their use in men vs women. When you do that, there is very good evidence that statins provide very good benefit for primary and secondary prevention in men, and there is good evidence, but not as good, that they provide benefit in secondary prevention in women. There is very little evidence that they provide benefit for primary prevention in women."

    With that in mind, it can be argued that the drugs shouldn't be used in primary prevention in women, although this is a minority opinion in medicine, said Karas. One reason it is unpopular is that there isn't any real physiological reason to suggest that statins would work differently in women from the way they do in men. Although there are subtle differences in lipid values between men and women, such as HDL cholesterol being more important in women, LDL cholesterol drives atherosclerosis in women, as it does in men.

    "Second, there is an important difference between an absence of information and information suggesting that it doesn't work," said Karas. "In this case, it is really just an absence of information. I treat women with statins for primary and secondary prevention, and the way I think about it is that the drug clearly works in these other settings. It makes sense to use statins for primary prevention in the absence of information."

    Different meta-analyses and different interpretations

    In their paper, Eisenberg and Wells note that a 1996-1997 study found that nearly one-quarter of statin users were women without coronary heart disease (CHD), including 1.7% of women under age 70 and 9.1% of women 70 years of age and older without a history of CHD.

    In their analysis of the data, including the ALLHAT, AFCAPS, ASCOT, PROSPER, and WOSCOPS studies, the authors concluded that the benefit of statin therapy does not extend to women in primary prevention. Although there was a significant 21% reduction in risk of cardiovascular events in men and women and a significant 28% reduction in events in men, there was no benefit when the analysis is restricted to women only. Excluding ALLHAT, a study challenged because one-third of usual-care participants started taking lipid-lowering drugs at some point during the study, and PROSPER, where the definition of primary and secondary prevention patients is less clear, did not alter the results, they note.

    Commenting on the analysis for heartwire, Dr James Stein (University of Wisconsin Medical School, Madison, WI) spoke to the clinical conclusions of the researchers.

    "This analysis relies on the distinction between those with and without heart disease or at high vs low or intermediate risk. By narrowing the focus so much, they create a very narrow bin of 'low-' or 'moderate-' risk women, in which a benefit is hard to show. Not enough women have been enrolled to show it definitively," he said. "But the weight of the evidence—[from] women with cardiovascular disease, women with diabetes, [data] from men, and what we know about how atherosclerosis develops—strongly suggests the benefit is there."

    Stein noted that the meta-analysis published by the Cholesterol Treatment Trialists in 2005 showed a significant 18% reduction in cardiovascular events among women treated with statins, a finding that was not significantly different from the benefit observed in men . This analysis included primary- and secondary-prevention patients, and there was no difference in statin benefits among those with or without previous cardiovascular disease.

    Karas agreed, telling heartwire there is "no doubt" that improving the lipid profile in women and men reduces cardiovascular disease risk. Karas and Stein both noted that the only differences are absolute risk reduction and the strength of the evidence, which is stronger in men since more men were enrolled in these studies. Karas said that the legal meta-analysis is restricted to atorvastatin (Lipitor, Pfizer) only, which is "important, because every time you reduce the amount of information, you have a harder time showing or learning anything."

    Prepping for court?

    In their paper, Eisenberg and Wells argue that their findings challenge the advertising of these drugs, specifically the advertising of atorvastatin, the best-selling drug in the world, with annual sales of more than $12 billion. The authors state that Pfizer's advertising omits label information that is relevant to women. For example, whereas the label states that results for women are inconclusive for the reduction of coronary events, the advertising of such cardioprotective claims makes no qualifications by gender and even fails to disclose that one clinical trial of Lipitor, the ASCOT-LLA study, found a modest increased risk of heart problems in women.

    "If we are correct about omissions from Pfizer's advertising, then neither market forces nor Food and Drug Administration (FDA) regulation has effectively regulated the mass marketing of Lipitor," write Eisenberg and Wells. "At a minimum, the FDA should use its authority under the Federal Food, Drug, and Cosmetic Act (FDCA) to address massive questionable marketing."

    Stein told heartwire he had no comment on Pfizer's advertising claims or the legal arguments put forth by the Cornell researchers, saying that, in general, he opposes direct-to-consumer advertising of medications. Karas said the analysis emerges from an "extremely legalistic perspective" and appears to "carefully construct a sawhorse for a lawsuit," but it will affect "not one bit" how he prescribes to female patients.

    The 2007 American Heart Association/American College of Cardiology update to the guidelines for cardiovascular-disease prevention states that LDL-cholesterol-lowering therapy is "useful and effective," a class I recommendation, in women with elevated LDL-cholesterol levels and multiple risk factors . In addition, the Adult Treatment Panel III (ATP III) guidelines do not discriminate between men and women
     
  8. cortex

    cortex كبير مراقبي منتدى الأخبار الطبيّة والصحيّة الحديثة طاقم الإدارة

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      08-11-2008 11:55
    Eyes trained on JUPITER: Cardiologists seek details to understand how statin use may expand

    Cardiologists already know the key result from JUPITER, the opening late-breaking clinical trial at the upcoming American Heart Association(AHA) 2008 Scientific Sessions: rosuvastatin was superior to placebo in reducing hard end points in apparently healthy people with low or normal LDL levels but elevated C-reactive protein (CRP). Still, experts who spoke with heartwire said that as-yet-unreported details from the trial, which has the potential to radically expand the number of people eligible for statin therapy, will be key for understanding how patient screening or statin usage may change.

    Dr Paul Ridker (Brigham and Women's Hospital, Boston, MA) will present the full results from JUPITER at 3:45 pm November 9 at the AHA 2008 meeting, in New Orleans.

    As previously reported by heartwire, AstraZeneca, the study sponsor, announced it had stopped the trial last spring, with 17 802 patients enrolled, after an interim analysis showed death, MI, and other adverse events to be reduced among patients randomized to 20-mg rosuvastatin. Critically, JUPITER participants had normal to low LDL levels (less than 130 mg/dL) but increased CRP levels (>2.0 mg/L); depending on nuances in the results, JUPITER could ultimately lead to the expansion of statins to millions of adults currently not eligible for statin therapy.

    Commenting on the potential impact of the study—without knowing the results—Dr Michael Miller (University of Maryland, Baltimore) pointed out that the anti-inflammatory effects of statins were known already, even in the absence of high LDL, as demonstrated in the ASCOT trial.

    But in ASCOT, he points out, patients also had risk factors for coronary heart disease other than high CRP—it will be important to see what other risk factors JUPITER patients may have had, Miller notes. "Was the high CRP in JUPITER present by itself, or was it always accompanied by other risk factors? Our analysis of the NHANES database found that a high CRP was present only in one in 2000 [people] in the absence of traditional risk factors, thereby suggesting that high CRP is a biomarker rather than a direct promoter of coronary heart disease," Miller said. "Hence, if the JUPITER paper shows a high prevalence of subjects who had no other risk factors beside high CRP as the basis for the increased event rates, then that would argue for routine CRP screening in this group of middle-aged subjects."

    Additional benefit of CRP

    Also commenting on the potential impact of JUPITER, Dr James Stein (University of Wisconsin, Madison) drew parallels between JUPITER and the METEOR study, which also addressed the question of treating low-risk patients on the basis of a biomarker, not a cholesterol cut point, but he adds that JUPITER was "much more important."

    "METEOR showed that if you have the biomarker of high carotid [intima media thickness] IMT but LDL cholesterol at a level that would not qualify for treatment, you have less disease progression on rosuvastatin. JUPITER extends that finding to a more widely available biomarker—[high-sensitivity] hs-CRP—and shows the outcome we care most about: cardiovascular events. It is a landmark study. It shows something we all have suspected—that there are people out there who are at higher-than-apparent risk, and if they get identified and treated, they do better."

    But the question will persist as to how much CRP adds to current screening, Stein suggested. "The rub is that hs-CRP is highly correlated with adiposity and abnormal levels of risk factors, so how many extra people do you identify with screening above just looking at those parameters?" he asked. Participants in JUPITER were older, overweight, with higher-than-normal blood pressure. "They were poster children for a biomarker test to see whether they were at higher-than-apparent risk," Stein said.

    The question for the medical community will be how to incorporate the JUPITER results into practice guidelines, Stein points out. "That mainly will depend on the magnitude of the benefit in absolute terms, rather than relative terms, as well as the cost of any screening strategies we implement," he said. "Do we screen for hs-CRP in everyone, or just certain subgroups? Or do we just lower our targets for treatment across the population and omit extra screening? Also, how do we account for the high intra-individual variability in hs-CRP? We can't begin to answer these questions until we see the final data and some of the subgroup analyses."



    Other trials at AHA 2008

    The JUPITER trial is expected to steal the show at this year's meeting, although a range of other trials should also help cardiologists to fine-tune treatments for both primary and secondary prevention of cardiovascular disease.

    Day two of the meeting features trials of clopidogrel, rivaroxaban (ATLAS ACS-TIMI 46), and an "intervention timing" trial for non-STE ACS (TIMACS). Diabetes is the focus of three late-breakers spread across different days of the meeting: two studies address atherosclerosis prevention in diabetic patients (the JPAD trial using aspirin and the APPROACH trial with rosiglitazone), while a third is a registry analysis of drug-eluting stents vs bare-metal stents in diabetic patients from the Massachusetts registry.

    Speaking with heartwire about the upcoming meeting, Dr Gordon Tomaselli (Johns Hopkins University, Baltimore, MD), chair of the program committee, pointed out that JPAD may provide some much-needed new information. "The utility of aspirin specifically in patients with diabetes really has been difficult to sort out, so the trial will help us understand whether there really is any effect," he said.

    The third late-breaking clinical-trial session, on Tuesday, is devoted to heart-failure trials: of these, the I-PRESERVE study, looking at the use of irbesartan in patients with preserved ejection fraction, has the power to pack the most punch, if positive, given the dearth of drugs for this form of heart failure. According to Tomaselli, "I-PRESERVE is really the first properly designed trial to address this question, so it could be very interesting." Additional late-breakers include results of a home INR-monitoring study (THINRS), the FIT study exploring a family-based exercise intervention for heart-disease prevention, and two randomized comparisons of vitamin-related strategies vs placebo for primary and secondary prevention.

    Of these last, Tomaselli highlighted the SEARCH study, looking at effects of secondary prevention using both statins and folic acid. "The homocysteine hypothesis hasn't been abandoned, we just haven't figured out the correct way to reduce homocysteine. . . . I think that it may further confirm the recent trials that suggest using folic acid to lower homocysteine levels is not the right way to go, but I don't think it's going to firmly put the nail in the biological plausibility of the homocysteine hypothesis."
     
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  9. cortex

    cortex كبير مراقبي منتدى الأخبار الطبيّة والصحيّة الحديثة طاقم الإدارة

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    5.044
      09-11-2008 23:52
    Landmark study shows statins benefit healthy individuals with high CRP levels

    New Orleans, LA - The Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) started the American Heart Association (AHA) 2008 Scientific Sessions here today with a bang, shaking up the field of primary prevention with new data showing that the treatment of apparently healthy patients with a statin cuts their risk of cardiovascular disease morbidity and mortality by almost half [1].

    In a study of individuals with low LDL cholesterol but elevated C-reactive-protein (CRP) levels, investigators showed that rosuvastatin (Crestor, AstraZeneca) 20 mg significantly reduced the primary end point—a composite of nonfatal MI, nonfatal stroke, hospitalization for unstable angina, revascularization, and confirmed death from cardiovascular causes—by 44% compared with individuals treated with placebo.

    Presented by Dr Paul Ridker (Brigham and Women's Hospital, Boston, MA) during the late-breaking clinical-trials session and published online in the New England Journal of Medicine to coincide with the AHA presentation, investigators showed that the benefits extended to all subgroups, including "robust reductions in cardiovascular events with statin therapy in women and black and Hispanic populations, for which data on primary prevention are limited," write the JUPITER investigators.

    Calling JUPITER "one of the most important clinical trials in the long history of statin studies," Dr Steven Nissen (Cleveland Clinic, OH) told heartwire that such large reductions in clinical events in less than two years among patients considered healthy by conventional definitions is likely to change the guidelines.

    "Ideally, if a patient comes to me with normal LDL-cholesterol levels—in JUPITER, the median LDL-cholesterol level was 108 mg/dL—I tell him to keep doing what he's doing and to go about his business," said Nissen. "Now, what happens when that same patient arrives in my office and I know his CRP is elevated? I know that treating him with intensive statin therapy, despite what the guidelines state, is going to cut his risk of cardiovascular morbidity and mortality in half."

    Dr James Stein (University of Wisconsin Medical School, Madison) echoed the sentiments of others when he said that the findings are going to pose challenges, particularly as clinicians grapple with changing how they think about and treat seemingly low-risk patients.

    "It is a true landmark in preventive cardiology, not only for its findings, but even more so for the challenges it raises to our current strategies for use of cholesterol-lowering medications and to our risk-assessment paradigms," said Stein.
     
  10. cortex

    cortex كبير مراقبي منتدى الأخبار الطبيّة والصحيّة الحديثة طاقم الإدارة

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      20-11-2008 13:07
    1. Situps and Crunches Will NEVER GET YOU Flat Abs- For years I would do hundreds of cruches everyday. My abs were always sore, but never were toned, and I always still had that extra belly fat covering them up. After just 3 weeks of using the unique moves in this program, I noticed some ridges in the mirror when I was in the bathroom. By the way, those ridges were my abs finally coming in!

    2. Eat Less Food and You Will Lose Weight is a crock of _____! I always believed that I was fat because I ate too much and if I would eat less I could lose weight. Let me tell you something... Eating less only made my body fat percentages sky rocket. I won't lie to you, I did lose weight... but guess what? I gained it all back. I couldn't understand why until I read that restricting calories for too long will cause you to lose muscle tissue and retain more body fat.

    Now I am following this cool meal plan in this program that actually allows me to eat MORE food, not less... and like I said, I can already see my ab muscles. Not to mention other areas of my body are looking firm and fit. I did tell you that my girlfriend can't keep her hands off me right?

    3. More Cardio Does NOT help lose more fat- If you are a member of any gym I am sure you have seen people run for an hour and then do a few hundred crunches and then go home. I know this because I use to follow the advice of all the magazines which told me to run 4 miles and then bike for 20 minutes and then do 6 "unique" sit up variations. It sounded good but...

    I still never saw my abs... until I STOPPED doing the long boring cardio and started doing the unique style of workouts I found in this program. I actually saved time by doing these shorter but more effective workouts that you'll discover in a minute.

    4. Fat Burner Pills, Magic Pills, Metabolic Pills Are All a Waste of Money... This one is my own damn fault. I use to stay up late and watch all those lame infomercial's that promised how their "extreme fat burners" were the key to unlocking my belly fat and washing it out of my body forever. Well $1,547 dollars later and I still didn't have the body that I wanted. I learned in this program about how to use natural foods that are better fat burners than ANY pills.

    5. Ab Loungers, Ab Rockers, Ab Scissors and Most Other Ab Machines are a WASTE OF TIME! I guess I didn't learn my lesson from ordering all those useless fat burning pills from the late night infomercial's. I mean I couldn't help it... all those fancy commercials look so appealing with the way they have these sexy models doing exercises and saying they got their bodies from using the "state of the art" ab machine that is scientifically proven to target your abs more than crunches and situps. I found out in this program that most of these ab machines are actually LESS effective than the unique exercises I learned that don't use any equipment at all.

    6. Fat Free Foods will Help You Burn Fat- Sadly this too is another myth. Fat free foods actually cause your body to store more body fat because of the chemicals and the way that the foods are over-processed. In this program, I actually learned about dozens of delicious natural foods that allowed me to lose my stomach fat faster than when I was eating "low fat" or "fat free" foods.

    7. Healthy Food Isn't Always Healthy- I always thought that just because something said it was healthy on the label, that it was. However I just learned that most of these so called healthy foods are nothing less than cleverly designed cover-ups for unhealthy junk food.
     
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