#571
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Александр Иванович, это не глубокий консерватизм, а недопонимание того, что означает формулировка IIb.
Есть масса ситуаций, когда НЕОТКУДА взять рекомендации классом выше. Возьмите, почитайте, например, гайдлайны по лечению инфекционного эндокардита. Там для эмпирической терапии кроме как IIb особо и вариантов-то нет доказательности. И не потому, что "все плохо, не рекомендуется", а потому что болезнь тяжелая и результаты лечения априори не бывают суперзамечательными до получения посевов. И что теперь, не начинать терапию до получения гемокультуры? А она ведь еще и не всегда оказывается положительной, даже при наличии всех остальных несомненных признаков ИЭ. В общем, это я так, просто в качестве примера. На самом деле, их несть числа. |
#572
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Интересное кино....
[Ссылки доступны только зарегистрированным пользователям ] Понятно, что нужны РКИ, но тенденция, однако. |
#573
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__________________
Александр Иванович с пожеланиями крепкого здоровья Канал в Телеграм: https://t.me/doctorkorzun |
#574
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#576
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The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials.
[Ссылки доступны только зарегистрированным пользователям ] |
#577
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FDA предупреждает: действуйте осторожно!
[Ссылки доступны только зарегистрированным пользователям ] Focus on lipids: Risks and benefits of statin therapy |
#578
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Нет худа без добра. Тромбозов больше, зато кровотечений - меньше.
[Ссылки доступны только зарегистрированным пользователям ] MIAMI — New data from the Assessment of Dual Antiplatelet Therapy with Drug Eluting Stents (ADAPT-DES) shows that clopidogrel hyporesponsiveness does not predict one-year mortality in drug-eluting-stent recipients because the increased risk of thrombosis is offset by a lower risk of bleeding [1,2]. In light of this result, "overcoming clopidogrel hyporesponsiveness with more potent antiplatelet agents is therefore unlikely to improve survival unless the beneficial effects of reducing stent thrombosis and myocardial infarction can be uncoupled from the likely increase in bleeding with greater platelet inhibition," ADAPT-DES investigator Dr Thomas Stuckey (Moses Cone Heart and Vascular Center, Greensboro, NC) said at TCT 2012, where he and Dr Gregg Stone (Columbia University, NY) presented an analysis of the relationship between clopidogrel hyporesponsiveness and subsequent adverse events in the ADAPT-DES patients. Commenting on the study, Dr Ajay Kirtane (New York-Presbyterian Hospital, NY) said, "We know that hyporesponsiveness is a risk factor for ischemic events, but the therapies we have to treat those ischemic events--more potent antiplatelet therapies--increase the risk of bleeding, so we do have figure out in whom should we use those therapies." Unfortunately, these data do not identify that patient population. Commenting on the analysis, Dr Alice Jacobs (Boston Medical Center, MA) said, "This is a testament to the conundrum that we're seeing with these newer [antiplatelet] agents. We haven't gotten to that sweet spot of matching the increased efficacy and the problem of bleeding. So I don't think these data will change anything now." Stuckey said: "We're trying to gain the advantage of newer and better agents but uncoupling them from the bleeding. There are a lot of issues related to that--the timing of the bleeding, the type of bleeding, procedure-related vs later. But if you tackle those things as separate issues, there may be a sweet spot where you can define people who are or are not at risk for bleeding and target the therapy like we have in many other areas," he predicted. Protection From Bleeding Balances Thrombosis Risk As reported by heartwire , the 8575-patient ADAPT-DES registry showed that absolute and relative levels of platelet inhibition independently predict stent thrombosis in patients with a DES, although the test used to measure platelet reactivity in the study, the VerifyNow (Accumetrics) assay, is not specific or sensitive enough to predict one-month stent-thrombosis risk in individual patients. The new ADAPT-DES data released at TCT 2012 show that, at one-year postprocedure, 70 patients (0.84%) had a stent thrombosis, 224 had an MI (2.7%), 531 suffered a major bleed (6.2%), and 161 died (1.9%). Clopidogrel hyporesponsiveness, defined as a VerifyNow score of 208 platelet reactivity units (PRU) or greater, was found in 42.7% of patients in the study. This clopidogrel hyporesponsiveness was significantly associated with stent thrombosis, as 1.3% of clopidogrel hyporesponsive patients suffered thrombosis vs only 0.5% of nonhyporesponsive patients. It was also associated with more MI, 3.9% vs 2.7%. However, clopidogrel hyporesponsiveness also predicted a lower risk of major bleeding in the study, 5.6% vs 6.7%. Clopidogrel hyporesponsive patients had a higher one-year mortality rate than nonhyporesponsive patients in the trial, 2.4% vs 1.5%, but multivariable modeling demonstrated no independent association between clopidogrel hyporesponsiveness and mortality. Aspirin hyporesponsiveness was defined as a score of over 550 aspirin reactive units on the VerifyNow assay. In these patients, hyporesponsiveness to aspirin predicted a slightly lower risk of bleeding but did not predict a difference in stent thrombosis, heart attack, or death. This calls into question the value of aspirin in patients treated with DES, since stent thrombosis is the most important risk associated with DES, Stuckey and Stone said. Dr Ted Feldman (Evanston Hospital, IL) agreed that the analysis leaves clinicians with no more clarity on how to balance bleeding and thrombosis risk in DES patients. "These are more data in the pool, but definitely only a glimmer and not a big blast of light. . . . I've been waiting to buy a bedside platelet assay testing machine, and I won't feel guilty about waiting a little longer." |
#579
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Beta blockers of no use in stable CAD patients
Очередной виток в дискуссии: так ли полезны [Ссылки доступны только зарегистрированным пользователям ]:
Цитата:
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#580
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Sexual Activity and Cardiovascular Disease
A Scientific Statement From the American Heart Association [Ссылки доступны только зарегистрированным пользователям ] Комментарии на русском языке [Ссылки доступны только зарегистрированным пользователям ] |
#581
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Sodium, Blood Pressure, and Cardiovascular Disease Further Evidence Supporting the American Heart Association Sodium Reduction Recommendations 2012
[Ссылки доступны только зарегистрированным пользователям ] |
#582
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Умеренное употребление кофе ассоциируется с более низким риском инсульта:
результаты метаанализа проспективных исследований. [Ссылки доступны только зарегистрированным пользователям ] |
#583
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Я уверен, что большинство в курсе. Но может быть кто-то еще не знает про любопытный сайт [Ссылки доступны только зарегистрированным пользователям ]
К слову, именно там будет проходить трансляция АНОиСЗР 16.11.2012. |
#584
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Цитата:
J Thromb Haemost. 2012 Oct 20. Coffee consumption is associated with a lower risk of venous thrombosis which is mediated through haemostatic factor levels. Roach R, Siegerink B, le Cessie S, Rosendaal F, Cannegieter S, Lijfering W. Background: Coffee consumption is associated with a lower risk of venous thrombosis, but the role of confounding and the pathophysiology behind these findings are unclear. Objective: To assess the role of haemostatic factors in the relation between coffee consumption and venous thrombosis. Methods: From a large case-control study, 1803 patients with a first venous thrombosis and 1803 partner controls were included. With conditional logistic regression, odds ratios (OR) and 95% confidence intervals for venous thrombosis were calculated for coffee consumption versus no coffee consumption. In addition, mean differences in haemostatic factor levels between these groups were calculated in the controls. Results: Coffee consumption yielded a 30% lower risk of venous thrombosis compared with no coffee consumption (OR 0.7, 0.5-0.9). Adjustment for several putative confounders (age, sex, BMI, smoking, hormonal factors, statin, aspirin, alcohol, malignancy and chronic disease) yielded an OR of 0.8 (0.6-1.1). Results were similar for provoked and unprovoked events, and for deep vein thrombosis and pulmonary embolism. In controls, von Willebrand factor was 11 (3 to 19) IU/dL lower and factor VIII levels were 11 (1 to 21) IU/dL lower in coffee consumers than in non consumers. After adjusting the risk estimates for these haemostatic factors, the inverse association between coffee consumption and venous thrombosis diminished: OR 1.0 (0.7-1.4). There was no association between coffee consumption and anticoagulant proteins, fibrinogen levels or fibrinolytic markers. Conclusions: Coffee consumption is associated with a lower risk of venous thrombosis, which seems to be mediated through von Willebrand factor and factor VIII.
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Искренне, Вадим Валерьевич. |
#585
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Несколько цитат из дискуссии экспертов на medscape "в защиту" дабигатрана по поводу риска ИМ в сравнении с варфарином и другими новыми антикоагулянтами
[Ссылки доступны только зарегистрированным пользователям ] (речь про дополнительный анализ RE-LY) ...looked for new Q waves (silent MIs) in patients who were not reported to have had a MI. They found 28 further cases. Now the total number of MIs were distributed as roughly 98 and 97 in the dabigatran arms vs 75 in the warfarin group. There was no longer a significant trend pointing to a signal of concern with dabigatran. ....We went further and said MI is not the only myocardial ischemic event that can happen and we therefore included acute coronary syndrome. We included coronary vascularization by coronary artery bypass graft or percutaneous coronary intervention. We included cardiac arrest, which is oftentimes caused by ischemia. We included cardiovascular death. If we enrich our endpoints by combining this then we can see that there is absolutely no difference in terms of outcomes between the 3 groups. If anything, the dabigatran groups tended to have lower event rates than the warfarin group. What we also did is we looked at the predefined net clinical benefit in this analysis, which is a composite of mortality with MI, stroke, peripheral embolism, and major bleeding pulmonary embolism. If we do this analysis we again increase the number of outcome events and then we can find that there is no statistical difference between the low-dose dabigatran and warfarin but that there is, in fact, a significant reduction in the high-dose dabigatran group as far as net clinical benefit is concerned. ...(и непрямое сравнение новых антикоагулянтов между собой) The comparability of the trial populations has just been published in the Journal of the American College of Cardiology online. RE-LY and ARISTOTLE were very close in their profile. In fact, when you look at the indirect comparison, the MI hazard ratio was not statistically significant between dabigatran and apixaban. |