Интересные ссылки

[Gilarov]

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[cactus1972]

Интересные выводы делают исследователи из Stanford Univercity

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Nitroglycerin, which treats impaired cardiac function through vasodilation as it is converted to nitric oxide, is used worldwide for patients with various ischemic and congestive cardiac diseases, including angina pectoris. Nevertheless, after continuous treatment, the benefits of nitroglycerin are limited by the development of tolerance to the drug. Nitroglycerin tolerance is a result of inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme essential for cardioprotection in animals subjected to myocardial infarction. Here, we tested the hypothesis that the tolerance that develops as a result of sustained nitroglycerin treatment increases cardiac injury by subsequent myocardial infarction. In a rat model of myocardial infarction, 16 hours of prior, sustained nitroglycerin treatment resulted in infarcts that were twice as large as those in untreated control animals and in diminished cardiac function at 3 days and 2 weeks after the myocardial infarction. We also sought to identify a potential treatment to protect against this increased cardiac damage. Nitroglycerin inhibited ALDH2 activity in vitro, an effect that was blocked by Alda-1, an activator of ALDH2. Co-administration of Alda-1 with the nitroglycerin prevented the nitroglycerin-induced increase in cardiac dysfunction after myocardial infarction in rats, at least in part by enhancing metabolism of reactive aldehyde adducts that impair normal protein functions. If our animal studies showing that nitroglycerin tolerance increases cardiac injury upon ischemic insult are corroborated in humans, activators of ALDH2 such as Alda-1 may help to protect patients with myocardial infarction from this nitroglycerin-induced increase in cardiac injury while maintaining the cardiac benefits of the increased nitric oxide concentrations produced by nitroglycerin.

Опубликовано в Science Translational Medicine 2 November 2011: Vol. 3, Issue 107, p. 107
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[disdas]

QT-Interval Duration and Mortality Rate
Results From the Third National Health and Nutrition Examination Survey

Yiyi Zhang, MHS; Wendy S. Post, MD, MS; Darshan Dalal, MD, PhD; Elena Blasco-Colmenares, MD, PhD; Gordon F. Tomaselli, MD; Eliseo Guallar, MD, DrPH


Arch Intern Med. 2011;171(19):1727-1733. doi:10.1001/archinternmed.2011.433

Background Extreme prolongation or reduction of the QT interval predisposes patients to malignant ventricular arrhythmias and sudden cardiac death, but the association of variations in the QT interval within a reference range with mortality end points in the general population is unclear.

Methods We included 7828 men and women from the Third National Health and Nutrition Examination Survey. Baseline QT interval was measured via standard 12-lead electrocardiographic readings. Mortality end points were assessed through December 31, 2006 (2291 deaths).

Results After an average follow-up of 13.7 years, the association between QT interval and mortality end points was U-shaped. The multivariate-adjusted hazard ratios comparing participants at or above the 95th percentile of age-, sex-, race-, and R-R interval–corrected QT interval (439 milliseconds) with participants in the middle quintile (401 to <410 milliseconds) were 2.03 (95% confidence interval, 1.46-2.81) for total mortality, 2.55 (1.59-4.09) for mortality due to cardiovascular disease (CVD), 1.63 (0.96-2.75) for mortality due to coronary heart disease, and 1.65 (1.16-2.35) for non-CVD mortality. The corresponding hazard ratios comparing participants with a corrected QT interval below the fifth percentile (<377 milliseconds) with those in the middle quintile were 1.39 (95% confidence interval, 1.02-1.88) for total mortality, 1.35 (0.77-2.36) for CVD mortality, 1.02 (0.44-2.38) for coronary heart disease mortality, and 1.42 (0.97-2.08) for non-CVD mortality. Increased mortality also was observed with less extreme deviations of QT-interval duration. Similar, albeit weaker, associations also were observed with Bazett-corrected QT intervals.

Conclusion Shortened and prolonged QT-interval durations, even within a reference range, are associated with increased mortality risk in the general population.

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[Igor73]

"Dronedarone increased rates of heart failure, stroke, and death from cardiovascular causes in patients with permanent atrial fibrillation who were at risk for major vascular events".
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[Chevychelov]

The VeriQ system for assessing graft flow during coronary artery bypass graft
surgery
Issued: November 2011
NICE medical technology guidance
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[Gilarov]

Bleeding risk assessment and management in atrial fibrillation patients
Executive Summary# of a Position Document from the European Heart Rhythm Association [EHRA], endorsed by the European Society of Cardiology [ESC] Working Group on Thrombosis
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[rsp]

[Ссылки доступны только зарегистрированным пользователям ] //Circulation published online January 19, 2012

[Gilarov]

Соду нафиг?
Sodium chloride vs. sodium bicarbonate for the prevention of contrast medium-induced nephropathy: a randomized controlled trial
Theresia Klima et al.

Aims The most effective regimen for the prevention of contrast-induced nephropathy (CIN) remains uncertain. Our purpose was to compare two regimens of sodium bicarbonate with 24 h sodium chloride 0.9% infusion in the prevention of CIN.

Methods and results We performed a prospective, randomized trial between March 2005 and December 2009, including 258 consecutive patients with renal insufficiency undergoing intravascular contrast procedures. Patients were randomized to receive intravenous volume supplementation with either (A) sodium chloride 0.9% 1 mL/kg/h for at least 12h prior and after the procedure or (B) sodium bicarbonate (166 mEq/L) 3 mL/kg for 1h before and 1 mL/kg/h for 6h after the procedure or (C) sodium bicarbonate (166 mEq/L) 3 mL/kg over 20min before the procedure plus sodium bicarbonate orally (500 mg per 10 kg). The primary endpoint was the change in estimated glomerular filtration rate (eGFR) within 48h after contrast. Secondary endpoints included the development of CIN. The maximum change in eGFR was significantly greater in Group B compared with Group A {mean difference −3.9 [95% confidence interval (CI), −6.8 to −1] mL/min/1.73 m2, P = 0.009} and similar between Groups C and B [mean difference 1.3 (95% CI, −1.7–4.3) mL/min/1.73 m2, P = 0.39]. The incidence of CIN was significantly lower in Group A (1%) vs. Group B (9%, P = 0.02) and similar between Groups B and C (10%, P = 0.9).

Conclusion Volume supplementation with 24 h sodium chloride 0.9% is superior to sodium bicarbonate for the prevention of CIN. A short-term regimen with sodium bicarbonate is non-inferior to a 7 h regimen.

Там же: Contrast-induced kidney injury: mechanisms, risk factors, and prevention
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[angio]

Любопытная ссылка - [Ссылки доступны только зарегистрированным пользователям ]

Скорее не для врачей, а для студентов и пациентов - собраны понятные и наглядные видеоролики, часть рекомендации по кардиологии, атласы по ЭКГ, ЭхоКС.
_______________________
P.S.: Имеется даже свой форум, который пытается набрать обороты (рекорд посещаемости 3, тем 5, ответов 7)

[rsp]

свежий [Ссылки доступны только зарегистрированным пользователям ] американцев о том когда и каким способом реваскуляризировать миокард

[Gilarov]

Для тех, кто жаждет ученых степеней:
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[Dr.Vad]

Сообщение от Gilarov

Вадим Валерьевич, а что делать с пациентом, если он закровил на варфарине? Витамина К1 в РФ нет...

Михаил Юрьевич, витамин К считается ОК, если у пациента высокое МНО, но нет кровотечения, в случае большого кровотечения на варфарине - лечение выбора -> СМП, причем согласно недавней публикации, если не удается выровнять МНО менее 1.5 в первый день, то у пациентов на варфарине с внутричерепным кровоизлиянием повышается риск умереть в 2.5 раза:

Among the subgroup of major bleeding patients with warfarin-associated ICH, those not correcting to INR of ≤1.5 with the use of FFP have an increased rate of mortality at 30 days (adjusted OR=2.55; 95% CI 1.04-6.28)...

Failure to Correct International Normalized Ratio and Mortality Among Patients with Warfarin-Related Major Bleeding: an Analysis of Electronic Health Records. Menzin J, Hoesche J, Friedman M, Nichols C, Bergman GE, Crowther M, Garcia D, Jones C. J Thromb Haemost. 2012 Jan 18

Другие публикации предлагают корректировать препаратом протромбинового комплекса как более эффективной/беzопасной опцией, но в Штатах это не всегда доступно...

Complete and rapid reversal of warfarin-induced bleeding can be achieved more successfully with PCC than with FFP. In addition, PCC is associated with a more rapid normalisation of the INR and a better clinical outcome due to the balanced ratio of four vitamin-K-dependent clotting factors plus the coagulation inhibitors protein C and Protein S. PCC products containing four factors are the preferred option for the emergency reversal of OAC, according to some clinical treatment guidelines. Other advantages of PCC over FFP include smaller infusion volumes, no blood group testing and virus-inactivated blood product.
Warfarin-induced bleeding complications - clinical presentation and therapeutic options.
Wiedermann CJ, Stockner I.
Thromb Res. 2008;122 Suppl 2:S13-8.
+++
Role of prothrombin complex concentrates in reversing warfarin anticoagulation: a review of the literature.
Leissinger CA, Blatt PM, Hoots WK, Ewenstein B.
Am J Hematol. 2008 Feb;83(2):137-43.

[Gilarov]

Вадим Валерьевич, спасибо за ссылку, но нам-то в РФ что делать? Лить плазму 15 мл на 1 кг живого веса? Нам и это не слишком доступно. PCC это вообще недостижимая мечта (диализ доступнее). Кстати, что Вы думаете о Новосевен?

[Dr.Vad]

Михаил Юрьевич, думаю, что неплохая опция, но очень дорогая даже по американским меркам и впечатляюще тромбогенна:

Stroke. 2010 Jul;41(7):1459-63.
Safety of recombinant activated factor VII in patients with warfarin-associated hemorrhages of the central nervous system.
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всякие сравнения коррекций в полном тексте еще здесь:

Int J Emerg Med. 2011 Jul 8;4(1):40.
Treatments for reversing warfarin anticoagulation in patients with acute intracranial hemorrhage: a structured literature review.
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[DoctorPetrov]

При наличии ингибиторов Xа фактора существование ингибиторов тромбина бессмысленно. У них нет никаких преимуществ, даже ценовых, а потенциальные риски длительного полного ингибирования тромбина никем не изучены. У тромбина полно других функций в организме, помимо участия в образовании фибрина, и подавление даже базального уровня антифизиологично.

Похоже, что над Прадаксой начинают сгущаться тучи. Количество кровотечений на дабигатране в реальной клинической практике намного превышает число кровотечений на варфарине.

Dabigatran (PRADAXA). This drug, which was launched in October 2010 to reduce the risk of stroke in patients with atrial fibrillation, generated hundreds of adverse event reports during the first quarter of 2011. Overall, 932 serious adverse events were linked to this drug, including 120 deaths, 25 cases of permanent disability, and 543 cases requiring hospitalization. Of the 932 events, 505 cases involved hemorrhage, more than any other monitored drug including warfarin, which ranked second with 176 cases of hemorrhage. The total included 120 cases that described the event with terms indicating hemorrhagic stroke, which is particularly problematic given that the drug’s primary indication is to prevent ischemic strokes.
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Похожие проблемы и в Японии.

In August 2011, the Japanese MHLW issued a safety advisory to warn of the potential for serious adverse events with dabigatran (Pradaxa®) which was approved in Japan in January 2011. This was following the death of five patients who were taking the drug. Between January and 11 August 2011, the patient exposure in Japan was about 64,000 people. At the time of publication of the advisory, there were 81 cases of serious side effects associated with dabigatran reported in Japan, including cases of gastrointestinal bleeding .

The five patients who had bleeding events contributory to their death were elderly, aged between 76 and 100 years old. They were prescribed with age-adjusted doses of dabigatran. The events leading to death include haemorrhage of the digestive tract, pulmonary alveolar haemorrhage, respiratory failure and haemorrhagic shock. The time to onset for these events ranged from eight days to 104 days. Two of these patients had taken aspirin concomitantly. Based on limited data available and a post-hoc estimation of creatinine clearance (CLcr), four of the patients were suspected to have severe renal impairment while on dabigatran therapy.

Physicians in Japan were advised to carefully monitor for signs of anaemia and bleeding and the need for immediate response should these side effects develop. They were also recommended to perform renalfunction tests before and during treatment, and to reduce the dose of dabigatran or stop treatment upon signs of renal impairment or bleeding.
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