#16
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Цитата:
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#17
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Рутинно ВСУЗИ делают наверное только на "live cases" (да и то на 80%)
По данным многочисленных голосований (различные зарубежные мероприятия) на практике регулярно используют IVUS только 25-30% интервенционных кардиологов Остальные 70-75%, как то обходятся без этого Лично я бы не прочь "поиметь/заиметь" IVUS |
#18
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Цитата:
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#19
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Цитата:
В частности, рекомендуется использовать ВСУЗИ у пациентов с отчетливо маленьким (по результатам КАГ) диаметром коронарных артерий, например, если диаметр ПМЖА в проксимальном сегменте представляется < 3 мм, а диаметр ПКА в проксимальном сегменте (при сбалансированном и, особенно, правом типе кровоснаюжения сердца) - <3,5 мм. Кроме того, ВСУЗИ контроль рекомендуется использовать во всех случаях стентирования кальцинированных стенозов (когда кальциноз виден при флюороскопии), т.к. наличие неравномерно кальцинированных участков бляшки существенно увеличивает риск этого самого "stent underexpansion". |
#20
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[I]Где-то читал статью о рестенозе у онкологических пациентов с соотв. противоопухолевой терапией, так у них бинарный рестеноз был на уровне 8%. Может, чем лучше иммунитет у пациента, тем выше рестеноз? (и наоборот).[/quote][/I]
Коллеги! Поскольку тема еще не закрыта, позволю себе вопрос. Был у нас пациент, у которого в анамнезе опухоль где-то в подчелюстной зоне и с неоднократными облучениями, химиотерапией. К нам попал с ОИМ. На КАГ "жуть" - множественные стенозы ЛКА, ПКА с кальцинатами. Пациент до 40 лет. Потом где-то прочитал, что облучение приводит к кальцинозу коронарных артерий. Втречались ли облученные больные, есть ли какая-то особенность поражения коронарного русла? |
#21
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У меня было несколько человек после лучевой терапии, эти пациенты "запомнились" тяжелым диффузным поражением коронарного русла.
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#22
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Цитата:
Med Phys. 2002 Oct;29(10):2391-403. Pathophysiological effects of radiation on atherosclerosis development and progression, and the incidence of cardiovascular complications. Basavaraju SR, Easterly CE. Radiation therapy while important in the management of several diseases, is implicated in the causation of atherosclerosis and other cardiovascular complications. Cancer and atherosclerosis go through the same stages of initiation, promotion, and complication, beginning with a mutation in a single cell. Clinical observations before the 1960s lead to the belief that the heart is relatively resistant to the doses of radiation used in radiotherapy. Subsequently, it was discovered that the heart is sensitive to radiation and many cardiac structures may be damaged by radiation exposure. A significantly higher risk of death due to ischemic heart disease has been reported for patients treated with radiation for Hodgkin's disease and breast cancer... ----------------------- ...A 36-year-old man was admitted to the clinic with unstable angina pectoris of one month duration. The patient had no coronary artery disease risk factor. The history of the patient revealed that he had mediastinal radiotherapy due to Hodgkin's disease at 10-year of age. Coronary arteriography showed total occlusion of the left anterior descending artery and 70% stenosis of the proximal right coronary artery. Both arteries are dilated with placement of two stents. Control coronary arteriography at the end of the first year showed patency of both stents and the patient is free of symptoms. Previous radiotherapy to the mediastinum should be considered as a risk factor for the development of premature coronary artery disease. Percutaneous transluminal coronary angioplasty with stent placement or surgical revascularization are the preferred methods of treatment. Preoperative assessment of internal thoracic arteries should be considered prior to surgery... Z Kardiol. 2003 Aug;92(8):682-5. Radiation-induced coronary artery disease. -------------------------------------------------- ...15 subjects (8 men and 7 women, aged 25-56 years, mean 44) examined in the cardiac catheterisation laboratory, who had significant coronary artery disease years after having radiation treatment to the chest and anterior mediastinum. In the early stages of the study angiography was performed because of typical symptoms of ischaemic heart disease. Later on it was performed because of a high index of suspicion in people with signs of extensive radiation heart damage. The patients were relatively young and had no risk factors. Seven patients had no signs or symptoms of ischaemic heart disease. Ten patients had ostial stenosis, which was associated with extensive involvement of other cardiac structures in nine of them. Seven required surgical treatment for coronary artery disease. Two died, one at surgery and the other one six months later. Five patients had complications associated with irradiation... Br Heart J. 1993 Jun;69(6):496-500. Severe coronary artery disease after radiation therapy of the chest and mediastinum: clinical presentation and treatment.
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Искренне, Вадим Валерьевич. |
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#23
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У таких пациентов атеросклероз прогрессирует быстрее. А еще у них бывают тяжкие констриктивные перикардиты (иногда через несколько лет после лучевой терапии).
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#24
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Цитата:
Restenosis after successful ostial stent implantation: the role of statins compared with conventional treatment. Horlitz M, Amin FR, Boerrigter G, Sigwart U, Clague JR. Department of Cardiology, HELIOS Klinikum Wuppertal, Heartcenter Wuppertal, University of Witten/Herdecke, Arrenberger Strasse 20, D-42117 Wuppertal, Germany. Despite the introduction of coronary stents and effective anticoagulation regimens, the treatment of ostial lesions is limited by high restenosis rates. Initial results have been published asserting that statin therapy is associated with a significant reduction in restenosis after stent deployment. However, no information is available about the effect of statins after ostial stenting. Between 1993 and 2000, 122 patients required ostial placement of coronary stents at the Royal Brompton Hospital in London, United Kingdom. Statin treatment was continued or begun in 52 patients with a documentated hypercholesterolemia. Follow-up was feasible in 97 patients undergoing successful stent implantation. Restenosis rate was lower in patients receiving statins, but did not differ significantly from the nonstatin group (34.6% as against 42.2%, P = 0.531). //////////////////////////////////////////////////////////////////////////////////// J Cardiol. 2005 Mar;45(3):107-13. Combined treatment with statin and angiotensin-receptor blocker after stenting as a useful strategy for prevention of coronary restenosis. Nishikawa H, Miura S, Shimomura H, Tsujita K, Okamura K, Zhang B, Iwata A, Shirai K, Matsuo K, Arai H, Saku K. Department of Cardiology, Fukuoka University School of Medicine, Fukuoka. OBJECTIVES: 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) enhances the inhibitory effects of angiotensin-receptor blocker (ARB) on vascular neointimal formation in mice. The present case-control study investigated the efficacy of combined treatment with statin and ARB for preventing restenosis in patients with coronary artery disease. METHODS: We examined 210 patients with angina pectoris undergoing elective coronary stenting for de novo lesions of native coronary arteries. All enrolled patients received aspirin and ticlopidine. The subjects included patients who received no statin (control group, n = 137) or started statin treatment (statin group, n = 73) with or without ARB treatment after stenting. RESULTS: The rate of restenosis at 6 months after stent implantation in the statin group (19%) was significantly lower than that in the control group (32%). The restenosis rate in self-expanding Radius stents. (23%) was significantly lower than that in balloon-expandable Velocity stents (42%) independent of statin treatment. Patients treated with statins and ARBs were least likely [odds ratio (95% confidence interval): 0.30 (0.12-0.74)] to develop coronary restenosis, as assessed by multiple logistic regression analysis. CONCLUSIONS: These findings indicate that combined treatment with statin and ARB after stenting is a useful strategy for the prevention of coronary restenosis. ----------------------------------------------------------------- J Atheroscler Thromb. 2005;12(6):302-6. Effect of statin on restenosis after radius stent implantation in patients with acute coronary syndrome. Nishikawa H, Miura S, Shimomura H, Kawamura A, Tsujita K, Shirai K, Matsuo K, Arai H, Saku K. Department of Cardiology, Fukuoka University School of Medicine, Fukuoka, Japan. Despite reports that statin treatment reduces the rate of coronary restenosis with a balloon expandable stent, there is no evidence that statins affect the incidence of restenosis with a self-expanding Radius stent. Ninety-five patients with acute coronary syndrome who had been implanted with a Radius stent were classified into two groups: those with hyperlipidemia and initial statin treatment (statin group, n = 38) and those without statin treatment (comparative group, n = 57). At six months after stent implantation, the rate of coronary restenosis was significantly lower in the statin group (10.5%) than control group (28.1%) (p = 0.033), while there were no differences in morphology, maximal inflation pressure or stent size between the two groups. Interestingly, there was no difference in the serum lipid profile between the two groups at the 6-month follow-up, although the statin group had a significantly lower rate of restenosis. In conclusion, initial statin therapy reduced the rate of coronary restenosis even when a Radius stent was implanted.
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Искренне, Вадим Валерьевич. |
#25
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Я бы сказал, что нет сейчас понятия академического интереса, а есть - коммерческо-академический.
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#26
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Уважаемый Вадим Валерьевич, Ваши сообщения как раз и подтверждают слова доктора Козлова. В первом абстракте - эффекта нет, а во втором непонятно, то ли статин помог, то ли БРА. К тому же речь о "железках". Да и размер исследований не впечатляет. В общем, ясности нет.
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#27
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Уважаемый Михаил Юрьевич,
Согласен, что пока эвиденс слабоватый, но как говорицца, дайте срок... Кстати, третья статья доступна свободно [Ссылки доступны только зарегистрированным пользователям ] в ней собран более весомый референс с обьяснялками, нежели приведен мною...
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Искренне, Вадим Валерьевич. |
#28
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Цитата:
Какой предполагаемый механизм действия (влияния) статинов на рестеноз? Каким образом они тормозят пролиферацию? Ранее при ангиопластике мы "проходили" антагонисты Ca+, ингибиторы АПФ, и многое другое, включая гигантские дозы аскорбиновой кислоты (японцы кстати) и где это теперь? Все разбилось (кроме пробукола) при первых слепых исследованиях. |
#29
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Ну, каким образом тормозят... За счет плеотропного эффекта (подавление пролиферации гладкомышечных клеток). Правда, был тут недавно мета-анализ, показавший, что положительные эффекты статинов напрямую зависят от степени снижения холестерина и ни от чего более.
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#30
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Уважаемые коллеги,
далеко не специалист в этом, но вот что писали зарубежные спецы об этом: Curr Drug Targets Cardiovasc Haematol Disord. 2005 Apr;5(2):135-44. Statin-induced vascular smooth muscle cell apoptosis: a possible role in the prevention of restenosis? Erl W. Institut fur Prophylaxe und Epidemiologie der Kreislaufkrankheiten, Ludwig-Maximilians-Universitat, Pettenkoferstr. 9, Munchen, 80336, Germany. Growing evidence suggests that statins are more than simple lipid-lowering drugs. The so called pleiotropic effects of statins include multiple actions on cells of the vasculature. A large number of studies have confirmed that these compounds exert beneficial effects by mechanisms unrelated to cholesterol metabolism. For example, statins have been shown to inhibit the migration and proliferation of vascular smooth muscle cells (VSMC), and to induce apoptosis in this cell type. It is not yet clear if the induction of apoptosis in VSMC by statins is beneficial or detrimental. In the context of post-angioplasty restenosis, recurrent plaque growth after intervention, the inhibition of neointimal proliferation as well as a reduction of neointimal cell numbers by apoptosis is appealing. Multiple animal studies and clinical trials have therefore been undertaken to investigate effects of statin treatment on the development of restenosis, with very controversial results. Conversely, in advanced atherosclerotic lesions VSMC in the intima may stabilize the plaque and prevent plaque rupture by synthesizing collagen. VSMC in media adjacent to plaque areas or restenotic lesions should not be exposed to apoptosis promoting agents. In this context, recent evidence suggests that pravastatin protects such lesions by inhibiting inflammation and macrophage activation Our recent findings together with observations from other groups suggest that neointima cells are more sensitive to the induction of apoptosis than media VSMC. Importantly, statins were found to preferentially induce apoptosis in neointimal VSMC in our study. Кстати, вот весьма элегантная статья от корейцев, доступная в полной версии, - они показали, что положительное анти-рестенотическое действие статинов отмечалось только у пациентов с исходно высокими значениями ЦРП (вот одна из возможных обяснялок, почему не у всех пациентов после стентов статины "работают") [Ссылки доступны только зарегистрированным пользователям ]
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Искренне, Вадим Валерьевич. |