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#16
11.10.2004, 11:19
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ПРОДОЛЖЕНИЕ
Recurrent PE in patients treated with thrombolytic therapy
In the UPET trial, the incidence of recurrent PE was assessed by serial lung scans that were performed 2, 5, and 14 days after therapy in 160 patients. Recurrent PE was judged to be proven only if there was clinical and lung scan evidence of recurrence. The incidence of recurrent PE was the same in patients treated with heparin or urokinase 6% vs. 7%. In the recent report by Konstantinides et al., recurrent PE after treatment with heparin or alteplase was documented by lung scan, spiral CT or pulmonary angiogram. The rate of documented recurrent PE was 3.4% in patients treated with alteplase and 2.9% in those treated with heparin. The fact that thrombolytic therapy does not reduce the rate of recurrent PE is the major reason that it does not reduce the mortality of PE in hemodynamically stable patients. Complications of thrombolytic therapy The primary complication of thrombolytic therapy is bleeding. High rates of bleeding occur with thrombolytic therapy for PE despite modifications in dose, type of agent, rate of administration, and care in avoiding arterial punctures and venipunctures. In a review of 227 patients treated for PE with rt-PA, Levine reported an incidence of major bleeding of 8.4%, and an incidence of fatal hemorrhage of 2.2%. Konstantinides et al. reported an incidence of major hemorrhage of 21.9% in 169 PE patients treated with thrombolytics, compared to 7.8% in 550 patients treated with heparin. The most serious and the most lethal bleeding complication is intracranial hemorrhage (ICH), which is accurately assessed by CT scan. The incidence of intracranial hemorrhage in PE patients treated with heparin is 0.2%. However the incidence of ICH in patients treated with thrombolytics is much higher; 2.1% in one series of 559 patients and 3.0% in another series of 304 PE patients. The finding of no cases of ICH in the 118 patients reported by Konstantinides et al. is at variance with prior reports. As shown in Table 3, the incidence of ICH in the 981 patients included in the two earlier reports and the report by Konstantinides et al. is 2.1%. The incidence of ICH in PE patients is much higher than in acute myocardial infarction patients treated with the same doses of thrombolytics: 0.5-0.7%. The reason for this difference in the rate of ICH is unknown. This very significant incidence of ICH, which is fatal in 75% of cases, is a very compelling impediment to the use of thrombolytic therapy in hemodynamically stable patients in whom the mortality with heparin therapy is less than 5%. Cost of thrombolytic therapy Given a cost of US$ 2974 for 100 mg of alteplase (wholesale price, University Medical Center, Tucson, AZ, USA in 2003), the additional cost of treating the approximately 50% of PE patients who have right ventricular dysfunction, but who are hemodynamically stable would be formidable. This expense can not be justified since we have no evidence that these patients would benefit from such therapy and they would be subject to a very significant risk of major hemorrhage including ICH. In summary, there is no evidence that thrombolytic therapy benefits PE patients who are hemodynamically stable with or without RV dysfunction. Thrombolytic therapy may be of benefit to patients with massive PE complicated by shock; however, this has not been established by a randomized clinical trial. 
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#17
11.10.2004, 11:23
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Journal of Thrombosis and Haemostasis
Volume 2 Issue 8 Page 1473 - August 2004 FORUM Thrombolysis in submassive pulmonary embolism S.Z. Goldhaber Debates about the pros and cons of pulmonary embolism (PE) thrombolysis permeate academic meetings and journals. This tradition was initiated by Arthur Sasahara, the protagonist, and James Dalen, the antagonist, in 1980. The formula remains alive and well. Year 2003 featured a debate between Stavros Konstantinides vs. James Dalen in the inaugural issue of the Journal of Thrombosis and Haemostasis. The American College of Chest Physicians continued this popular sport by hosting a debate between Dalen and me at its Scientific Session in Orlando in October 2003. Debates on this topic appeal to journal editors and conference organizers because they attract readers who cite the articles and increase the 'impact factor' and crowds at conferences who find the showdowns memorable and return to the meeting the following year, thereby boosting attendance. Yet, debates serve as poor substitutes for data. As a cardiologist, I emerge from a culture where we solve debates with rigorous clinical trials. Occasionally, the trials will involve hundreds of patients. For major issues such as the utility of thrombolysis, the trials have required enrollment of thousands and at times tens of thousands of patients. We enroll patients in the trials with the conviction that we will obtain a definitive 'yes' or 'no' answer to a fundamental clinical question. We choose the question by determining where there is disagreement among colleagues and clinical equipoise, with sufficient uncertainty that a thoughtful clinician can advocate randomization to each arm of a therapeutic strategy. With Coronary Care Units pervasive throughout the world, and with acute myocardial infraction (MI) easily identified by history, electrocardiogram, and cardiac biomarkers, we can find eligible patients efficiently and move forward. In the field of PE thrombolysis, we have only enrolled 771 patients in 10 randomized clinical trials of thrombolysis plus anticoagulation vs. anticoagulation alone. An overview indicates a possible 25% reduction in mortality, with very wide confidence intervals. The same overview demonstrates a doubling of major bleeding complications, with narrow confidence limits. I feel we are obligated to determine whether the hint of mortality reduction is real or due to the play of chance. If the benefit is illusory, we must curtail thrombolysis except for patients with massive PE. If real, however, we must coordinate protocols to enhance patient safety and minimize bleeding complications. Why have we moved so slowly to answer the PE thrombolysis debate? First, we who are interested in this issue are dispersed in many specialties and subspecialties. This makes trial organization more difficult. Second, PE itself may be difficult to detect because it mimics so many other illnesses. Third, the patients stricken with PE may have medical comorbidities that make them far from ideal candidates for this type of clinical trial. Fourth, thrombolytic agents are considered 'mature drugs', with commercial patents expiring and usage declining as percutaneous coronary intervention displaces thrombolysis as the routine management strategy for acute MI. Consequently, industry sponsorship is meager. Fifth, with regard to Federal funding, PE thrombolysis is not necessarily viewed as a high priority area compared with hot topics such as preventing bioterrorism. Nevertheless, the time for excuses has expired. Harry Büller has demonstrated that a large number of patients with symptomatic PE can be successfully recruited into an international randomized clinical trial of patients with acute symptomatic PE. He and his colleagues, the 'Matisse Investigators', enrolled 2213 patients to compare the efficacy and safety of fondaparinux with unfractionated heparin. We must follow his example to settle the PE thrombolysis question. By enrolling high-risk patients with submassive PE, we can determine whether routine thrombolysis is worthwhile. Patients can now be diagnosed rapidly and accurately with chest CT scanning. Immediately after diagnosis, patients can be stratified to a high-risk group despite normal blood pressure by using a combination of echocardiography and cardiac biomarkers. Randomization to thrombolysis plus anticoagulation vs. anticoagulation alone can then take place. Please let me know if you would like to collaborate in solving this enduring clinical question.
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#18
11.10.2004, 11:26
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Journal of Thrombosis and Haemostasis
Volume 2 Issue 8 Page 1474 - August 2004 FORUM Thrombolysis in submassive pulmonary embolism A. Perrier For quite a number of years, the controversy whether or not to administer thrombolytics to patients with pulmonary embolism (PE) has been a popular source of 'pro' and 'contra' debates in scientific meetings. The small number of randomized studies (of which the largest was also the oldest) and their inclusion criteria that mixed patients with a wide spectrum of clinical severity precluded any meaningful conclusion. The issue has been somewhat focused by the identification of a subset of patients with a poorer prognosis despite the absence of overt arterial hypotension or shock. Those patients - termed as having submassive PE - share echocardiographic features of subclinical hemodynamic compromise, i.e. right ventricular (RV) hypokinesis, and have a mortality of 4% compared with around 1% for patients without RV dysfunction. However, merely identifying a higher risk group did not demonstrate that thrombolytic treatment would reduce mortality in that group and the evidence in favor of that hypothesis was only circumstantial. It relied on observational studies in which the assignment to thrombolytic treatment was not randomized and the mortality difference in favor of thrombolytic treatment might have been due to the preferential prescription of thrombolytics to younger patients with less comorbid conditions. Finally, other registry data showed no clear mortality difference. This prompted a team of German investigators to perform a large-scale randomized trial comparing heparin plus thrombolysis to heparin alone in patients with submassive PE. Thanks to that highly commendable endeavor, the evidence is available at last. Yet the controversy goes on and two experts recently reached diametrically opposite conclusions in the Journal of Thrombosis and Haemostasis based on the same study. What are the facts? The investigators randomized 256 patients with submassive PE into two groups (heparin-alteplase, 118; heparin-placebo, 138). The primary endpoint was composite and combined death or escalation of treatment (catecholamine administration or rescue thrombolysis) required by clinical deterioration. Clinical deterioration was defined as any of the following: worsening clinical symptoms, particularly dyspnea, or worsening respiratory failure due to PE; arterial hypotension or shock; and persistent or worsening pulmonary hypertension or right ventricular dysfunction detected by echocardiography or right heart catheterization; endotracheal intubation; cardiopulmonary resuscitation; and emergency surgical embolectomy or thrombus fragmentation by catheter. There was no difference in mortality (3.4% in the thrombolysis group and 2.2% in the heparin alone group). Therefore, the 13.6% absolute difference in favor of thrombolysis was driven only by clinical deterioration and rescue thrombolysis was administered to 23.2% of patients in the heparin group compared with 7.6% in the initial thrombolysis group. The indication for rescue thrombolysis in the 32 patients from the heparin group was worsening respiratory failure in 24, only 3 of whom were intubated. Finally, major bleeding rates were unusually low (0.8% in the thrombolysis group and 3.6% in the heparin group). Should we then interpret those data with enthusiasm or skepticism regarding thrombolysis? Actually, since patients from both groups achieved the same outcome in terms of mortality from PE, the only meaningful difference is the cost of thrombolysis, both in terms of major and intracerebral bleedings and of financial resources. Indeed, as commented by Dalen, the trial by Konstantinides et al. is clearly an outlier in terms of bleeding: the average figures from trials on thrombolysis in PE are a 10% major bleeding rate and a 2% fatal bleeding rate, consisting mostly of fatal hemorrhagic strokes. Applying systematic thrombolytic treatment to all patients with submassive PE would result in 14 excess deaths and a 43% increase in total costs. Although those figures are only crude estimates, they are probably quite realistic. In summary, what does the German trial teach us? First, that we should only thrombolyze those patients with submassive PE whose clinical condition worsens under heparin treatment, if any (since all such patients from the heparin group were thrombolyzed, there is no way of knowing how they would have fared without rescue thrombolysis and the trial does not demonstrate that thrombolytic treatment improved their outcome). Second, that data alone is not enough and a rigorous interpretation of the evidence is necessary. Variation in recommendations based on high levels of evidence is a well-known problem. This should remind us that data are neutral, those who interpret them are not.
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#19
11.10.2004, 11:30
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Journal of Thrombosis and Haemostasis
Volume 2 Issue 8 Page 1476 - August 2004 FORUM Thrombolysis in submassive pulmonary embolism A. Torbicki The controversy regarding indications for thrombolysis in submassive pulmonary embolism (PE) continues. Two eminent experts took opposing positions regarding this important clinical problem in the June issue of this journal. Clearly, more solid evidence is needed to resolve this debate. However, most importantly the definition of submassive PE, currently based on echocardiographic signs of right ventricular (RV) overload/dysfunction in an otherwise stable patient (no shock, no hypotension) should be reshaped, if it is to be used as indication for thrombolysis. In its present form this definition seems too liberal to justify potentially dangerous treatment. How does one identify those patients who might need more aggressive treatment? Management strategies and Prognosis of Pulmonary Embolism-3 Trial Investigators (MAPPET-3) gave an answer - by close observation and rapid intervention, whenever needed. Indeed, a patient with submassive PE is by definition stable. What we need to know is whether he improves or deteriorates despite promptly introduced anticoagulation. However, the monitoring of a patient with submassive PE should probably be different in 2004 than it was before. The concept of vulnerable, acutely overloaded RV, which can suffer further due to inadequate coronary supply and ultimately fail even in the absence of PE recurrence, suggests the need for close monitoring of indices related to RV ischemia and/or dysfunction. Serial echocardiography is not an attractive solution: it is complex, costly and probably not very precise: in particular the right ventricle-right artery (RV-RA) peak gradient might be a tricky measurement, since it can decrease both with effective treatment and with progressive RV failure. RV dimension changes might be difficult to follow with echocardiography because of complex RV geometry and problems with reproducibility. Doppler-assessed RV ejection pattern does not seem to be prognostically relevant. Serial assessment of troponin, B-type natriuretic peptides and myoglobin seem more promising. Troponin detected in plasma at presentation or during the first days of observation of a patient with acute PE was invariably found to indicate worse in-hospital prognosis. However, while monitoring the presence and intensity of troponin leakage from the RV myocytes may be useful in following patients with chronic pulmonary hypertension, troponin may have too long plasma half-life for optimal decision-making in acute PE. Indeed, just as it occurs in acute myocardial infarction, initially elevated plasma troponin may remain elevated for hours, despite improved hemodynamics and restored RV myocyte integrity. Therefore B-type natriuretic peptide, with its half-life of approx. 20 min might prove a more sensitive marker of improvement or deterioration. Though more related to stretching rather than to damage of the myocardium, it has been also reported as prognostically relevant in acute PE. Recently, the Warsaw group reported on the prognostic significance of an even more rapid responder, myoglobin. Those three biochemical markers, of which the former two are widely available as point of care tests, might provide us in the near future with an improved strategy detecting the response to initial anticoagulant treatment of patients with submassive PE. As prospective and adequately controlled trials assessing such strategies have yet to come, we need to define our local decision algorithms now. When deciding on such controversial issues I try to imagine myself as a patient with confirmed acute submassive PE, but remaining, despite tachycardia and dyspnea, without hypotension. Would I like to get thrombolysis, knowing what I know about its risks and benefits? Well, if my troponin was detectable and brain natriuretic peptide (BNP) was high I would feel quite concerned, but I would probably prefer to wait while watching the results of a reassuring infusion of heparin flowing into my vein. I would probably pay much attention to the direction of changes in my heart rate and blood pressure as well as pulsoximetry. If they were relatively stable I would probably wait 3-12 h or even longer to see the results of serial BNP and troponin point-of care testing, even in the absence of obviously increased personal risk of bleeding on thrombolytic therapy Frankly speaking when choosing this strategy I would also feel much safer, if I knew that my proximal deep veins and right heart chambers do not contain thrombi. On the other hand I would not feel reassured even with initially negative troponin, especially if my signs/symptoms were of short duration. Also then I would rely on what happens to me and to my biomarkers during the first 3-12 h of heparin infusion in the ICU. And while waiting for what will happen I would feel sorry that my colleague Tomkowski was not able so far to prospectively test his idea on very low-dose bolus of rt-PA on top of heparin as an initial treatment in submassive PE. And I would be also thinking how long it will take to verify and implement into clinical practice the message from a recent fascinating experimental report from a Chinese group, suggesting that urokinase bound to lung endothelium-specific antibody can induce local thrombolysis of PE without increasing systemic bleeding risk.
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#20
11.10.2004, 11:49
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Цитата: только вот пожизненно варфарин - это может быть слишком круто. Но 6 месяцев минимум.
Зависит от факторов риска и вида тромбофилии, напр.: Patients with distal VTE or VTE due to a transient risk factor are at a low risk of recurrence and short-term anticoagulation is indicated (3 months). Patients with an idiopathic event or with known thrombophilic defects such as FV Leiden or the G20210A prothrombin mutation are candidates for a longer course of therapy (6 months). Patients with cancer, antiphospholipid antibodies syndrome, recurrent idiopathic event, antithrombin deficiency, protein C or protein S deficiency, homozygosity for FV Leiden, and double heterozygosity are candidates for extended long-term anticoagulation. Из Semin Vasc Med. 2003 Aug;3(3):303-14. Oral anticoagulant therapy in venous thromboembolism. Cosmi B, Palareti G.
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#21
11.10.2004, 14:53
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И в совсем недавних рекомендациях:
4.2.1. For most patients with PE, we recommend clinicians not use systemic thrombolytic therapy (Grade 1A). In selected patients, we suggest systemic administration of thrombolytic therapy (Grade 2B). For patients who are hemodynamically unstable, we suggest use of thrombolytic therapy (Grade 2B). 4.2.2. We suggest clinicians not use local administration of thrombolytic therapy via a catheter (Grade 1C). 4.2.3. For patients with PE who receive thrombolytic regimens, we suggest use of thrombolytic regimens with a short infusion time over those with prolonged infusion times (Grade 2C). ----------- 5.1.1. For patients with a first episode of PE secondary to a transient (reversible) risk factor, we recommend long-term treatment with a VKA for at least 3 months (Grade 1A). 5.1.2. For patients with a first episode of idiopathic PE, we recommend treatment with a VKA at least 6 to 12 months (Grade 1A). 5.1.3. We suggest that patients with first-episode idiopathic PE be considered for indefinite anticoagulant therapy (Grade 2A). Underlying values and preferences. This recommendation ascribes a relatively high value to preventing recurrent thromboembolic events and a relatively low value on bleeding and cost. 5.1.4. For patients with PE and cancer, we recommend LMWH for the first 3 to 6 months of long-term anticoagulant therapy (Grade 1A). These patients should then receive anticoagulant therapy indefinitely or until the cancer is resolved (Grade 1C). 5.1.5. For patients with a first episode of PE who have documented antiphospholipid antibodies or who have two or more thrombophilic conditions (eg, combined factor V Leiden and prothrombin 20210 gene mutations), we recommend treatment for 12 months (Grade 1C+). For these patients, we suggest indefinite anticoagulant therapy (Grade 2C). Underlying values and preferences. This recommendation ascribes a relatively high value to preventing recurrent thromboembolic events and a relatively low value on bleeding and cost. 5.1.6. For patients with a first episode of PE who have documented deficiency of antithrombin, deficiency of protein C or protein S, or the factor V Leiden or prothrombin 20210 gene mutation, homocysteinemia, or high factor VIII levels (> 90th percentile of normal), we recommend treatment for 6 to 12 months (Grade 1A). We suggest indefinite therapy as for patients with idiopathic PE (Grade 2C). Underlying values and preferences. This recommendation ascribes a relatively high value to preventing recurrent thromboembolic events and a relatively low value on bleeding and cost. 5.1.7. For patients with two or more episodes of objectively documented PE, we suggest indefinite treatment (Grade 2A). 5.1.8. We recommend that the dose of VKA be adjusted to maintain a target INR of 2.5 (range, 2.0 and 3.0) for all treatment durations (Grade 1A). We recommend against high-intensity VKA therapy (INR range, 3.1 to 4.0) [Grade 1A]. We recommend against low-intensity therapy (INR range, 1.5 to 1.9) compared to INR range of 2.0 to 3.0 (Grade 1A). 5.1.9. In patients who receive indefinite anticoagulant treatment, the risk-benefit of continuing such treatment should be reassessed in the individual patient at periodic intervals (Grade 1C). 5.2 LMWH for the long-term treatment of PE The use of LMWH for the long-term treatment has been evaluated in three randomized trials in patients with DVT. The findings indicate that in patients with cancer, LMWH was more effective than VKA for preventing recurrent VTE. The recommendation about the use of LMWH in patients with cancer and PE is based on these studies. Recommendation 5.2.1. For most patients with PE and concurrent cancer, we recommend treatment with LMWH for at least the first 3 to 6 months of long-term treatment (Grade 1A) Remark: The LMWH regimens that have been established to be effective for long-term treatment are dalteparin, 200 IU/kg body weight qd for 1 month followed by 150 IU/kg qd thereafter, and tinzaparin at 175 IU/kg body weight SC qd. Из Chest. 2004;126:401S-428S. Antithrombotic Therapy for Venous Thromboembolic Disease The Seventh American College of Chest Physicians (ACCP) Conference on Antithrombotic and Thrombolytic Therapy Harry R. Büller, MD, Chair; Giancarlo Agnelli, MD; Russel D. Hull, MBBS, MSc, FCCP; Thomas M. Hyers, MD, FCCP; Martin H. Prins, MD and Gary E. Raskob, PhD
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#22
11.10.2004, 22:01
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Цитата:
 Уважаемый Alex, А если пересчитать с учетом данных, которые привел уважаемый Dr.Vad (Wan S et al. Thrombolysis compared with heparin for the initial treatment of pulmonary embolism: a meta-analysis of the randomized controlled trials. Circulation. 2004;110:744-9? Цитата:
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#23
12.10.2004, 05:53
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Да и смертность 5% маловата... От 8% для субмассивной и до 30% при массивной ТЭЛА, как в ICOPER. И риск ВМК не 3%, а 1.0 - 1.5% (а реально и того меньше).
30% смертность при наличии нестабильной гемодинамики, при стабильной гемодинамике риск смерти менее 5% (для массивной) Dalen JE. Pulmonary embolism: what have we learned since Virchow?: treatment and prevention. Chest. 2002;122:1801-1817., а реально и того меньше. В отношении диагностики гиперкоагуляции - выявление дефектов свертывающей системы будет обязывать к пожизненной антикоагуляции, что скорее всего имеет место в случае с описанной пациенткой. Так, что зря вы так насчет того, что тактика не меняется. Да, и вообще, все разговры о пользе вмешательства, которое нельзя продемонстрировать по снижению смертности могут носить только кулуарный характер - подальше от постели больного. Насчет стратификации полность с вами согласен, именно поэтому сейчас и проходит рекрутирование в новое исследование по тромболитикам с использованием критериев риска (наверное будет что-то типа TIMI). Насчет этического коммитета волноваться не стоит, ведь тромболитики нигде не являются стандартом лечения таких пациентов (в чем нам дали еще одну возможность убедиться приведенные ваше гайдлайнсы)
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#25
16.10.2004, 06:40
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Цитата:
1. При поступлении естественно была бы выполнеа спиральная томография грудной клетки и таза и нижнух конечностей и забрана кровь на антифосфолипидные антитела, фактор С, фактор S, фактор V Leiden, PT/PTT 2. У данной пациентки нет показаний к немедленному введению тромболитиков, поэтому был бы назначен низкомолекулярный гепарин. У нас используется эноксопарин (Lovenox) в дозе 1 мг на кг каждые 12 часов. 3. После поступления в блок интенсивной терапии скорее было бы выполнено ЭХО. 4. При необходимости тромболитики были бы назначены к порядке акселерации терапии при ухудшении клинической симптоматики (как в MAPETT 3) как вариант возможна тромэмболэктомия. Возможно был бы установлен инвазивный мониторинг гемодинамики (в основном следить на степенью легочной гипертензии). В данном случае скорее всего через бедренную вену. 5. При обнаружении тромбофилий пациенке варфарин показан перманентно. При идеопатической ТЭЛА на 6 месяцев.
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#26
20.10.2004, 14:04
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Цитата:
У больной имелся такой существенный фактор риска как прием оральных контрацептивов (+ ожирение). Надо, конечно, уточнить семейный анамнез и сроки приема контрацептивов. Но если в семье не было тромбоэмболических проблем и принимала регулон она уже несколько лет, то вероятность наличия тромбофилия не более 30%. И скорее всего – это будет лейденовская мутация или гена протромбина G20210А. Даже если, это окажется дефицит C, S или антитромбина, то врядли тромбофилия проявившаяся на фоне контрацептивов имеет высокий эмболический потенциал в дальнейшем...IMHO. Если больная не будет использовать оральные контрацептивы (что очевидно) да еще похудеет, то зачем ее обрекать на пожизненный прием варфарина с ежегодным риском фатального геморража 0.25 – 0.33%? Как вариант можно после отмены варфарина (например, через 6 месяцев) определить уровень D-димера и относительно полученного результата принимать решение о продолжении антикоагулянтной терапии [4, 5]. Хотя, если есть возможность без нечеловеческих усилий диагностировать тромбофилию, то почему бы и нет? В Москве, кажется, это делают только в гемцентре. Стоит около 800$. Цитата:
Уважаемый Alex, как в вашей клинике относятся к флотирующим тромбам - ограничиваются ли антикоагулянтами или ставят фильтры? P.S. Интересно, что с больной... 1. Lindmarker P, Schulman S, Sten-Linder M et al. The risk of recurrent venous thromboembolism in carriers and non-carriers of the G1691A allele in the coagulation factor V gene and the G20210A allele in the prothrombin gene. DURAC Trial Study Group. Duration of Anticoagulation. Thromb Haemost. 1999; 81(5):684-9. 2. Eichinger S, Weltermann A, Mannhalter C et al. The risk of recurrent venous thromboembolism in heterozygous carriers of factor V Leiden and a first spontaneous venous thromboembolism. Arch Intern Med. 2002; 162(20):2357-60. 3. van den Belt AG, Sanson BJ, Simioni P et al. Recurrence of venous thromboembolism in patients with familial thrombophilia. Arch Intern Med. 1997; 157(19):2227-32. 4. Palareti G, Legnani C, Cosmi B et al. Predictive value of D-dimer test for recurrent venous thromboembolism after anticoagulation withdrawal in subjects with a previous idiopathic event and in carriers of congenital thrombophilia. Circulation. 2003;108(3):313-8 5. Eichinger S, Minar E, Bialonczyk C et al. D-dimer levels and risk of recurrent venous thromboembolism. JAMA. 2003; 290(8):1071-4.
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#27
20.10.2004, 15:06
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Уважаемый Thorn (уж не Константин Станиславович?)!
цитата: Хотя, если есть возможность без нечеловеческих усилий диагностировать тромбофилию, то почему бы и нет? В Москве, кажется, это делают только в гемцентре. Стоит около 800$. Не могли бы Вы подсказать какие из тестов включены в "тромбофилическую батарею"? Хотя, подозреваю, что крановщица из Новосиба вряд ли воспользуется этим "заманчивым" предложением. Уж лучше (дешевле) тогда Д-димер после 6-12 мес. курса ОАК (полагаю, в Новосибе и его трудновато сыскать), но это еще не дефинитивная общепринятая тактика. Согласен, чти после первого даже идиопатич. тромбоза несколько жутковато сразу планировать пожизненно ОАК, проще и безопаснее профилактировать тромбозы в последующем в наиболее "тромбогенные" периоды жизни, но большинство наших докторов к этому не привыкло, в крайнем случае кто назначит аспирин...
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#28
20.10.2004, 15:32
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Цитата:
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#29
21.10.2004, 04:39
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Согласен с Вами, что не совсем понятна роль обследования на дефекты коагуляции у пациентов с DVT. Кроме этого в остром периоде определение факторов коагуляции часто не имеет смысла (за исключение генетических методик включай фактор V leiden и протромбин). DVT само по себе не является показанием для хронической антикоагуляции, вот при PE (тем более скорее всего хронических повторных PE - все-таки интересно было бы посмотреть давление в легочной артерии напрямую и данные СТ ангиографии) назначение варфарина пожизненно видимо более оправдано. Безусловно при этом нужно учитывать комплекс параметров, включающих степень легочной гипертензии, образ жизни, возможность для определения протромбинового времени и т.д.
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#30
02.11.2004, 14:24
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Цитата:
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Линейный вид
