Donc pas de preuve EBM de l'int�r�t d'une anticoagulation imm�diate des AVC associ�s � une FA. C'est ce que l'article qui a initi� cette discussion, r�v�lait et j'ai donc appris des choses. merci. PT
=?iso-8859-1?Q?Martin_Ch=E9nier?= a *crit : > Voici des extraits de la m�ta-analyse de Cochrane qui m'apparaissent fort > int�ressants. On consid�re l'anticoagulation aigu lorsqu'effectu�e dans les > 2 SEMAINES de l'�pisode. Aucune cat�gorie de patients ne semble b�n�ficier > du traitement. Certains passages mettent en doute la pertinence de > l'anticoagulation prophylaxique pour la MTE dans ce contexte. Ceux qui sont > int�ress�s � avoir le texte complet peuvent me le faire savoir (PDF de 437 > kb). > > "...Acute stroke treatments should aim to prevent disability as well as > death, lest patients survive their acute stroke only to remain severely > disabled. The present randomised evidence indicates that routine immediate > anticoagulation does not provide any net short or long-term reduction in > death or disability. Although immediate anticoagulation leads to fewer > recurrent ischaemic strokes, avoiding nine ischaemic strokes per 1000 > patients treated, this benefit is entirely offset by a similar-sized > increase in the number of intracranial haemorrhages. The net result is no > short- or long-term benefit..." > > "iii) Prevention of deep vein thrombosis and pulmonary embolism in acute > ischaemic stroke. > > In patients with presumed or confirmed ischaemic stroke, allocation to > immediate anticoagulation was associated with a highly significant 79% > reduction in the odds of deep vein thrombosis during the treatment period, > similar to that seen with the use of prophylactic heparin in patients > undergoing different types of surgery (Collins et al 1988). > > In this systematic review, the reductions in deep vein thrombosis with acute > anticoagulation were substantial, with 281 deep vein thromboses prevented > per 1,000 patients treated. However, as mentioned previously, this estimate > is based on relatively small numbers of patients, and most of the deep vein > thromboses detected were asymptomatic. In addition, there was significant > heterogeneity in the effects of treatment which was difficult to explain. > > If however, one accepts the estimate of treatment effect, it is then > difficult to assess the extent to which it may be generalisable. The stroke > patients included in the trials of anticoagulants to prevent deep vein > thrombosis generally had quite severe strokes, and paralysis of one leg > (with the attendant high risk of deep vein thrombosis) was almost invariably > present at randomisation. Furthermore, with the widespread intorduction of > Stroke Units, with policies of early mobilisation and good hydration, the > risk of deep vein thrombosis may well be lower. > > In addition to deep vein thrombosis prevention, the risk of pulmonary > embolism was also reduced significantly with the use of anticoagulants (OR > 0.61; CI 0.45 - 0.83), with an additional four pulmonary emboli avoided per > 1000 patients treated. The overall risk of pulomary embolism appeared to be > low, and the absolute benefit was small, and so the apparent reduction in > deep vein thrombosis may have little clinical relevance if there is not a > correspondingly large reduction in pulmonary embolism. However, there may > well have been under-ascertainment of pulmonary embolism in all of the > trials, since pulmonary emboli were not sought systematically. In addition, > deep vein thrombosis can lead to morbidity (eg. post-phlebitic leg and > varicose ulcers), but data on these outcomes were not available from the > trials. > > If anticoagulants result in no net increase or decrease in long-term death > or disability, but do lead to a reduction in the number of deep vein > thromboses and pulmonary emboli (albeit in immobile patients at higher > risk), then the benefit of fixed heparin regimens associated with a low risk > of bleeding (eg. low fixed-dose unfractionated heparin) may yet outweigh the > increased risk of haemorrhage. Unfortunately, there were insufficient > randomised data comparing low-dose heparin to aspirin, or to > non-pharmacological interventions such as compression stockings or early > mobilisation, to determine what the most effective and safe antithrombotic > regimen for deep vein thrombosis prophylaxis might be. > > However, it is interesting to note from the IST (IST 1997) that the > frequency of fatal and non-fatal symptomatic pulmonary embolism (perhaps a > surrogate for the occurrence of deep vein thrombosis) was very similar among > patients allocated low dose subcutaneous heparin alone (0.8%) and aspirin > alone (0.7%). Aspirin alone may therefore be an adequate antithrombotic > agent to be used for routine deep vein thrombosis prophylaxis in many > patients with acute ischaemic stroke. There is substantial evidence to > support the use of antiplatelets in deep vein thrombosis and pulmonary > embolism prophylaxis in other categories of high-risk patients (APT 1994b). > > Finally, it is possible that once anticoagulants are stopped, rebound > thrombosis could occur, and deep vein thromboses may begin to develop. We > were unable to exclude this possibility because no trials sought deep vein > thrombosis systematically after the treatment period. " > > v) Different categories of patient.. > > This systematic review provides information about the use of anticoagulants > in stroke patients in general, as well as limited information about various > subgroups. It is recognised that the evaluation of subgroups should only be > undertaken with caution due to the increased potential for error due to the > smaller numbers of patients and outcomes being evaluated. With that > qualification in mind, the small amounts of (randomised) sub-group data > evaluated here do not provide any evidence to support the routine use of > anticoagulants in any specific category of stroke patient, including those > with: cardioembolic stroke, 'stroke in progression', vertebrobasilar > territory stroke, or following thrombolysis for acute ischaemic stroke to > prevent re-thrombosis of the treated cerebral artery." > > MC > > ----- Original Message ----- > From: "paulaye" <[EMAIL PROTECTED]> > To: "URG-L Mailing List" <[EMAIL PROTECTED]> > Sent: Monday, December 10, 2001 5:21 AM > Subject: URG-L: RE: URG-L: Re: URG-L: RE: URG-L: FA et accident isch�mique > c�r�bral. > > ATTENTION!!! > Ne me faites pas dire ce que je n'ai pas dit. > - Il faut faire le SCAN en urgence!!! > - IL est FORMELLEMENT indiqu� d'administrer de l'HBPM SC � DOSES PREVENTIVES > dans l'AVC isch�mique, ce en pr�vention de la maladie thromboembolique. La > discussion portait sur l'anticoagulation curative > Par ailleurs, il persiste de rares indications � l'anticoagulation > th�rapeutique : > 1- les porteurs de valve m�canique (relais des AVK) > 2- 2 situations, o� m�me en l'absence de preuve certaine, il y a un fort > consensus professionnel : la dissection carotidienne, et la thrombophl�bite > c�r�brale (voir �tude de l'�quipe de Heidelberg)
