Cerebral venous thrombosis is an uncommon condition with difficulties in diagnosis and treatment. There is limited study on the best treatment option. The mainstay of treatment remains systemic anticoagulation with a lengthy duration of oral anticoagulants, which has a troublesome unpredictable drug effect, various drug and food interactions, and increased risk of bleeding. Recent availability novel anticoagulants provides an alternative treatment option for other medical conditions, such a prevention in stroke for Non-valvular Atrial Fibrillation patients (ROCKET, RE-LY or ARISTOTLE i.e.) . Do you think that a multi-center design protocol for standard treatment vs according to best medical and scientific practice could be made on this scenario
Dear Miguel
As you well pointed, cerebral venous thrombosis is an uncommon condition. This low incidence and its great clinical and etiological variability will limit the development of multi-center design protocol for standard treatment.
Probably in the next years several short series and isolated case-control studies will be published with the "off label" experience of patients with the antivitamin K indication changed/moved to NACOs. Most of them will be anticoagulant patients with bad control, inestability INR levels, or logistical problems to be well managed.
I agree with my colleague ; I think direct oral anticoagulant should be reserved to validated indications, as CVT is often linked with an abnormal condition as cancer or hemopahy, conditions in which DOA have not been evaluated properly.
I agree with all of you. Still, the bleeding risk is similar when it comes to DOA's in our population vs AVK. Have to read this new french study : "Etude des risques hémorragiques et thromboemboliques artériels liés au changement de traitement d’un médicament antivitamine K (AVK) vers un anticoagulant oral direct (AOD) chez les individus nécessitant une anticoagulation à long-terme en conditions réelles d’utilisation (02/07/2014) (1453 ko) - Etude ANSM
Given the rarity of the condition, an off-label use of NOADs is possible. However, the dosages of these drugs need to be calibrated such that they can be safely and effectively used. There should be caution in the use of these agents that a specific antidote is not available. Large clinical trials may be warranted to establish the evidence for the use of NOACs in cerebral vein thrombosis.
There is no argument to think against the possible use of NOA in this setting. However, large number of centers are needed to get an evidence in a relatively short time period. Of course, the genetic background should also be taken into account, especially for those with G20210A prothrombin mutation, given the type of action of these novel agents.
Dear colleagues:
I really appreciate your excellent comments regarding this topic. As a matter of fact, NOA have been placed as a good option, according the favorable pharmacological profile of these drugs, for Off-label conditions in thrombotic scenarios. But as many of you say, we should be careful when we translate pharmacological properties and apply them in other pathological conditions. I must confess, that sounds great when you see the results from other conditions, and also how patients behave with these drugs, but even with these "bonus stars", we must be impartial when we read evidence from many studies related to NOA, and for new possible applications, randomized controlled trials could be a reasonable answer, keeping in mind how versatile is cerebral vein thrombosis and its many pathophysiological approaches.
A good reading for NOA controversy could be found in Stroke 2014; 45:2158-2159