ESOC Session Highlight – Intracerebral Haemorrhage (I)

Christine Roffe and Roland Veltkamp from UK were the chairs of this first interesting session on ICH, don’t miss the main messages summarized here!

“ICH remains the most devastating presentation of stroke and documented treatment options in ICH remain scarce”. However, new knowledge is emerging, and this session will provide an overview.

The first speaker, Dr Marco Pasi from Boston, brought news insights on cerebellar bleeding and their underlying vasculopathy.  Cerebellar haemorrhages represent 10% of overall ICH, more than 70% of them are spontaneous. Small vessel disease (SVD) and cerebral amyloid angiopathy (CAA) are the most common causes. Interestingly, recently published data suggest that deep cerebellar ICH were often due to SVD, likely because of the intensive anastomosis in the nucleus caudate and its sensitivity to HTA. Cortical, superficial and vermis ICH were related to CAA, and are associated to supratentorial lobar cerebral microbleeds. Acute complications, associated with midline location, include brain stem compression, herniation and hydrocephalus and contribute to the huge overall mortality which is about 30-40%. To date, few and heterogeneous data are available on long-term outcome, because of differences on patient selection and clinical management… Join the important effort of the international collaboration on cerebellar ICH!

Second presentation by Pr Charlotte Cordonnier from University of Lille reported on ICH related to oral anticoagulants. About 15% of patients presenting at EDs for an ICH are under oral anticoagulant (both direct anticoagulant, DOAC and Anti-vitamin K, AVK): these patients suffer for larger volume ICHs, often have more comorbidities, and higher mortality rate. Volume expansion plays a pivotal role on poor outcome: time is brain!  Focusing on DOAC, do they bleed less? Yes, but definitions are crucial: data from Orange study showed that intracranial bleeding were less frequent in DOAC, nevertheless proportion of spontaneous ICH was the same in the DOAC vs AVK group! And even if intracranial bleedings are less frequent, we have more and more older patient that have atrial fibrillation! Concerning prognosis of DOAC-related ICH compared to AVK, observational data suggest that mortality rate is lower under DOAC, but clinically severity do not differ. Up to date, biological data do not provide clues in clinical practice and in particular, rivaroxaban plasma levels seem not to be associated with ICH volume. Waiting new data on antidotes for therapeutic management… do not forget the essentials! Stroke unit, intensive lowering of blood pression and reversion therapy!

Coming back to physiopathology and basic research, Pr Vincent Berezowski from Lille University reported data from animal models of ICH: what have they taught us? A lot! The complex mechanistic and biochemical cascade of events following RBC lysis has been unraveled with the two main models that have been available until now: direct blood injection, which permit control of haemorrhage volume and collagenases inject. Collagenase causes extensive vascular damage and triggers large hematoma expansion, with extensive activation of neuro-inflammation. New model of underlying vasculopathies are needed… and what about models for microbleeds? We are waiting for them!

The presentation of Pr Hagen Hutter, from University of Erlangen in Germany, reported on thorny questions on whether and when resuming anticoagulant after ICH. Randomized data are lacking, and only observational data are available to date. Risk of re-bleeding remains the major concern, nevertheless, for about 20% anticoagulant (AVK) are restart at 1 month:  in these patient’s risk of thrombo-embolic complications is reduced and risk of re-bleeding was not increase. However, important bias attributable to observational design should be considered: younger patients, better outcome, less cerebral microbleeds. Once again: we need to randomize! Is there a subgroup who could benefit more? Scores can be useful to stratify? Which is the best timing? Probably 4-6 weeks after ICH, with less concerns for deep ICH? Waiting for the exciting RCTs data!

During the last presentation, Pr Theodoros Karapanayiotides from Aristotle University of Thessaloniki, Greece, reported on “Management of statins in ICH patients: what should we do? Is there a higher risk of re-bleeding if we continue, discontinue or initiate a statin after ICH? Many unanswered questions are still open. Statins discontinuation has been associated with higher in-hospital mortality, but data are heterogeneous, and confounders likely impact these results. Puzzle is pretty complicated from a biochemical and physio-pathological point of view, different risk profiles depending on HDL and LDL has been discussed and more evidence is needed to conclude on clinical indications..

Barbara Casolla