The Vessel Has Been Recanalized: Now What?

Abstract

When treating acute ischemic stroke patients in our daily clinical practice, we strive to achieve recanalization of the occluded blood vessel as fast as possible using pharmacological thrombolysis and mechanical clot removal. However, successful recanalization does not equal successful reperfusion of the ischemic tissue due to mechanisms such as microvascular obstruction. Even if successful reperfusion is achieved, numerous other post-recanalization tissue damage mechanisms may impair patient outcomes, namely blood–brain barrier breakdown, reperfusion injury and excitotoxicity, late secondary changes, and post-infarction local and global brain atrophy. Several cerebroprotectants are currently evaluated as adjunctive treatments to pharmacological thrombolysis and mechanical clot removal, many of which interfere with post-recanalization tissue damage pathways. However, our current lack of knowledge about the prevalence and importance of the various post-recanalization tissue damage mechanisms makes it difficult to reliably identify the most promising cerebroprotectants and to design appropriate clinical trials to evaluate them. Serial human MRI studies with complementary animal studies in higher order primates could provide answers to these critical questions and should be first conducted to allow for adequate cerebroprotection trial design, which could accelerate the translation of cerebroprotective agents from bench to bedside to further improve patient outcomes.