Intracerebral Hemorrhage: Large Disease Burden but Less Therapeutic Progress

The current issue of Journal of Stroke publishes three review articles regarding intracerebral hemorrhage (ICH).ICH is caused by diverse etiologies including hypertension, cerebral amyloid angiopathy, trauma, vascular malformation, and drugs.Compared to ischemic strokes, the incidence of ICH is lower.However, the 2010 Global Burden of Disease (GBD) Study showed that the absolute number of hemorrhagic strokes increased 47% worldwide for the last two decades, 1 mainly due to increased ICH in lowand middle-income countries.Moreover, as the population is aging, prevalence of ICH associated with amyloid angiopathy and anticoagulation is also increasing.Warfarin-associated ICH is associated with high mortality and disability.Currently, new oral anticoagulants (NOACs) rapidly replace vitamin K antagonists for stroke prevention in patients with atrial fibrillation; however, only one NOAC, dabigatran, has an antidote available.Management of NOAC-related ICH has become an emerging issue.Blood pressure (BP) is usually elevated in the acute phase of ICH.Studies have been performed to determine whether intensive BP lowering is more beneficial than standard BP treatment in the early phase of ICH.The INTERACT-2 study showed that early intensive BP lowering (target systolic BP < 140 mmHg) was moderately associated with lower mortality or major disability rate than standard BP lowering (target systolic BP < 180 mmHg). 2 However, the reasons for improved outcomes are unclear because changes in hematoma growth did not differ between the two groups.The ATACH-2 trial, which randomly assigned patients to the same BP targets as in INTERACT-2, showed that the outcomes were not different between the intensive and standard treatment groups. 3The hypothesis of these trials was based on the idea that intensive BP control might inhibit rebleeding or hematoma growth.However, the lower is not always the better.A