Cerebral Microbleeds

Growing evidence suggests a link between cerebral microbleeds (CMBs) and increased risk of intracerebral hemorrhage (ICH), leading to concerns on the safety of administering antithrombotic drugs in patients with CMBs. This review summarized studies on the association among CMBs, ICH, and antithrombotic therapy (defined as antiplatelet and anticoagulant agents). Recommendations for future studies on this topic were also proposed.CMBs are small perivascular hemosiderin deposits (usually with macrophages) from leakage through cerebral small vessels, which can be visualized as small, rounded, homogeneous, and hypointense lesions on T2*-weighed gradient-recalled echo or susceptibility-weighted imaging MRI.1 CMBs indicate hemorrhage-prone pathological states, and studies have shown that the presence of CMBs is associated with increased risk of future ICH (odds ratio [OR], 8.52; 95% confidence interval [CI], 4.23–17.18),1 which is also the most feared complication associated with antithrombotic drugs. Thus, it is natural to wonder whether antithrombotic therapy should be averted in patients with CMBs. Different perspectives should be considered to address this question. In this review, we will seek to clarify this topic by answering the following questions: (1) What is the pathophysiology of CMBs? (2) Are CMBs common in populations who might require antithrombotic therapy? (3) Do patients taking antithrombotic therapy develop more CMBs? (4) Under antithrombotic therapy, do patients with CMBs have an increased risk of future ICH compared with patients without CMBs? (5) Does the increased risk of ICH outweigh the benefit of antithrombotic therapy in patients with CMBs? What Is the Pathophysiology of CMBs?Figure 1 illustrates our current understanding on the pathophysiology of CMBs. At least 2 pathological mechanisms may lead to CMBs: cerebral amyloid angiopathy (CAA) and hypertensive microangiopathy. CAA, characterized by amyloid-β deposition in vessel walls, is related to apolipoprotein E genotype.2 Amyloid-β, especially inflammatory amyloid, induces local inflammation ranging from mild changes to a granulomatous angiitis with apoptosis …