Alexander E. Merkler, MD 

Turc G, Sallem A, Moulin S, Tisserand M, Machet A, Edjlali M, Baron JC, et al. Microbleed Status and 3-Month Outcome After Intravenous Thrombolysis in 717 Patients With Acute Ischemic Stroke. Stroke. 2015

Patients who receive intravenous tPA within 3 hours are 30% more likely to have minimal or no disability at 3 months – but does this hold true for every patient with an acute ischemic stroke? What if a patient’s initial MRI has cerebral microbleeds – are these patients at higher risk for hemorrhage and poor functional outcome?

Cerebral microbleeds are small areas of signal void seen on T2*, SWI, or SWAN imaging often due to hypertensive vasculopathy, amyloid angiopathy, or a combination thereof. Cerebral microbleeds are present on pre-treatment MRIs in 15-35% of patients with acute ischemic stroke. Whether or not cerebral microbleeds are associated with an increased risk of symptomatic hemorrhage or poor functional outcome at 3 months is uncertain and prior studies have conflicting results.

In the current study, Turc et al evaluated whether presence of cerebral microbleeds was associated with poor 3 month functional outcome in 717 patients who received IV tPA for acute ischemic stroke and who received a pre-treatment MRI. The authors assessed whether presence or burden of cerebral microbleeds was associated with poor functional 3 month outcome, whether underlying etiology of cerebral microbleeds (amyloid versus hypertensive) was associated with poor functional 3 month outcome, and as a secondary outcome, whether cerebral microbleeds were associated with symptomatic ICH.

On pre-treatment imaging, 20.9% of patients had at least one cerebral microbleed, 33 patients (4.6%) had 2-4 microbleeds, and 25 (3.5%) had ≥ 5 microbleeds. Amyloid was thought to be the etiology of the cerebral microbleeds in 40% of patients, hypertension in 22.7% of patients, and undetermined in 37.3% of patients.

The authors found no significant association between either presence or burden of cerebral microbleeds and poor 3-month outcome. Neither etiology of cerebral microbleed nor microbleed location was associated with poor 3 month outcome. In addition, there was no association between cerebral microbleeds and increased rates of symptomatic hemorrhage.

Two noteworthy limitations included 1) the fact that T2*/1.5 T MRIs were performed and perhaps newer modalities such as SWI or SWAN could have detected cerebral microbleeds in patients who were thought to have none and 2) the number of patients with a high burden of cerebral microbleeds was low, and perhaps the study was underpowered to detect a relationship in this subgroup of patients previously found to be at very high risk for poor functional outcome after IV tPA.

Overall, previous data regarding the association between cerebral microbleeds and poor functional outcome after IV tPA is conflicting. This large study supports the practice of not withholding tPA in an otherwise eligible patient with an acute ischemic stroke even in the presence of cerebral microbleeds on a pre-treatment MRI. However, as the authors mention, future studies are needed to detect whether there is a subset of patients with cerebral microbleeds who may be at higher risk of hemorrhage or poor functional outcome after tPA.