Developing a computer-aided image analysis and visualization tool to predict region-specific brain tissue “at risk” for developing acute ischemic stroke
Background and Purpose
Endothelial progenitor cells (EPCs) migrate from bone marrow to systemic circulation in response to tissue ischemia where they differentiate into mature endothelial cells for in situ angiogenesis. This study tested the hypothesis that the level of circulating EPCs is substantially increased and predictive of prognostic outcomes after acute ischemic stroke.
Methods
The level of circulating EPCs [staining markers: CD31/CD34 (E
1
), CD62E/CD34 (E
2
) and KDR/CD34 (E
3
)] was examined using flow cytometry at 48 h after acute ischemic stroke in 138 consecutive patients. The EPC level was also evaluated once in twenty healthy volunteers and in forty at-risk controls.
Results
Level of circulating EPCs (E
1–3
) was significantly higher in ischemic stroke patients than in at-risk control subjects (
p
<0.05). Additionally, EPC (E
1–3
) level was significantly lower in patients with severe neurological impairment [defined as a score ≥12 on the National Institute of Health Stroke Scale (NIHSS)] than in patients with less severe impairment (NIHSS < score 12) at 48 h after ischemic stroke (
p
<0.0001). Moreover, the EPC (E
3
) level was strongly correlated with improved NIHSS ≥ 4 on day 21 after ischemic stroke (
p
=0.0004). Furthermore, low circulating EPC level was independently predictive of severe neurological impairment (NIHSS ≥ 12) at 48 h (E
1–3
) and combined major adverse clinical outcomes (defined as recurrent ischemic stroke, any cause of death, or NIHSS of ≥ 12) on day 90 (E
1
) following ischemic stroke (
p
<0.001).
Conclusions
Level of circulating EPCs is independently predictive of prognosis after ischemic stroke.
Purpose of ReviewTo explore factors associated with infarct progression in the early and late phase of acute ischemic stroke in patients undergoing endovascular therapy.Recent FindingsFollowing ischemic stroke, brain injury can progress at a variable rate, at the expense of “penumbral tissue,” which is the ischemic tissue at risk of infarction. Despite dramatic advances in endovascular stroke therapies with early revascularization in more than 80% of cases, nearly half of patients do not achieve functional independence despite successful recanalization. This is largely attributed to the irreversible damage that is already extensive at the time of revascularization.SummaryThe underlying pathophysiology and determinants of the core infarct progression are complex and multifactorial, depending on a balance between brain energy consumption and collateral perfusion supply. It is crucial to develop creative and individualized theranostics to predict infarct progression and to “freeze” the tissue at risk prior to recanalization.
One of the reasons for the insufficient effectiveness of treatment of acute ischemic stroke may be secondary inflammation of the brain tissue, which, according to the results of modern studies, significantly worsens the consequences and outcome of the disease.