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“No-reflow” phenomenon in acute ischemic stroke
Abstract
Acute
ischemic stroke (AIS) afflicts millions of individuals worldwide.
Despite the advancements in thrombolysis and thrombectomy facilitating
proximal large artery recanalization, the resultant distal
hypoperfusion, referred to “no-reflow” phenomenon, often impedes the
neurological function restoration in patients. Over half a century of
scientific inquiry has validated the existence of cerebral “no-reflow”
in both animal models and human subjects. Furthermore, the correlation
between “no-reflow” and adverse clinical outcomes underscores the
necessity to address this phenomenon as a pivotal strategy for enhancing
AIS prognoses. The underlying mechanisms of “no-reflow” are
multifaceted, encompassing the formation of microemboli, microvascular
compression and contraction. Moreover, a myriad of complex mechanisms
warrant further investigation. Insights gleaned from mechanistic
exploration have prompted advancements in “no-reflow” treatment,
including microthrombosis therapy, which has demonstrated clinical
efficacy in improving patient prognoses. The stagnation in current
“no-reflow” diagnostic methods imposes limitations on the timely
application of combined therapy on “no-reflow” post-recanalization. This
narrative review will traverse the historical journey of the
“no-reflow” phenomenon, delve into its underpinnings in AIS, and
elucidate potential therapeutic and diagnostic strategies. Our aim is to
equip readers with a swift comprehension of the “no-reflow” phenomenon
and highlight critical points for future research endeavors.
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