Table 2.

Competing and interacting mechanisms of post-thrombectomy microvascular failure.

Mechanism	Potential relationship to glycocalyx dysfunction	Representative evidence context	Potential readout	Key limitation
Distal embolization	Upstream, parallel, or independent; can sustain local low flow and endothelial stress.	Human procedural primary (24) + experimental	DSA/CTA; distal occlusion; perfusion defects	Not glycocalyx-specific; can directly cause perfusion failure.
Microthrombosis	Potential downstream amplifier, parallel pathway, or bidirectional interaction.	Experimental primary (26); indirect human	Coagulation/fibrinolysis markers; perfusion imaging	Multiple drivers including thrombin, stasis, emboli, inflammation.
Leukocyte plugging	Potential downstream amplifier after loss of anti-adhesive surface.	Animal no-reflow primary (25); indirect human	Leukocyte/endothelial activation markers; experimental microscopy	No direct human proof that glycocalyx loss is the upstream trigger.
Pericyte contraction	Parallel/interacting pathway via NO, oxidative stress, edema.	Animal/ex vivo primary (30, 31)	Experimental microscopy; perfusion	Direct glycocalyx-pericyte coupling after MT untested.
Endothelial swelling	Parallel or interacting endothelial injury mechanism.	Experimental/indirect clinical; broader no-reflow synthesis (5)	Perfusion imaging; pathology	Hard to separate from edema and other endothelial injury.
BBB disruption/edema/HT	Potential downstream and parallel pathway.	Experimental cerebral (9, 16) + human MT/EVT primary (28, 29)	Permeability imaging; edema; HT	Multifactorial and not glycocalyx-specific.
Complement activation	Upstream/parallel inflammatory stressor.	Experimental cerebral primary (20) + cross-disease	C3a/C5a; inflammatory panels	Temporal complexity; pleiotropic effects.
Impaired autoregulation/vasomotor mismatch	Parallel/interacting; potentially amplified by impaired mechanosensing.	Human imaging primary (27) + mechanistic inference	BOLD-CVR; CTP/MRP/ASL	Not specific to luminal-surface injury.
Glycocalyx dysfunction	Proposed interface/amplifier linking blood-facing stress to adhesion, coagulation, mechanosensing, and barrier biology.	Human biomarker primary (38–43) + experimental/cross-disease	Serial compartment-annotated shedding markers + imaging	No direct in-vivo cerebral glycocalyx visualization immediately after human MT.