Home Ischemic Stroke The No-Reflow Paradox: Unblocking the Vessel, Not the Damage?

The No-Reflow Paradox: Unblocking the Vessel, Not the Damage?

by Admin1122


 Well shit, you’re describing Capillaries that don’t open due to pericytes;

 known since September 2011. The whole stroke medical world IS COMPLETELY FUCKING INCOMPENT FOR NOT SOLVING THAT PROBLEM!

The No-Reflow Paradox: Unblocking the Vessel, Not the Damage?

  • Shravan Sivakumar

    , MD

    , @sshravanMD

Rivet
S, Churilov L, Yassi N, Kleinig TJ, Thijs V, Wu T, Dewey H, Desmond PM,
Parsons MW, Donnan GA, et al. Persistent Tissue-Level Hypoperfusion
(No-Reflow) Negates the Clinical Benefit of Successful Thrombectomy. Stroke. 2025.

In real-world clinical practice, a substantial number of ischemic
stroke patients fail to achieve functional independence, even after
technically successful thrombectomy with excellent angiographic
reperfusion scores (TICI 2C-3). This discordance has been described as
futile recanalization and may be attributable to a phenomenon referred
to as “no-reflow.” This has been conceptualized as the failure of
downstream microvascular reperfusion at the tissue level despite
successful macrovascular recanalization. Several mechanisms including
microvascular obstruction by microthrombi, edema-related microvascular
compression, and pericyte-induced capillary contraction may be at play.1
Its clinical relevance is magnified in the context of recent trials
expanding thrombectomy to patients with large core infarcts and
perfusion mismatch — groups where optimizing tissue-level perfusion may
be especially crucial. Prior research supports use of CTP imaging as a
better predictor of outcomes following successful recanalization than CT
angiogram alone and was even utilized as an indicator of therapeutic
success in recent thrombolytic trials.

The authors Rivet et al. aimed to investigate the clinical impact of
this no-reflow mechanism on functional outcomes by comparing patient
characteristics between patients with “no-reflow” mechanism on perfusion
imaging and varying degrees of angiographic recanalization (TICI
scores). They conducted a post hoc analysis on the data from three
clinical trials: EXTEND-IA (Endovascular Therapy for Ischemic Stroke
with Perfusion-Imaging Selection) and EXTEND-IA TNK (Tenecteplase Versus
Alteplase Before Thrombectomy for Ischemic Stroke) part 1 and 2 trials.
Both qualitative and quantitative evidence of tissue perfusion
evaluation for “no-reflow” were evaluated in a two-step process through
application of commercially available fully automated software (RAPID;
iSchemaView, Menlo Park, CA) on post-thrombectomy follow-up 24-hour
perfusion imaging (CTP or MR Perfusion). The authors identified 2
distinct regions of interest (ROI) which were superimposed into
perfusion maps and excluded signals associated with hemorrhagic
transformation of infarct. No-reflow was defined when both qualitative
and quantitative criteria were met — that is, visually demonstrable
reduced intralesional rCBV or rCBF and >15% interside reduction in
median rCBV or rCBF value2 (Figure 1). It is
worth noting that since the primary studies were not primarily designed
to evaluate for this phenomenon, not all patients had both MRP and CTP.

Figure 1. Imaging analysis method.
Figure 1. Imaging analysis method.

They compared both clinical and radiological characteristics of
patients with combinations of no-reflow or completeFlow with different
levels of angiographic success (full-TICI 2c3, partial-2b,
unsuccessful-0-2a). No significant difference in the rate of no-reflow
detection according to imaging modality (CT perfusion 13.6% [n=9/66]
versus MRP 25.0% [n=21/84]; P=0.10) was observed. No-reflow
mechanism occurred more frequently in successful angiographic
recanalization (TICI 3) (n=17/30, 56.7%). Among patient characteristics
across varying degrees of technical success, it is worth noting a
statistically significant difference among time of onset and proportion
of patients receiving thrombolytic (alteplase or tenecteplase).

The primary outcome of functional independence (mRS score of 0–2) was
achieved in 43.33% (n=13/30) of patients with eTICI 2c3–NoReflow,
versus 67.50% (n=81/120) of patients with eTICI 2c3–CompleteFlow, 63.03%
(n=150/238) of patients with eTICI 2b and 50.00% (n=34/68) of patients
with unsuccessful thrombectomy. In unadjusted analysis, patients with
no-reflow  were less likely to experience functional independence
despite technical success, TICI 2c-3 compared to completeFlow (odds
ratio [OR], 0.37 [95% CI, 0.16–0.83]; P=0.02) or those with eTICI 2b (OR, 0.45 [95% CI, 0.21–0.97]; P=0.04) but had similar rate to patients with unsuccessful thrombectomy (OR, 0.76 [95% CI, 0.32–1.82]; P=0.54).
When adjusted for age, premorbid mRS, baseline NIHSS, and baseline core
volume, multivariable analysis confirmed lower odds of functional
independence with no-reflow and full/partial recanalization, and similar
odds of functional independence with unsuccessful thrombectomy.
Furthermore, exploratory analysis of functional infarct volumes (FIV)
showed that despite similar volumes, patients with no-reflow had worse
outcomes despite full recanalization compared to partial recanalization.

These findings suggest that “no-reflow” phenomenon negates benefit of
macrovascular recanalization in achieving favorable clinical outcome.
The authors further caution that no-reflow mechanism tends to occur more
frequently with prolonged periods of ischemic injury, suggesting that
this prevalence could be underestimated by this study given the
inclusion of patients within the 4.5-hour time window. Their major
strength includes use of prospectively collected data from clinical
trials. As we push the boundaries of thrombectomy eligibility, tackling
the no-reflow phenomenon may be the next frontier in improving
patient-centered outcomes — representing a crucial step not only in
restoring macrovascular blood flow but also in minimizing downstream
ischemic injury, thereby broadening the therapeutic benefit for patients
with acute ischemic stroke.



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