Serial immune-inflammatory recovery trajectories after acute ischemic stroke: associations with early neurological deterioration and 90-day functional outcome in a retrospective cohort

 

'Associations' don't get you recovered, or are you too fucking stupid to see that? What prevents early neurological deterioration is the needed research, not this crapola! You've known of the need for almost a decade but INCOMPETENTLY did this instead! You're fired!

• Early neurological deterioration (36 posts to January 2017)

Serial immune-inflammatory recovery trajectories after acute ischemic stroke: associations with early neurological deterioration and 90-day functional outcome in a retrospective cohort

• 

  Ruihan Ni 1

• 

  Lan Chu 1,2*

• 1. Suzhou Medical College, Soochow University, Suzhou, Jiangsu, China

• 2. Department of Neurology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China

Abstract

Background: 

Systemic inflammation after acute ischemic stroke is usually assessed using admission biomarkers, which may not distinguish transient stress from sustained immune-inflammatory activation. We examined whether serial immune-inflammatory recovery trajectories were associated with early neurological deterioration (END) and 90-day functional outcome.

Methods: 

This single-center retrospective cohort included 760 adults with acute ischemic stroke identified from a hospital stroke database. NLR, SII, SIRI, and hs-CRP measured at admission, 24 h, 72 h, and day 7 were log-transformed and standardized, and equally weighted values were averaged at each observed time point. Latent class mixed models with 2–5 classes were compared without using outcome information, and a five-class solution was selected before association and prediction analyses. The primary outcome was 90-day mRS 3–6. END was defined as an NIHSS increase of ≥2 points within 72 h; the landmark END analysis excluded END within 24 h and tested 0–24 h immune change for END from 24 to 72 h.

Results: 

The five LCMM classes comprised 182 low-stable, 223 transient moderate, 161 delayed recovery, 122 persistent high, and 72 extreme persistent high patients. Among 751 patients with 90-day outcome data, the observed rate of mRS 3–6 increased from 21.5 to 30.6%, 44.2, 71.9, and 98.6% across these classes. After adjustment, persistent high (OR 2.46, 95% CI 1.31–4.61; p = 0.005) and extreme persistent high inflammation (OR 20.24, 95% CI 2.48–165.26; p = 0.005) were associated with mRS 3–6; a bias-reduced sensitivity estimate for the extreme class remained large (OR 13.61, 95% CI 2.34–79.26). Ordinal analysis showed progressively worse mRS for delayed recovery (common OR 2.73), persistent high (4.18), and extreme persistent high (6.72). The 0–24 h composite immune-change metric was not associated with landmark END (OR 1.12, 95% CI 0.92–1.36; p = 0.265). Adding LCMM-5 to the clinical model increased AUC from 0.828 to 0.841, but did not clearly outperform adding admission NLR/SII.

Conclusion: 

Longitudinal classification identified five immune-inflammatory recovery trajectories with a marked gradient in 90-day disability. Persistent-high and extreme persistent-high classes retained independent associations with poor functional outcome.