Prolonged Heightened Blood Pressure Following Mechanical Thrombectomy for Acute Stroke is Associated with Worse Outcomes.

BACKGROUND: Most data evaluating the relationship of post-mechanical thrombectomy (MT) blood pressure (BP) management and outcomes of patients with large vessel occlusion (LVO) focus on early BP control within the first 24 h. We investigated the correlation of daily BP trends up to the third day following MT with patient outcomes. METHODS: We retrospectively reviewed our prospectively maintained database for LVO patients treated with MT from February 2015 to December 2017. Recorded BP values for 72 h post-reperfusion were reviewed. Daily peak systolic and diastolic blood pressures (SBP, DBP) were extracted for each day post-procedure. The association and importance between BP increments of 10 mmHg and mortality, hemorrhage, and functional independence (FI = mRS ≤ 2) was analyzed in a multivariable logistic regression and random forest (RF) analyses modeling. RESULTS: A total of 212 thrombectomies were included. An increase in peak 24-h SBP was independently associated with higher likelihood of symptomatic hemorrhage (OR 1.2, p = 0.048) and decreased functional independence (OR 0.85, p = 0.03). Higher day 2 and day 3 peak SBP was strongly correlated with decreased functional independence and higher mortality. Third day SBP < 140 was independently associated with higher likelihood of functional independence (OR 4.3, p = 0.0004). Post-MT patients with and without functional independence demonstrated a similar relative decrease in peak SBP between the first 2 days following thrombectomy (p = 0.26); however, those without functional independence experienced a significant rebound increase in peak SBP on the third day following MT (mean change from day 2 to 3: FI - 3.5 mmHg, non-FI + 3.9 mmHg; p = 0.005). CONCLUSION: High daily maximum SBP and a rebound SBP on the third day following MT is independently associated with increased likelihood of functional dependence.

Endothelial dysfunction in cerebral aneurysms

Endothelial cell (EC) dysfunction is known to contribute to cerebral aneurysm (CA) pathogenesis. Evidence shows that damage or injury to the EC layer is the first event in CA formation. The mechanisms behind EC dysfunction in CA disease are interrelated and include hemodynamic stress, hazardous nitric oxide synthase (NOS) activity, oxidative stress, estrogen imbalance, and endothelial cell-to-cell junction compromise. Abnormal variations in hemodynamic stress incite pathological EC transformation and inflammatory zone formation, ultimately leading to destruction of the vascular wall and aneurysm dilation. Hemodynamic stress activates key molecular pathways that result in the upregulation of chemotactic cytokines and adhesion molecules, leading to inflammatory cell recruitment and infiltration. Concurrently, oxidative stress damages EC-to-EC junction proteins, resulting in interendothelial gap formation. This further promotes leukocyte traffic into the vessel wall and the release of matrix metalloproteinases, which propagates vascular remodeling and breakdown. Abnormal hemodynamic stress and inflammation also trigger adverse changes in NOS activity, altering proper EC mediation of vascular tone and the local inflammatory environment. Additionally, the vasoprotective hormone estrogen modulates gene expression that often suppresses these harmful processes. Crosstalk between these sophisticated pathways contributes to CA initiation, progression, and rupture. This review aims to outline the complex mechanisms of EC dysfunction in CA pathogenesis.

In vivo cerebral aneurysm models.

Cerebral aneurysm rupture is a devastating event resulting in subarachnoid hemorrhage and is associated with significant morbidity and death. Up to 50% of individuals do not survive aneurysm rupture, with the majority of survivors suffering some degree of neurological deficit. Therefore, prior to aneurysm rupture, a large number of diagnosed patients are treated either microsurgically via clipping or endovascularly to prevent aneurysm filling. With the advancement of endovascular surgical techniques and devices, endovascular treatment of cerebral aneurysms is becoming the first-line therapy at many hospitals. Despite this fact, a large number of endovascularly treated patients will have aneurysm recanalization and progression and will require retreatment. The lack of approved pharmacological interventions for cerebral aneurysms and the need for retreatment have led to a growing interest in understanding the molecular, cellular, and physiological determinants of cerebral aneurysm pathogenesis, maturation, and rupture. To this end, the use of animal cerebral aneurysm models has contributed significantly to our current understanding of cerebral aneurysm biology and to the development of and training in endovascular devices. This review summarizes the small and large animal models of cerebral aneurysm that are being used to explore the pathophysiology of cerebral aneurysms, as well as the development of novel endovascular devices for aneurysm treatment.

Extended Window for Stroke Thrombectomy.

OBJECTIVE: Mechanical thrombectomy is the standard treatment for large vessel occlusion (LVO) in acute ischemic stroke (AIS) up to 6 h after onset. Recent trials have demonstrated a benefit for wake-up strokes and patients beyond 6 h. METHODS: A systematic literature review was conducted for multicenter randomized clinical trials (RCTs) investigating endovascular stroke treatment using perfusion imaging to identify patients that may benefit from mechanical thrombectomy for AIS beyond 6 h of onset. Random effects meta-analysis was used to analyze the following outcomes: 90-day functional independence rates with modified Rankin Scale (mRS ≤2), 90-day mortality, and symptomatic intracranial hemorrhage (sICH) rates. Further stratification was carried out by age and presentation. RESULTS: Two multicenter RCT's were included as follows: DAWN and DEFUSE-3. Pooled 90-day functional independence rates favored endovascular management (odds ratio [OR] 5.01; P < 0.00001). Subgroup analysis demonstrated continued 90-day functional independence benefit for endovascular management regardless of age (≥80 years, OR 5.65, P = 0.01; ≤80 years, OR 4.92, P < 0.00001). When stratified for the manner of stroke discovery, 90-day functional independence rates favored endovascular management for wake-up strokes (OR 8.74, P < 0.00001) and known-time onset strokes (OR 5.08, 95% confidence interval [CI] 2.04-12.65, P = 0.0005), although no benefit was observed for unwitnessed strokes (OR 1.64, 95% CI 0.17-16.04, P = 0.67). No difference observed in 90-day mortality rates (OR 0.71; P = 0.14) or in SICH rates (OR 1.67; P = 0.29). CONCLUSIONS: This meta-analysis reinforces that endovascular management is superior to standard medical management alone for the treatment of AIS due to LVO beyond 6 h of onset in patients with perfusion-imaging selection.