Afia, Mahmoud

The effect of induced hypertension (iHTN) on functional outcomes in noncardioembolic acute ischemic stroke (AIS) with early neurological deterioration remains unclear. We performed a systematic review and meta-analysis evaluating the safety and efficacy of iHTN vs medical management. A literature search of PubMed/MEDLINE, Web of Science, Ovid Embase, and Scopus from inception through November 6th, 2025. The protocol was registered in PROSPERO (CRD420261282211). Studies evaluating iHTN within 72 h of AIS onset and reporting 90-day functional independence (modified Rankin Scale [mRS] 0-2) were included. Safety outcome was hemorrhagic transformation. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) were estimated using random-effects model based on Restricted Maximum-Likelihood (REML) methods. Three studies were included, comprising 366 patients (iHTN, n = 180; control, n = 186). Mean age was 65.8 ± 11.8 years, 60.9% were men, and the mean initial NIHSS was 5.4 ± 3.5. Target systolic blood pressure (SBP) was a 15-25% increase from baseline SBP using phenylephrine. Functional independence at 90-days occurred more often in the iHTN group than in controls (68.8% vs 50.5%; RR = 1.37; 95% CI, 1.09-1.73; P = 0.007). Hemorrhagic transformation was uncommon and did not differ significantly between groups (3.3% vs 0.5%; RR = 2.08; 95% CI, 0.05-88.07; P = 0.70). In our study, phenylephrine-induced hypertension was associated with greater 90-day functional independence in selected AIS subtypes,without a significant increase in hemorrhagic transformation. However, the limited studies, predominance of retrospective designs, exclusively Asian cohorts, and heterogeneity in treatment protocols and populations warrant cautious interpretation and underscore the need for larger multicenter RCTs.

Background: Previous studies have reported the mean difference in homocysteine level in patients with and without silent brain infarction. However, evidence regarding the rate of silent brain infarcts in the presence versus absence of hyperhomocysteinemia remains limited. Objective: We aim to perform a systematic review and meta-analysis to compare the rate of silent brain infarcts in patients with hyperhomocysteinemia compared with patients with normal or low homocysteine levels. Methods: A systematic search of PubMed, Embase, Web of Science, Scopus were searched from inception to June 18, 2025. Eligible studies compared the rate of image-confirmed silent brain infarcts in patients with hyperhomocysteinemia versus those with normal homocysteine levels. The primary outcome was the rate of silent brain infarcts; the secondary outcome was cognition assessed by the Mini-Mental State Examination (MMSE). Pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated using a random-effects model, and heterogeneity was assessed using I 2 statistics. Subgroup analyses were performed according to increasing hyperhomocysteinemia cutoffs (>12 μmol/L and 9–12 μmol/L) as defined in the included the studies. Results: Four observational studies involving 2331 patients were included (mean age was 58.0±6.4 years, 45.8% women). Of these, 1087 had hyperhomocysteinemia and 1244 had normal levels. The rate of silent brain infarcts was 23.3% (253/1087) in patients with hyperhomocysteinemia versus 22.8% (284/1244) in controls (OR 1.82; 95% CI 1.11-3.00; P = 0.02, Figure 1A). The association was higher in studies using a > 12 µmol/L cutoff (OR 3.08; 95% CI 1.85-5.11; P < 0.0001, Figure 1B). Patients with hyperhomocystinemia had lower MMSE score compared with controls (mean difference of -1.55; 95% CI -3.60-0.50; P = 0.14, Figure 2). Conclusions: Hyperhomocysteinemia is associated with increased risk of silent brain infarcts and numerically lower cognitive performance. Findings suggest a possible dose-dependent relationship between homocysteine level and silent stroke risk. Prospective studies are needed to determine whether homocysteine is a modifable therapeutic tharget for reducing silent infarcts and cognitive decline.