Journal of Stroke最新文献

Background and purpose: Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture.

Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture.

Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27-0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05).

Conclusion: The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Background and purpose: This study aimed to investigate the association between residual inflammatory risk (RIR) and vulnerable plaques using high-resolution magnetic resonance imaging (HRMRI) in symptomatic intracranial atherosclerotic stenosis (ICAS).

Methods: This retrospective study included 70%-99% symptomatic ICAS patients hospitalized from January 2016 to December 2022. Patients were classified into four groups based on high-sensitivity C-reactive protein (hs-CRP) and low-density lipoprotein cholesterol (LDL-C): residual cholesterol inflammatory risk (RCIR, hs-CRP ≥3 mg/L and LDL-C ≥2.6 mmol/L), RIR (hs-CRP ≥3 mg/L and LDL-C <2.6 mmol/L), residual cholesterol risk (RCR, hs-CRP <3 mg/L and LDL-C ≥2.6 mmol/L), and no residual risk (NRR, hs-CRP <3 mg/L and LDL-C <2.6 mmol/L). Vulnerable plaque features on HRMRI included positive remodeling, diffuse distribution, intraplaque hemorrhage, and strong enhancement.

Results: Among 336 included patients, 21, 60, 58, and 197 were assigned to the RCIR, RIR, RCR, and NRR groups, respectively. Patients with RCIR (adjusted odds ratio [aOR], 3.606; 95% confidence interval [CI], 1.346-9.662; P=0.011) and RIR (aOR, 3.361; 95% CI, 1.774-6.368, P<0.001) had higher risks of strong enhancement than those with NRR. Additionally, patients with RCIR (aOR, 2.965; 95% CI, 1.060-8.297; P=0.038) were more likely to have intraplaque hemorrhage compared with those with NRR. In the sensitivity analysis, RCR (aOR, 2.595; 95% CI, 1.201-5.608; P=0.015) exhibited an additional correlation with an increased risk of intraplaque hemorrhage.

Conclusion: In patients with symptomatic ICAS, RIR is associated with a higher risk of intraplaque hemorrhage and strong enhancement, indicating an increased vulnerability to atherosclerotic plaques.

Background and purpose: Lipoprotein(a) [Lp(a)] is a lipoprotein structurally similar to low-density lipoprotein and is considered a genetically determined risk factor for cardiovascular disease. Although Lp(a) has been linked to ischemic stroke, its role in secondary stroke prevention, particularly in stroke recurrence, remains unclear.

Methods: A systematic search of MEDLINE and Scopus databases was conducted to identify randomized controlled trials (RCTs) and observational studies reporting Lp(a) levels in patients with ischemic stroke or transient ischemic attack. The primary outcome was stroke recurrence, and secondary outcomes included poor functional outcome, all-cause mortality, and recurrent vascular events. Pooled odds ratios (ORs) were calculated using a random-effects model.

Results: A total of 12 studies, including one RCT post hoc analysis and 11 observational studies, comprising 17,903 patients (mean age 63 years, 38% female), were included. Elevated Lp(a) levels were significantly associated with increased stroke recurrence (OR: 1.69; 95% confidence interval [CI]: 1.09-2.63; P=0.020) and poor functional outcome (OR: 2.09; 95% CI: 1.40-3.11; P<0.001). No significant associations were found between Lp(a) levels and all-cause mortality (OR: 2.20; 95% CI: 0.89-5.43; P=0.088) or recurrent vascular events (OR: 2.66; 95% CI: 0.95-7.44; P=0.063).

Conclusion: Elevated Lp(a) levels are linked to increased stroke recurrence and poor functional outcome in stroke patients. Lp(a) may represent a novel therapeutic target in secondary stroke prevention in addition to a promising biomarker.

Anticoagulation is crucial to reducing the risk of cardioembolic strokes, particularly in vulnerable populations such as patients with atrial fibrillation, artificial heart valves, or left ventricular thrombus. Though successful, anticoagulation failure (the occurrence of an ischemic stroke or systemic embolism while receiving therapy) remains a major stroke-care issue. The reason for anticoagulation failure can be below the required threshold, inability to follow up, drug-drug interactions, preexisting hypercoagulable states, or anticoagulant resistance. This failure undermines stroke prevention and requires tailored management, often requiring more drastic or alternative interventions. This review examines what drives anticoagulation failure and explores predictors of this failure in clinical, imaging, and laboratory data. It also discusses current management techniques for improving control and points to new treatments and possible futures, such as high-resolution imaging and personalized medicine based on biomarkers, to help tackle this critical clinical problem.

Background and purpose: The Treat Stroke to Target (TST) was a randomized clinical trial involving French and Korean patients demonstrating that a lower low-density lipoprotein cholesterol (LDL-C, <70 mg/dL) target group (LT) experienced fewer cerebro-cardiovascular events than a higher target (90-110 mg/dL) group (HT). However, whether these results can be applied to Asian patients with different ischemic stroke subtypes remains unclear.

Methods: Patients from 14 South Korean centers were analyzed separately. Patients with ischemic stroke or transient ischemic attack with evidence of atherosclerosis were randomized into LT and HT groups. The primary endpoint was a composite of ischemic stroke, myocardial infarction, coronary or cerebral revascularization, and cardiovascular death.

Results: Among 712 enrolled patients, the mean LDL-C level was 71.0 mg/dL in 357 LT patients and 86.1 mg/dL in 355 HT patients. The primary endpoint occurred in 24 (6.7%) of LT and in 31 (8.7%) of HT group patients (adjusted hazard ratio [HR]=0.78; 95% confidence interval [CI]=0.45-1.33, P=0.353). Cardiovascular events alone occurred significantly less frequently in the LT than in the HT group (HR 0.26, 95% CI 0.09-0.80, P=0.019), whereas there were no significant differences in ischemic stroke events (HR 1.12, 95% CI 0.60-2.10, P=0.712). The benefit of LT was less apparent in patients with small vessel disease and intracranial atherosclerosis than in those with extracranial atherosclerosis.

Conclusion: In contrast to the French TST, the outcomes in Korean patients were neutral. Although LT was more effective in preventing cardiovascular diseases, it was not so in stroke prevention, probably attributed to the differences in stroke subtypes. Further studies are needed to elucidate the efficacy of statins and appropriate LDL-C targets in Asian patients with stroke.