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.

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.

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.

Background: and Purpose Secondary progressive multiple sclerosis (SPMS) presents with a challenging clinical phenotype, and siponimod has a potential to treat the active clinical phenotype of this disease. This single-center longitudinal study aimed to determine the therapeutic effects of siponimod in patients with active SPMS over 12 months. Methods: The clinical and radiological parameters of 50 patients with active SPMS treated using siponimod were assessed at baseline and after a 1-year follow-up period using the annual relapse rate (ARR), the Expanded Disability Status Scale (EDSS), the occurrence of gadolinium-enhanced lesion (GdE+), the Modified Fatigue Impact Scale (MFIS), and the Symbol Digit Modalities Test. The urine bladder postvoid residual (PVR) volume was also measured in a subcohort of 39 participants. Participants with an EDSS score ≥5.0 at baseline were finally assessed separately in prespecified subgroup analyses. Results: There were significant reductions in ARR (p<0.001), GdE+ (p<0.001), and MFIS score (p=0.001) during the follow-up period. The progression of physical and cognitive disabilities remained stable (p>0.05). The PVR-volume analysis revealed a significant decrease in urine bladder PVR volume (p<0.001). These observations were consistent for the subgroup with EDSS score ≥5.0. Conclusions Siponimod demonstrated efficacy in reducing ARR, GdE+, fatigue levels, and PVR volume, while maintaining stability in the cognitive and physical disability statuses of patients with SPMS. Similar findings were documented in the subgroup with EDSS score ≥5.0.

Background: and Purpose Secondary progressive multiple sclerosis (SPMS) presents with a challenging clinical phenotype, and siponimod has a potential to treat the active clinical phenotype of this disease. This single-center longitudinal study aimed to determine the therapeutic effects of siponimod in patients with active SPMS over 12 months. Methods: The clinical and radiological parameters of 50 patients with active SPMS treated using siponimod were assessed at baseline and after a 1-year follow-up period using the annual relapse rate (ARR), the Expanded Disability Status Scale (EDSS), the occurrence of gadolinium-enhanced lesion (GdE+), the Modified Fatigue Impact Scale (MFIS), and the Symbol Digit Modalities Test. The urine bladder postvoid residual (PVR) volume was also measured in a subcohort of 39 participants. Participants with an EDSS score ≥5.0 at baseline were finally assessed separately in prespecified subgroup analyses. Results: There were significant reductions in ARR (p<0.001), GdE+ (p<0.001), and MFIS score (p=0.001) during the follow-up period. The progression of physical and cognitive disabilities remained stable (p>0.05). The PVR-volume analysis revealed a significant decrease in urine bladder PVR volume (p<0.001). These observations were consistent for the subgroup with EDSS score ≥5.0. Conclusions Siponimod demonstrated efficacy in reducing ARR, GdE+, fatigue levels, and PVR volume, while maintaining stability in the cognitive and physical disability statuses of patients with SPMS. Similar findings were documented in the subgroup with EDSS score ≥5.0.

Background: and Purpose Secondary progressive multiple sclerosis (SPMS) presents with a challenging clinical phenotype, and siponimod has a potential to treat the active clinical phenotype of this disease. This single-center longitudinal study aimed to determine the therapeutic effects of siponimod in patients with active SPMS over 12 months. Methods: The clinical and radiological parameters of 50 patients with active SPMS treated using siponimod were assessed at baseline and after a 1-year follow-up period using the annual relapse rate (ARR), the Expanded Disability Status Scale (EDSS), the occurrence of gadolinium-enhanced lesion (GdE+), the Modified Fatigue Impact Scale (MFIS), and the Symbol Digit Modalities Test. The urine bladder postvoid residual (PVR) volume was also measured in a subcohort of 39 participants. Participants with an EDSS score ≥5.0 at baseline were finally assessed separately in prespecified subgroup analyses. Results: There were significant reductions in ARR (p<0.001), GdE+ (p<0.001), and MFIS score (p=0.001) during the follow-up period. The progression of physical and cognitive disabilities remained stable (p>0.05). The PVR-volume analysis revealed a significant decrease in urine bladder PVR volume (p<0.001). These observations were consistent for the subgroup with EDSS score ≥5.0. Conclusions Siponimod demonstrated efficacy in reducing ARR, GdE+, fatigue levels, and PVR volume, while maintaining stability in the cognitive and physical disability statuses of patients with SPMS. Similar findings were documented in the subgroup with EDSS score ≥5.0.

Cardioembolic stroke is a major cause of morbidity, with a high risk of recurrence, and anticoagulation represents the mainstay of secondary stroke prevention in most patients. The implementation of endovascular treatment in routine clinical practice complicates the decision to initiate anticoagulation, especially in patients with early hemorrhagic transformation who are considered at higher risk of hematoma expansion. Late hemorrhagic transformation in the days and weeks following stroke remains a potentially serious complication for which we still do not have any established clinical or radiological prediction tools. The optimal time to initiate therapy is challenging to define since delaying effective secondary prevention treatment exposes patients to the risk of recurrent embolism. Consequently, there is clinical equipoise to define and individualize the optimal timepoint to initiate anticoagulation combining the lowest risk of hemorrhagic transformation and ischemic recurrence in cardioembolic stroke patients. In this narrative review, we will highlight and critically outline recent observational and randomized relevant evidence in different subtypes of cardioembolic stroke with a special focus on anticoagulation initiation following endovascular treatment. We will refer mainly to the commonest cause of cardioembolism, non-valvular atrial fibrillation, and examine the possible risk and benefit of anticoagulation before, during, and shortly after the acute phase of stroke. Other indications of anticoagulation after ischemic stroke will be briefly discussed. We provide a synthesis of available data to help clinicians individualize the timing of initiation of oral anticoagulation based on the presence and extent of hemorrhagic transformation as well as stroke severity.