Stroke In Systemic Lupus Erythematosus Research Articles

OA19 Acute confusion, reduced conscious levels and stroke in systemic lupus erythematosus resulting from cerebral vasculitis

OA19 Acute confusion, reduced conscious levels and stroke in systemic lupus erythematosus resulting from cerebral vasculitis

Pathological Findings of Embolus Retrieved by Mechanical Thrombectomy in Cerebral Embolism with Libman-Sacks Endocarditis: A Report of Two Cases.

Libman-Sacks endocarditis is an important cause of embolic stroke in systemic lupus erythematosus, although the detailed pathogenesis of stroke remains unclear. We herein report two cases of stroke with Libman-Sacks endocarditis in which the emboli were retrieved by mechanical thrombectomy. The embolus consisted of eosinophilic homogeneous acellular structures, whereas fibrin-platelet thrombi were hardly observed in the embolus. Immunohistochemistry showed immunoglobulin deposits in the embolus, suggesting that immunological mechanisms were involved in the growth of the embolus. A pathological analysis of the embolus retrieved by mechanical thrombectomy provided useful information on the etiology, leading to optimal treatment.

Lupus, antiphospholipid syndrome, and stroke: An attempt to crossmatch.

Cerebrovascular accidents (CVAs) or strokes are part of the common thrombotic manifestations of Systemic Lupus Erythematosus (SLEs) and Antiphospholipid syndrome (APS). Such neurological thrombotic events tend to occur in patients with SLE at a higher frequency when Antiphospholipid antibodies (aPLs) are present, and tend to involve the large cerebral vessels. The mechanism of stroke in SLE can be driven by complement deposition and neuroinflammation involving the blood-brain barrier although the traditional cardiovascular risk factors remain major contributing factors. Primary prevention with antiplatelet therapy and disease activity controlling agent is the basis of the management. Anticoagulation via warfarin had been a tool for secondary prevention, especially in stroke recurrence, although the debate continues regarding the target international normalized ratio (INR). The presence of either of the three criteria antiphospholipid antibodies (aPLs) and certain non-criteria aPL can be an independent risk factor for stroke. The exact mechanism for the involvement of the large cerebral arteries, especially in lupus anticoagulant (LAC) positive cases, is still to be deciphered. The data on the role of non-criteria aPL remain very limited and heterogenous, but IgA antibodies against β2GPI and the D4/5 subunit as well as aPS/PT IgG might have a contribution. Anticoagulation with warfarin has been recommended although the optimal dosing or the utility of combination with antiplatelet agents is still unknown. Minimal data is available for direct oral anticoagulants (DOACs).

Isolated Insular Stroke: An Interesting Report of Two Cases.

Isolated Insular Stroke: An Interesting Report of Two Cases.

White Matter Hyperintensities as a Risk Factor for Ischemic Stroke in Patients With Systemic Lupus Erythematosus.

Objective: The occurrence of ischemic stroke in patients with systemic lupus erythematosus (SLE) can cause extended periods of reduced daily activities. However, the risk factors for ischemic stroke in SLE patients are not fully elucidated. Herein, we examined the effect of white matter hyperintensities (WMH) on the occurrence of ischemic stroke in SLE patients.Methods: We analyzed the relationship between WMH burden and ischemic stroke using follow-up brain magnetic resonance imaging (MRI) data of 79 patients with SLE. Of these patients, 16 developed stroke during the observation period. WMH on MRI were classified into periventricular hyperintensities and deep white matter hyperintensities (DWMH), while the lesion extent was graded using the Fazekas scale.Results: Kaplan–Meier curves showed that ischemic stroke events were significantly associated with age at initial brain MRI of ≥40 years (p = 0.015) and history of anti-phospholipid syndrome (p = 0.030). Additionally, ischemic stroke events were significantly associated with a one grade deterioration of periventricular hyperintensities (p = 0.003) and a one grade deterioration of DWMH (p = 0.002). Multivariate analysis using the logistic regression model showed that a one grade deterioration of DWMH was an independent risk factor for ischemic stroke (hazard ratio, 6.0; 95% confidence interval, 1.3–27.4).Conclusions: Although several factors affect the occurrence of ischemic stroke, SLE patients show increased risk of ischemic stroke via development of DWMH. An observation of DWMH deterioration on follow-up brain MRI may be useful for assessing the risk of ischemic stroke in SLE patients.

Stroke in systemic lupus erythematosus: epidemiology, mechanism, and long-term outcome

To determine stroke prevalence, mechanisms, and long-term outcome in a cohort of Hispanic patients with systemic lupus erythematosus (SLE). We analyzed demographical data, the timing between SLE diagnosis and stroke onset, stroke type, recurrence, and outcomes from an institutional database of 4451 patients with SLE followed from 1993 to 2018. We observed 139 strokes (3.1%), for an incidence rate of 1.25 per 1000 person-years: 81 (58.3%) acute ischemic stroke (AIS), 19 (13.7%) subarachnoid hemorrhage (SAH), 17 (12.2%) cerebral venous thrombosis, 13 (9.4%) intracerebral hemorrhage (ICH), and 9 (6.5%) transient ischemic attack. Median time from SLE diagnosis to acute stroke was 60 months (interquartile range 12-132 months). AIS had a bimodal presentation with 26% occurring within the first year and 30% >10 years after SLE diagnosis. In contrast, 75% of ICH cases occurred >3 years (and 34% >10 years) after SLE diagnosis. The most important cause of AIS was secondary antiphospholipid syndrome (48%). Hypertension was associated with 69% of ICH cases, while aneurysmal rupture was observed in 78% of SAH cases. Excellent recovery at hospital discharge was observed in 65%. Stroke recurrence was observed in 7%. The long-term all-cause fatality rate was 8%. The prevalence of stroke in this cohort was 3.1%. Ischemic strokes had a bimodal presentation, occurring either early after SLE diagnosis or after a several-year delay. Half of the hemorrhagic strokes occurred >10 years after the diagnosis of SLE. Clinical outcome was usually good with a relatively low recurrence rate.

Evaluation of oxygen extraction fraction in systemic lupus erythematosus patients using quantitative susceptibility mapping

The purposes of this study are to assess the oxygen extraction fraction (OEF) changes on MRI-based quantitative susceptibility mapping (QSM) in systemic lupus erythematosus (SLE) patients and to determine whether QSM-OEF is associated with disease activity in SLE. We enrolled 42 SLE patients and 20 healthy subjects (HS) who had no pathologies on conventional brain MRI. Disease activity was assessed using SLE Disease Activity Index (SLEDAI). For the measurement of QSM-OEF, QSM data were analysed using the Perfusion Mismatch Analyzer software program. Spearman's or Pearson's correlation coefficients were calculated, and independent predictors were identified through a multiple linear regression analysis. QSM-OEF was significantly higher in SLE than that in HS (51.3 ± 10.1 vs. 40.5 ± 3.7, p < 0.001). QSM-OEF was positively correlated with SLEDAI and the presence of neuropsychiatric symptom (NPS) scores (ρ = 0.663, p < 0.001 and ρ = 0.340, p = 0.028). At multiple linear regression analysis, SLEDAI and NPS were independently associated with QSM-OEF (standardized β = 0.426, p = 0.016 and standardized β = 6.148, p = 0.029). In the SLE patients, QSM-OEF is associated with disease activity, which might predict an increased risk of stroke in SLE.

Abstract TP205: Cerebrovascular Diseases in Hispanic Patients With Systemic Lupus Erythematosus

Introduction: Systemic Lupus Erythematosus (SLE) is an autoimmune disease that increases the risk for stroke. Here, we determined prevalence, stroke type, mechanism, and long-term outcome of patients with SLE-associated stroke. Methods: From an institutional cohort of 4454 patients with SLE, we identified 131 with stroke. We collected demographical data, time elapsed between SLE diagnosis and stroke onset, and data related to specific stroke type. Results: Prevalence of stroke in SLE was 2.9%. Figure shows the distribution of the stroke by type, as well as potential mechanisms. Median time from SLE diagnosis to stroke onset was 60 months (IQR 12-141) with high variability among stroke types. In 60% of patients with CVT and 30% of those with ischemic stroke, events occurred within the first 12 months of SLE diagnosis; indeed, stroke occurred prior to SLE (6%) or SLE was diagnosed during the clinical evaluation to ischemic stroke or CVT (10%). In contrast, 30% of ischemic strokes and 80% of hemorrhagic strokes occurred several years after diagnosis of SLE. An excellent clinical recovery at hospital discharge was observed in 68%. During a median follow-up of 84 months in 124 survivors of the acute phase, case fatality rate was 8.3%. Recurrence was observed in 7.2%. Conclusion: Prevalence of stroke in this large cohort of SLE patients was 2.9%. CVT commonly occurred early after SLE diagnosis. Patients with ischemic strokes had a bimodal presentation, occurring either prior to -or shortly after- the diagnosis of SLE, or after a delay of several years. In contrast, 80% of hemorrhagic strokes occurred several years after diagnosis of SLE. Long-term clinical outcome was usually favorable.

Mortality and Functionality after Stroke in Patients with Systemic Lupus Erythematosus.

To investigate mortality and functional impairment after stroke in systemic lupus erythematosus (SLE). Using Swedish nationwide registers, we identified 423 individuals with SLE and 1652 people without SLE who developed a first-ever ischemic or hemorrhagic stroke (1998-2013) and followed them until all-cause death or for 1 year. HR for death after ischemic or hemorrhagic stroke and the risk ratio of functional impairment (dependence in either transferring, toileting, or dressing) 3 months after ischemic stroke were estimated. One year after stroke, 22% of patients with SLE versus 16% of those without SLE died. After ischemic stroke, patients with SLE had an increased risk of death (HR 1.85, 95% CI 1.39-2.45), which was attenuated after controlling for SLE-related comorbidities (HR 1.41, 95% CI 1.04-1.91). Functional impairment at 3 months was increased in SLE by almost 2-fold (risk ratio 1.73, 95% CI 1.16-2.57). After hemorrhagic stroke, patients with SLE had an HR of 2.30 (95% CI 1.38-3.82) for death, which was increased even during the first month. Compared to subjects without SLE, mortality after ischemic stroke increases after the first month in individuals with SLE, and functionality is worse at 3 months. SLE is associated with all-cause death after hemorrhagic stroke even during the first month. A shift of focus to patient functionality and prevention of hemorrhagic strokes is required.

Stroke in systemic lupus erythematosus: a Swedish population-based cohort study

ObjectiveTo study the occurrence of ischaemic and haemorrhagic stroke in systemic lupus erythematosus (SLE) compared with the general population by age, sex and time since SLE diagnosisMethodsAdults with incident SLE...

Stroke in systemic lupus erythematosus and antiphospholipid syndrome: risk factors, clinical manifestations, neuroimaging, and treatment.

Neurologic disorders are among the most common and important clinical manifestations associated with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), mainly those that affect the central nervous system (CNS). Risk of cerebrovascular events in both conditions is increased, and stroke represents one of the most severe complications, with an incidence rate between 3% and 20%, especially in the first five years of diagnosis. This article updates the data regarding the risk factors, clinical manifestations, neuroimaging, and treatment of stroke in SLE and APS.

Temporal Trends of Mortality in Acute Ischemic Stroke in Systemic Lupus Erythematosus: A Propensity-Matched Analysis of Nationwide Inpatient Data (P2.295)

Temporal Trends of Mortality in Acute Ischemic Stroke in Systemic Lupus Erythematosus: A Propensity-Matched Analysis of Nationwide Inpatient Data (P2.295)

Transient ischemic attack and stroke in systemic lupus erythematosus

Ischemic stroke is increased in systemic lupus erythematosus (SLE) patients. The differential diagnosis of stroke in SLE is complex. Transient ischemic attack and ischemic stroke share pathophysiologic mechanisms, but prognosis may vary depending on severity and cause, and definitions are dependent on the timing and extent of the diagnostic evaluation. In SLE patients with a history of transient ischemic attacks, stroke occurred in 57%. Cerebrovascular events account for 20% to 30% of deaths in patients with SLE. In SLE, both disease-specific and traditional stroke risk factors are important.

Atypical aneurysms, vasculitis and stroke in systemic lupus erythematosus

(2001). Atypical aneurysms, vasculitis and stroke in systemic lupus erythematosus. British Journal of Neurosurgery: Vol. 15, No. 2, pp. 195-196.

Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus.

The frequency of coronary heart disease (CHD) and stroke are increased in systemic lupus erythematosus (SLE), but the extent of the increase is uncertain. We sought to determine to what extent the increase could not be explained by common risk factors. The participants at two SLE registries were assessed retrospectively for the baseline level of the Framingham study risk factors and for the presence of vascular outcomes: nonfatal myocardial infarction (MI), death due to CHD, overall CHD (nonfatal MI, death due to CHD, angina pectoris, and congestive heart failure due to CHD), and stroke. For each patient, the probability of the given outcome was estimated based on the individual's risk profile and the Framingham multiple logistic regression model, corrected for observed followup. Ninety-five percent confidence intervals (95% CIs) were estimated by bootstrap techniques. Of 296 SLE patients, 33 with a vascular event prior to baseline were excluded. Of the 263 remaining patients, 34 had CHD events (17 nonfatal MIs, 12 CHD deaths) and 16 had strokes over a mean followup period of 8.6 years. After controlling for common risk factors at baseline, the increase in relative risk for these outcomes was 10.1 for nonfatal MI (95% CI 5.8-15.6), 17.0 for death due to CHD (95% CI 8.1-29.7), 7.5 for overall CHD (95% CI 5.1-10.4), and 7.9 for stroke (95% CI 4.0-13.6). There is a substantial and statistically significant increase in CHD and stroke in SLE that cannot be fully explained by traditional Framingham risk factors alone.

Stroke in systemic lupus erythematosus.

We investigated the clinical and pathologic characteristics of stroke in 234 patients with systemic lupus erythematosus. Thirteen patients (5.6%) developed cerebrovascular disease. Cerebral infarction was noted in eight, cerebral hemorrhage in two, and subarachnoid hemorrhage in three. In seven (54%) of these 13 patients, stroke occurred less than or equal to 5 years after systemic lupus erythematosus was diagnosed. Among the predisposing risk factors for stroke, hypertension was the most important. Lupus anticoagulant was detected in three (38%) and anticardiolipin antibody in three (43% of seven investigated) of the patients with infarction. Evaluation of the clinical manifestations and autoantibodies indicated that renal involvement and high titers of anti-deoxyribonucleic acid antibody were more frequent in the stroke group than in the non-stroke group. Autopsy studies on six of the patients with stroke revealed small infarcts and hemorrhages in all, but in no case was true angiitis observed. Libman-Sacks endocarditis was found in two of the three patients with infarction. In conclusion, the important contributory factor to the development of stroke in patients with systemic lupus erythematosus is considered to be hypertension mediated by immunologic abnormalities. Antiphospholipid antibodies and Libman-Sacks endocarditis are closely associated with occlusive cerebrovascular disease.

Prevention of stroke in patients with systemic lupus erythematosis.

HomeStrokeVol. 21, No. 1Prevention of stroke in patients with systemic lupus erythematosis. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBPrevention of stroke in patients with systemic lupus erythematosis. A Achiron and I Sarova-Pinhas A AchironA Achiron Search for more papers by this author and I Sarova-PinhasI Sarova-Pinhas Search for more papers by this author Originally published1 Jan 1990https://doi.org/10.1161/01.STR.21.1.154Stroke. 1990;21:154–155"Prevention of stroke in patients with systemic lupus erythematosis.." Stroke, 21(1), pp. 154–155 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Wierzbicki A (2014) Stroke in systemic lupus erythematosus, Expert Review of Neurotherapeutics, 10.1586/14737175.2.3.385, 2:3, (385-390), Online publication date: 1-May-2002. Hinchey J and Sila C (1997) CEREBROVASCULAR COMPLICATIONS OF RHEUMATIC DISEASE, Rheumatic Disease Clinics of North America, 10.1016/S0889-857X(05)70331-8, 23:2, (293-316), Online publication date: 1-May-1997. January 1990Vol 21, Issue 1 Advertisement Article InformationMetrics Copyright © 1990 by American Heart Associationhttps://doi.org/10.1161/01.STR.21.1.154 Originally publishedJanuary 1, 1990 PDF download Advertisement