Search

Vascular disease recurrence following stroke is the main cause of morbidity and mortality. The MITICO study was designed to assess the prognostic value of markers of inflammation in relation to the risk of recurrence of vascular disease. Multi-centered prospective observational study, in patients with ischemic stroke not receiving anti-coagulation therapy and who were recruited within 1–3 months from stroke onset. Blood samples were obtained at baseline and follow- up for the determination of high-sensitive C reactive protein (CRP), IL-6, IL-10, ICAM-1, VCAM- 1, MMP-9 and cellular fibronectin. Four follow-up visits within the first year were to rule out recurrence. Of 965 patients from 65 hospitals, 780 (aged 67.5±11.2 years, 33.6 % female) were valid for main analysis. One-hundred and three patients (13.2 %) had a new adverse vascular event and 116 patients (14.9 %) a vascular event or vascular death (66.4 % stroke, 21.5 % coronary and 12.1 % peripheral). Levels of IL-6 > 5 pg/mL and VCAM-1 > 1350 ng/mL (ROC curve analyses) were associated with vascular disease recurrence risk (OR: 28.7; 95 % CI: 14.2–58.0 vs. OR: 4.1; 95 % CI: 2.4–7.1, respectively) following adjustment for confounding variables. Risk of adverse vascular event or death from vascular disease were associated with IL-6 (OR: 21.2; 95 % CI: 11.6–38.7) and VCAM-1 (OR: 3.8; 95 % CI: 2.3–6.4). Baseline values of IL-6 > 5 pg/mL and VCAM-1 > 1350 ng/mL increase 21-fold and 4-fold, respectively, the risk of new vascular disease event or death from vascular disease in patients with ischemic stroke not receiving anti-coagulation treatment. [ABSTRACT FROM AUTHOR]

Background and purpose Enlarged perivascular spaces (EPVS) have been recently considered a feature of cerebral small vessel disease. They have been related to aging, hypertension and dementia but their relationship with hypertension related variables (i.e. target organ damage, treatment compliance) and mild cognitive impairment (MCI) is not fully elucidated. Our aims were to investigate the relation between basal ganglia (BG) and centrum semiovale (CSO) EPVS with vascular risk factors, hypertension related variables and MCI. Methods In all, 733 hypertensive individuals free of stroke and dementia from the Investigating Silent Strokes in Hypertensives, a magnetic resonance imaging Study (ISSYS) underwent brain magnetic resonance imaging and cognitive testing to diagnose MCI or normal cognitive aging. Results The numbers of participants presenting high grade (>10) EPVS at the BG and CSO were 23.3% and 40.0%, respectively. After controlling for vascular risk factors, high grade BG EPVS were associated with age (odds ratio 1.68; 95% confidence interval 1.37, 2.06), poor antihypertensive compliance (1.49; 1.03, 2.14) and the presence of microalbuminuria (1.95; 1.16, 3.28), whereas in the CSO only age (1.38; 1.18, 1.63) and male sex were associated with EPVS (1.73; 1. 24, 2.42). MCI was diagnosed in 9.3% of the participants and it was predicted by EPVS in the BG (1.87; 1.03, 3.39) but not in the CSO. This last association was greatly attenuated after correction for lacunes and white matter hyperintensities. Conclusions Basal ganglia EPVS are associated with the presence of microalbuminuria and poor adherence to antihypertensive drugs. The BG EPVS relation with MCI is not independent of the presence of other cerebral small vessel disease markers. [ABSTRACT FROM AUTHOR]

Summary Patients with malignant middle cerebral artery (MCA) infarctions who have undergone craniectomy are susceptible to the development of vascular epilepsy. Our objective was to study the factors that might influence the occurrence of seizures in this group of patients. Materials and methods All patients who developed malignant MCA infarction and had undergone decompressive craniectomy in our center between November 2002 and January 2014 were evaluated. In the subsequent follow-up, we evaluated the clinical outcomes and attempted to identify the factors that were related to the occurrence of seizures. Results We evaluated a total of 80 patients. The median time at which the craniectomy was performed was 40.5 h after the stroke. Seizures occurred in 47.5% of all patients. The mortality rate within the first week was 16%, and of those who survived 53.7% developed seizures; 9% of these seizures were acute symptomatic, and 44.8% were remote. The median onset of remote seizures was seven months, and the majority of these were motor seizures with generalization. Notably, the patients with seizures exhibited longer delays from stroke to craniectomy, greater involvements of the temporal lobe and a higher rate of post-craniectomy recanalization of the occluded artery. Regarding the timing of the surgeries, a significantly greater proportion of those who underwent surgery more than 42 h after the stroke developed epilepsy ( p = 0.004). Logistic regression revealed that only prolonged delay (>42 h) independently predicted the development of epilepsy (OR 5.166; IC 95% 1.451–18.389; p = 0.011). Conclusions More than half of patients with malignant MCA infarcts who underwent decompressive craniectomy developed epilepsy. The occurrence of seizures in these patients was related to the delay to the performance of the craniectomy. [ABSTRACT FROM AUTHOR]

Background and purpose Recently, brain and vascular imaging have been added to clinical variables to identify patients with transient ischaemic attack ( TIA) with a high risk of stroke recurrence. The aim of our study was to externally validate the ABCD3-I score and the same score taking into account intracranial circulation. Methods We analyzed data from 1137 patients with TIA from the PROMAPA study who underwent diffusion-weighted magnetic resonance imaging ( DWI) within 7 days of symptom onset. Clinical variables and diagnostic work-up were recorded prospectively. The end-points were subsequent stroke at 7 and 90 days follow-up. Results A total of 463 (40.7%) subjects fulfilled all inclusion criteria. During follow-up, eight patients (1.7%) had a stroke within 7 days, and 14 (3.1%) had a stroke within 3 months. In the Cox proportional hazard multivariate analyses, the combination of large-artery atherosclerosis and positive DWI remained as independent predictors of stroke recurrence at 7- and 90-day follow-up [ HR 8.23, 95% confidence interval ( CI) 2.89-23.46, P < 0.001]. The ABCD3-I score was a powerful predictor of subsequent stroke. The area under the receiver operating characteristic curve was 0.83 (95% CI 0.72-0.93) at 7 days and 0.69 (95% CI 0.53-0.85) at 90 days. When we include intracranial vessel disease in the score, the area under the curve increases but the difference observed was non-significant. Conclusion The inclusion of vascular and neuroimaging information to clinical scales ( ABCD3-I score) provides important prognostic information and also helps management decisions, although it cannot give a complete distinction between high-risk and low-risk groups. [ABSTRACT FROM AUTHOR]

The risk of recurrent stroke is likely related to etiology. Therefore it is important to identify which patients are at highest early risk. We evaluated whether selected blood biomarkers may aid in the diagnosis of stroke etiology. We studied consecutive non-lacunar stroke patients between November 2006 and January 2007, and selected undetermined origin strokes. Blood samples were drawn at arrival to test brain natriuretic peptide (BNP), D-dimer, CK-MB, myoglobin, and troponin. Second harmonic transthoracic echocardiography (SHTTE) and ECG-24 h monitoring were also performed within the first 24 h. We evaluated 294 patients with ischemic stroke; 89 had an initial undetermined origin. After a cardiological work-up, 49 were diagnosed as embolic including atrial fibrillation (4), severe aortic arch atheromatosis (24), severe wall abnormalities (12), valve disease (3), dilated cardiomyopathy (1), and patent foramen (5). Higher levels of CK-MB, BNP, and myoglobin were found in patients with embolic source in SHTTE, but only CK-MB >1.5 ng/ml and BNP >64 pg/ml remained as independent predictors: BNP (OR 8.86; CI 95 % 2.79-28.09), CK-MB (OR 6.28; CI 95 % 1.66-23.69). BNP showed specificity of 75 %, sensitivity of 63.4 %, and positive predictive value (PPV) of 75.6 %. CK-MB had specificity of 85 %, sensitivity of 47.9 %, and PPV of 79.3 %. Measuring both biomarkers improves the finding of embolic source, increasing specificity to 95 % and PPV to 88.2 %. High-level CK-MB and BNP during the acute phase of ischemic stroke are associated with an embolic source. Measurement of both biomarkers may improve the diagnosis, guiding the need to perform a heart exploration. [ABSTRACT FROM AUTHOR]

Osteopontin (OPN) is a multifunctional protein which has shown neuroprotective properties in animal models of cerebral ischemia. Nevertheless, its role in acute human stroke has not yet been established. Therefore, we aimed to determine human serum OPN level during acute ischemic stroke and its relationship with patient outcome. We measured OPN levels in 178 consecutive patients with a middle cerebral artery (MCA) occlusion who received fibrinolytic therapy and in 40 control subjects. OPN level was determined by an enzyme-linked immunosorbent assay (ELISA). Bad functional outcome was defined by modified Rankin Scale (mRS) score >2 at 3 months after stroke onset. A logistic regression analysis was performed to determine factors that could be independently associated with poor prognosis. OPN levels among stroke patients did not differ from the controls' OPN levels (16.65 vs. 17.83 ng/mL, p = 0.404). Interestingly, OPN level was increased among those patients who showed worse prognosis at 3 months (19.96 vs. 15.48 ng/mL, p = 0.040). In a logistic regression model, an OPN level >27.22 ng/mL was found to be an independent factor for a bad outcome (OR 5.01, 95% CI 1.60-15.72, p = 0.006) after adjusting for potential confounders. Those patients showing higher OPN levels before tPA administration displayed a worse prognosis compared to those with lower OPN levels. Further research is necessary to elucidate the role of OPN in ischemic stroke pathophysiology and validate OPN as a useful tool to predict long-term stroke outcome. [ABSTRACT FROM AUTHOR]

Delay in arrival to the emergency room (ER) may negatively influence outcome of stroke patients. We aim to analyze factors that influence extra-hospital delay in stroke patients. Two hundred and ninety-two consecutive stroke patients admitted in the ER were prospectively studied. Analysis was made to identify variables associated with <1- and <3 h delays from onset. About 18.8% of patients arrived before 1 h and 57.5% before 3 h. Factors independently associated with <3 h delay were decision to go immediately to ER (OR = 8.17; 95% IC = 4.47–18.8), ambulance transportation (OR = 2.35; 1.36–4.05) and total anterior circulation syndrome (TACS) (OR = 3.74; 1.51–9.24). History of >1 vascular risk factor was associated with a greater delay (OR = 0.47; 0.26–0.86). Factors associated with a <1 h delay were: (i) immediate decision to attend the ER (OR = 3.55; 1.85–6.81), (ii) stroke on Sunday (OR = 3.46; 1.56–7.66), (iii) aphasia (OR = 2.41; 1.23–4.74), (iv) absence of stairs at home (OR = 0.37; 0.17–0.81) and (v) absence of diabetes mellitus (OR = 0.42; 0.20–0.88). In our area, nearly 60% of stroke patients arrive to ER before 3 h from onset. Immediate decision to attend the ER has the strongest association with a short delay. Patients with TACS arrived mainly before 3 h and those with isolated aphasia arrived before 1 h. Patients with vascular risk factors attended the hospital later. Ambulance transportation is associated with <3 h delay, but not with <1 h. [ABSTRACT FROM AUTHOR]

Background: We aimed to evaluate the prognostic value of myocardial perfusion gated SPECT in patients with symptomatic intracranial large-artery atherosclerosis (ILA). Methods: Seventy-two consecutive first-ever symptomatic ILA patients without known heart disease underwent a stress myocardial perfusion gated SPECT, and long-term follow-up was conducted thereafter. Results: During an average follow-up of 15.2 ± 9 months, 9 patients (13.8%) presented major coronary events (CEs). Survival analyses (Kaplan-Meier and Cox regression) identified presence of moderate-to-severe myocardial perfusion defects (log rank p = 0.004) and ejection fraction <50% (p = 0.014) as predictors of future CEs. Neurovascular ischemic events were not predicted by SPECT variables. Conclusion: Myocardial perfusion scintigraphy predicts future CEs in patients with symptomatic ILA and may be helpful to guide therapeutic strategies in this subgroup of stroke patients. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Papillary fibroelastoma (PFE) is a rare benign tumour that attaches to the endocardial surface, mostly on cardiac valves. Though usually asymptomatic, it can be the source of several complications. To date, 49 cases have been reported of embolic stroke with a PFE as the probable origin. Case reports: (i) a 39-year-old male presented with ischemic embolic stroke; the presence of a PFE was assessed by means of transoesophageal echocardiography and confirmed by pathological findings; (ii) a 32-year-old woman presented with sudden onset of left hemiparesis; a cardiogenic embolic stroke was suspected, and a diagnosis of PFE was made based on echocardiographic and pathological findings. In both cases, surgical excision of the tumours was performed with no recurrences at follow-up. Two mechanisms can explain the formation of emboli in PFE: dislodgement of the tumour leaves or fibrin-platelet aggregation on the endocardial surface of these leaves. Transthoracic echocardiography may lead to the suspicion of a PFE, but transoesophageal echocardiography is required for confirmation. Prompt surgical excision is indicated in most cases. Anticoagulation is only recommended in situations of high surgical risk and during the wait for surgery. [ABSTRACT FROM AUTHOR]

Background: Cerebral amyloid angiopathy (CAA) is a well-established cause of lobar intracerebral hemorrhage (ICH). Familial forms of CAA are because of mutations in the gene encoding the beta-amyloid precursor protein ( APP) and duplications of this gene can cause early-onset Alzheimer's disease associated with CAA. However, the contribution of APP genetic variants in the development of sporadic CAA remains unknown. Methods: The presence of genetic variants in the APP was examined in 78 patients with CAA-related ICH by sequencing exons 16 and 17 coding the β-amyloid protein and analyzing the presence of possible duplications of APP by microsatellite analysis and quantitative PCR. Results: We did not identify any pathogenic mutation or chromosomal duplication of APP. Conclusions: Our results suggest that APP genetic variants, point mutations and locus duplication, are not a common cause of CAA-related ICH in the Spanish population. [ABSTRACT FROM AUTHOR]