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V Obach

Publications and source records attributed to V Obach.

At least 19 recordsLinked to original sources
PubMed2006

Aspirin or anticoagulants in stenosis of the middle cerebral artery: A randomized trial.

BACKGROUND: We report the results of an open, randomized, multicenter trial that compared the efficacy of aspirin to oral anticoagulants (OA) for the prevention of vascular events in patients with symptomatic stenosis of the middle cerebral artery (MCA). METHODS: Participants were randomly assigned to receive 300 mg/day of aspirin or a dose of OA (target INR 2-3). The MCA stenosis was demonstrated by conventional angiography or by at least two noninvasive examinations. Patients had either transient ischemic attack or cerebral infarct (CI) attributable to the MCA stenosis within 90 days before inclusion. The primary endpoint was: nonfatal CI, nonfatal acute myocardial infarct, vascular death and major hemorrhage. The patients were followed-up for a minimum of 1 year and a maximum of 3 years. RESULTS: The study included 28 patients (14 in each treatment group); the average age was 67 +/- 9.9 years. Men constituted 68% of the patients. After a mean follow-up of 23.1 +/- 10.9 months, there were no recurrences of CI in both groups. No endpoint was reported in the aspirin group, but 2 patients in the OA group (14.3%) exhibited vascular events: 1 acute myocardial infarct and 1 intracerebral hemorrhage). However, this difference was not statistically significant (p = 0.48). CONCLUSIONS: Our study suggests that aspirin is the treatment of choice for the prevention of vascular events in patients with symptomatic MCA stenosis.

Aged↗
PubMed2006

Cortical laminar necrosis related to prolonged focal status epilepticus.

Cortical laminar necrosis (CLN) is radiologically defined as high intensity cortical lesions on T1 weighted MRI images following a gyral distribution. Histopathologically, CLN is characterised by pannecrosis of the cortex involving neurones, glial cells, and blood vessels. It has been reported to be associated with hypoxia, metabolic disturbances, drugs, and infections. We present two patients who developed CLN and permanent neurological deficits after prolonged and repeated focal status epilepticus. The possible mechanisms leading to CLN in these patients are discussed, together with the implications of prompt and aggressive treatment in similar cases.

Adult↗
PubMed2006

Interleukin 10, monocytes and increased risk of early infection in ischaemic stroke.

BACKGROUND AND PURPOSE: The pathophysiology of stroke-associated infection (SAI) is uncertain. The cytokine profile and peripheral white cell response were assessed in patients with or without SAI. METHODS: The incidence of SAI was assessed in 110 patients with ischaemic stroke allocated antibiotic prophylaxis or placebo within 24 h of clinical onset. Peripheral white cell counts, interleukin (IL)6, tumour necrosis factor (TNF)alpha and IL10 were measured in plasma. RESULTS: 17 (15%) patients developed infection and showed time-dependent increases of total white cell count, neutrophils, monocytes, lymphocytes, IL6 and IL10, whereas TNFalpha and the TNFalpha/IL10 ratio decreased. In logistic regression, IL10 (odds ratio (OR) 1.08, 95% confidence interval (CI) 1.01 to 1.16), monocyte count (OR 1.42, 95% CI 1.08 to 1.87) and National Institute for Health Stroke Survey score on admission (OR 1.17, 95% CI 1.05 to 1.31) were independent predictors of systemic infection. CONCLUSIONS: SAI is associated with stroke severity, excessive IL10-mediated response and an increased number of circulating monocytes. These results support the finding that acute ischaemic brain injury triggers a blood-borne anti-inflammatory response that decreases the antimicrobial drive of the immune system.

Aged↗
PubMed2005

The Early Systemic Prophylaxis of Infection After Stroke study: a randomized clinical trial.

BACKGROUND AND PURPOSE: Early infection after stroke is frequent but the clinical value of antibiotic prophylaxis in acute stroke has never been explored. OBJECTIVE AND METHODS: The Early Systemic Prophylaxis of Infection After Stroke (ESPIAS) is a randomized, double-blind, placebo-controlled study of antibiotic prophylaxis in patients older than 18 years with nonseptic ischemic or hemorrhagic stroke enrolled within 24 hours from clinical onset. Interventions included intravenous levofloxacin (500 mg/100 mL/d, for 3 days) or placebo (0.9% physiological serum) in addition to optimal care. A sample size of 240 patients was calculated to identify a 15% absolute risk reduction of the primary outcome measure, which was the incidence of infection at day 7 after stroke. Secondary outcome measures were neurological outcome and mortality at day 90. RESULTS: Based on a preplanned futility analysis, the study was interrupted prematurely when 136 patients had been included. Levofloxacin and placebo patients had a cumulative rate of infection of 6% and 6% (P=0.96) at day 1; 10% and 12% (P=0.83) at day 2; 12% and 15% (P=0.66) at day 3; 16% and 19% (P=0.82) at day 7; and 30% and 33% (P=0.70), at day 90. Using logistic regression, favorable outcome at day 90 was inversely associated with baseline National Institutes of Health Stroke Scale (OR, 0.72; 95% CI, 0.59 to 0.89; P=0.002) and allocation to levofloxacin (OR, 0.19; 95% CI, 0.04 to 0.87; P=0.03). CONCLUSIONS: Prophylactic administration of levofloxacin (500 mg/100 mL/day for 3 days) is not better than optimal care for the prevention of infections in patients with acute stroke.

Aged↗
PubMed2004

The -174G/C polymorphism of the interleukin 6 gene is a hallmark of lacunar stroke and not other ischemic stroke phenotypes.

BACKGROUND AND PURPOSE: The CC genotype of the -174 G/C interleukin (IL)-6 polymorphism has been associated with lacunar stroke. However, it remains unsettled whether this polymorphism is also associated with other ischemic stroke phenotypes. METHODS: The -174 G/C IL-6 polymorphism was genotyped in patients with lacunar stroke (n = 89), stroke due to large vessel disease (n = 82), cardioembolism (n = 53), stroke of undetermined cause (n = 49) and in white controls without any history of stroke (n = 105) by PCR and restriction enzyme analysis. Independent predictors of the -174 G/C IL-6 genotypes were assessed using multivariate logistic regression models adjusted for demographics, risk factors and disease state. RESULTS: The prevalence of the CC genotype was 8.5% in large vessel disease, 7.5% in embolism, 19.1% in lacunar stroke, 14.3% in stroke of undetermined cause and 8.6% in controls. The CC genotype was independently associated with lacunar stroke only (adjusted OR 3.22, 95% CI 9.09-1.12). Contrarily, there were no significant differences in genotype and allele distribution in the remainder of ischemic stroke phenotypes. Pooling of patients with nonlacunar stroke did not show any independent association with the CC genotype as compared with controls (OR 1.01, 95% CI 2.77-0.36). CONCLUSIONS: The unique association between the CC genotype of the -174 G/C IL-6 polymorphism and lacunar stroke suggests a particular susceptibility of small deep penetrators of cerebral arteries to IL-6-mediated inflammatory damage.

Aged↗
PubMed2002

[Antithrombotic treatment of fusiform aneurysms of the basilar artery].

Fusiform aneurysms are unusual, and they are most found in the vertebrobasilar system. Although the presence of such aneurysms has been related to atheromatous degeneration of the arterial wall, in many cases the cause of their formation is unknown. The clinical manifestations of fusiform aneurysms of the vertebrobasilar system are generally due to mass effect with compression of adjacent structures or to ischemic events; exceptionally they are due to subarachnoidal haemorrhage. We present the case of a patient with symptoms suggestive of brainstem ischemic damage, in which neuroimaging showed a fusiform aneurysm of the basilar artery with an intraaneurysmatic thrombus. Antiaggregation did not prevent new ischemic events, so anticoagulation therapy was initiated. The patient remained asymptomatic at 8 months of follow-up. The treatment of fusiform aneurysms is controversial; however, there are some evidences in the literature supporting that patients with ischemic events may be treated with long term anticoagulation, especially in cases of non-giant aneurysms of the vertebrobasilar system not accompanied by aneurysms in other sites.

Anticoagulants↗
PubMed2001

Analysis of the coding and the 5' flanking regions of the alpha-synuclein gene in patients with Parkinson's disease.

Missense mutations of the alpha-synuclein gene have been reported to explain a few kindreds with autosomal dominant Parkinson's disease (PD). In order to identify mutations in our PD patients, we have screened the coding region and 5'flanking region of the gene. DNA samples from 50 patients with familial PD were screened via single-strand conformation polymorphism (SSCP) for mutations in the alpha-synuclein gene. The 5' flanking region was examined in 117 additional PD patients (27 patients with unclear family history for PD, and 90 patients without family history) and in 169 control subjects. We found one change (G199A) in exon 4 in one family with a pattern of autosomal dominant PD. However, this mutation did not result in an amino acid substitution (valine) and did not segregate completely with PD. The analysis of the 5' flanking region also showed a new polymorphism, a nucleotide insertion (- 164insA) linked to a nucleotide substitution (C-116G), in patients and in controls. The -164insA/C-116G allele was present in 52.3% of the patients and in 47.6% of the controls. We did not find significant differences regarding the allelic and genotype frequencies between PD and control groups. These results suggest that mutations in the alpha-synuclein gene are a very rare cause of familial PD and that the novel -164insA/C-116G polymorphism in the 5' flanking region does not confer susceptibility to develop PD.

Aged↗
PubMed2001

alpha(1)-antichymotrypsin polymorphism: a risk factor for hemorrhagic stroke in normotensive subjects.

BACKGROUND AND PURPOSE: Although genetic factors may be important in the pathogenesis of ischemic stroke (IS), little is known on the potential role of genes in most cases of hemorrhagic stroke (HS). Preliminary data showed that the TT genotype of the alpha(1)-antichymotrypsin (ACT) gene polymorphism was associated with HS, although it remained unsettled whether prevalence of this polymorphism might differ between hypertensive and normotensive HS. METHODS: Ninety-nine patients with HS, 182 patients with IS (symptomatic control subjects), and 80 asymptomatic control subjects were genotyped for the ACT polymorphism using polymerase chain reaction amplification. Chronic hypertension was recorded in 66 patients with HS. RESULTS: The ACT-TT genotype was more prevalent in patients than in asymptomatic or symptomatic control subjects: 26%, 15%, and 16%, respectively. The ACT-TT genotype was obtained in 33% of HS who lacked arterial hypertension (P<0.05). After adjustment for age, gender, and vascular risk factors, the ACT-TT genotype remained independently associated with HS (OR 2.80, 95% CI 1.19 to 6.58, compared with asymptomatic control subjects; OR 1.79, 95% CI 0.95 to 3.40, compared with symptomatic control subjects). In analyses restricted to HS in normotensive patients, the ORs were 3.10 (95% CI 1.10 to 8.68) and 2.53 (95% CI 1.04 to 6.18), respectively. CONCLUSIONS: These findings confirm in a larger series of patients the association between the ACT-TT genotype and HS. This polymorphism is more prevalent in normotensive bleedings. Pathological studies will be required to establish whether the ACT-TT genotype facilitates proteolytic rupture of vessels that harbor amyloidotic changes or another form of nonhypertensive cerebral angiopathy.

Aged↗
PubMed2000

Comparison of the acute-phase response in patients with ischemic stroke treated with high-dose heparin or aspirin.

Experimental studies have suggested that unfractionated heparin (UH) has antiinflammatory properties. It is unknown whether UH also has these properties in patients with acute ischemic stroke. Within 12-24 h of treatment onset we measured the acute-phase response as reflected by the erythrocyte sedimentation rate (ESR) and total number of leukocytes (x10(9)/l) in 706 consecutive patients with acute ischemic stroke treated with full-dose UH (n=450), or 300 mg/day aspirin (n=256). Clinical outcome (Mathew scale) at hospital discharge and the effect of factors such as treatment (UH and aspirin), and acute phase response were assessed using multivariate analyses adjusted for baseline confounders and incident complications. Separate models were created for patients with lacunar and nonlacunar stroke. Whereas there were not differences at baseline between the two treatment groups, total leukocyte counts (8. 0+/-4.1 vs. 8.6+/-3.2, P<0.01) and ESR (21.7+/-20.9 vs. 25.2+/-22.9, P<0.05) were statistically significantly lower in patients treated with UH. This effect of UH was more accentuated in patients with nonlacunar stroke. Overall, leukocytes (7.2+/-2.3 vs. 8.4+/-4.0, P<0. 01), and ESR (15.7+/-17.2 vs. 24.3+/-22.2, P=0.0001) were lower in patients with complete early recovery and this effect was restricted to patients with nonlacunar stroke. Whereas baseline impairment, symptomatic bleeding and stroke recurrence were independent negative outcome predictors, the use of UH was positively associated with early recovery in all patients. This study shows that full-dose UH reduces the acute-phase reaction that follows ischemic stroke more effectively than aspirin. The prognostic implications of such effect seem more notable in patients with nonlacunar stroke.

Acute-Phase Reaction↗
PubMed2000

No evidence of linkage to 6p markers in spanish families with juvenile myoclonic epilepsy.

Juvenile myoclonic epilepsy (JME) is a common subtype of hereditary generalized epilepsy with an uncertain pattern of inheritance. Different studies in multiple families have provided evidence for and against linkage of the disease to chromosome 6p. We performed linkage analysis using microsatellite markers from 6p (D6S109, D6S248, D6S291, D6S426, D6S272, D6S466, D6S294, D6S257) and from centromeric 6q region (D6S402) in seven small families of Spanish origin. The highest LOD scores were obtained under an autosomal dominant inheritance model with a penetrance of 70% but a significant positive LOD score (Z>3) was not reached. LOD scores<-2 were obtained at different markers in three of our families. These results support the concept of genetic heterogeneity in the disease.

Adult↗
PubMed2000

Alpha(1)-antichymotrypsin gene polymorphism in patients with stroke.

BACKGROUND AND PURPOSE: A role for proteolytic enzymes has been suggested in the pathogenesis of stroke. In a search for new genetic factors, we investigated the gene polymorphism of the serine protease inhibitor alpha(1)-antichymotrypsin (ACT) in patients with stroke. METHODS: Two hundred twenty patients with acute ischemic stroke (n=182) and primary intracerebral hemorrhage (n=38) and 70 control subjects without clinical cerebrovascular disease were genotyped for the ACT polymorphism. RESULTS: The ACT-TT genotype was more frequent in patients with primary intracerebral hemorrhage than in patients with ischemic stroke (31.6% versus 16.4%, P:<0.05) or in control subjects (21.4%, P:=0.1). After adjusting for age, gender, and vascular risk factors, the ACT-TT genotype was associated with primary intracerebral hemorrhage, with an OR of 2.3 (95% CI 1.0 to 5. 2) compared with ischemic stroke and an OR of 1.8 (95% CI 0.85 to 9. 65) compared with controls. CONCLUSIONS: Pending confirmation in a larger study, our results suggest that the ACT-TT genotype might be a risk factor for primary cerebral hemorrhage.

Acute Disease↗
PubMed1999

Ex vivo response to aspirin differs in stroke patients with single or recurrent events: a pilot study.

The dose of aspirin for secondary stroke prevention and the clinical meaning of ex vivo platelet abnormalities are debated. We assessed prospectively 39 noncardioembolic stroke patients in which 300 mg/day aspirin had proved effective (n=24) or ineffective (n=15) to prevent recurrent ischemic events. We evaluated platelet aggregation induced by arachidonic acid, adenosine diphosphate and epinephrine, and the sensitivity of platelets to increasing concentrations of the synthetic thromboxane mimetic U46619. Aggregation studies were repeated while subjects received 300 (study phase 1), and 600 (study phase 2) mg/day aspirin, respectively. Overall, arachidonic acid-induced platelet aggregation was less effectively inhibited during study phase 1 compared to phase 2. Arachidonic acid and epinephrine promoted a stronger platelet aggregation in aspirin nonresponders than in aspirin responders while taking 300 mg/day aspirin. On the other hand, 600 mg/day effectively inhibited platelet function in both clinical groups. A lower sensitivity to thromboxane receptors was also found during phase 1 of the study, although the response was similar between aspirin responders and nonresponders. This pilot study suggests that 300 mg/day aspirin is less effective than 600 mg/day to block the cyclooxygenase pathway in noncardioembolic stroke and, incomplete cyclooxygenase inhibition is associated with recurrent thromboembolic events despite adequate aspirin compliance. It is likely that patients could receive a more efficacious stroke prevention if the dose of aspirin is tailored to individual needs as reflected by laboratory findings.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1999

Dopamine receptor D2 intronic polymorphism in patients with Parkinson's disease.

An association between the intronic allele 3 of the dopamine receptor D2 (DRD2) gene and European Parkinson's disease (PD) cases has been reported recently. We initiated the present work in order to determine whether this association between the DRD2 locus and PD is also present in our population from Spain. The DRD2 gene polymorphism has been genotyped in 154 patients and in 125 controls. The allele 3 is present in 60.3% of the patients and in 55.2% of the controls. The genotype 3/3 is present in 36.3% of the patients and in 34.4% of the controls. No statistical differences in the genotype and allelic frequencies between the two groups have been found. No differences were also found when the patients were classified according to different criteria such as onset, family history, gender or clinical presentation. Thus our results do not support a role for the DRD2 locus to develop PD.

Adult↗
PubMed1999

Alpha1-antichymotrypsin gene polymorphism and susceptibility to Parkinson's disease.

OBJECTIVE: To determine whether the alpha1-antichymotrypsin AA genotype (ACT-AA) confers susceptibility for developing Parkinson's disease (PD) in the Spanish population. BACKGROUND: A correlation between the ACT-AA genotype and the risk of developing PD has been recently reported in the Japanese population. METHODS: The ACT genotypes of 71 patients diagnosed with clinically definite PD were compared with those of 109 age-matched healthy control subjects. RESULTS: The authors found that the ACT-AA polymorphism frequency was not increased significantly in the PD group (31%) compared with the control group (28.4%). The ACT allelic distribution was also similar for familial and sporadic PD, for female and male patients, and for the different clinical subtypes of PD. The age at onset of PD was significantly lower in the ACT-AA patients compared with non-ACT-AA patients. When the actual age was considered, the ACT-AA frequency was higher in PD patients < or =50 years old (50%) compared with that present in patients >50 years old (26.8%), but the same effect was found in control subjects. CONCLUSIONS: The ACT-AA polymorphism is not related to an increased risk of developing PD in the Spanish population. The ACT-AA overrepresentation in PD and control subjects < or =50 years old suggests that this polymorphism could be associated with life-threatening conditions other than PD.

Adult↗