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Biomedical subjects

A Chamorro

Publications and source records attributed to A Chamorro.

At least 37 records · Page 2Linked to original sources
PubMed2000

Proinflammatory cytokines and early neurological worsening in ischemic stroke.

BACKGROUND AND PURPOSE: The mechanisms for clinical deterioration in patients with ischemic stroke are not completely understood. Several proinflammatory cytokines are released early after the onset of brain ischemia, but it is unknown whether inflammation predisposes to neurological deterioration. We assessed the implication of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in early neurological worsening in ischemic stroke. METHODS: Two hundred thirty-one patients consecutively admitted with first-ever ischemic cerebral infarction within the first 24 hours from onset were included. Neurological worsening was defined when the Canadian Stroke Scale (CSS) score fell at least 1 point during the first 48 hours after admission. IL-6 and TNF-alpha were determined in plasma and cerebrospinal fluid (CSF; n=81) obtained on admission. RESULTS: Eighty-three patients (35.9%) deteriorated within the first 48 hours. IL-6 in plasma (>21.5 pg/mL; OR 37.7, CI 11.9 to 118.8) or in CSF (>6.3 pg/mL; OR 13.1, CI 2.2 to 77.3) were independent factors for early clinical worsening, with multiple logistic regression. The association was statistically significant in all ischemic stroke subtypes as well as in subjects with cortical or subcortical infarctions. IL-6 in plasma was highly correlated with body temperature, glucose, fibrinogen, and infarct volume. CSF and plasma concentrations of TNF-alpha were also higher in patients who deteriorated, but the differences observed did not remain significant on multivariate analysis. CONCLUSIONS: In addition to participating in the acute-phase response that follows focal cerebral ischemia, IL-6 levels on admission are associated with early clinical deterioration. The association between IL-6 and early neurological worsening prevails without regard to the initial size, topography, or mechanism of the ischemic infarction.

Aged↗
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↗
PubMed2000

Doppler sonography of the intertransverse segment of the vertebral artery.

We assessed the utility of a Doppler ultrasonographic examination of the vertebral artery, limited to the intertransverse segment, in diagnosis of disease at any level of vertebrobasilar circulation. The vertebral artery was identified in all the patients, with a successful evaluation of the presence of disease in 112 of 116 (96.5%) vertebral arteries. All of the occlusions and subclavian steal syndromes were diagnosed. All of the vertebral arteries with abnormal Doppler findings had a pathologic angiographic study. In conclusion, Doppler ultrasonography of the intertransverse segment of the vertebral artery is useful owing to its applicability and accuracy.

Aged↗
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

Cytokine-induced inflammation and long-term stroke functional outcome.

Inflammatory reactions are involved in the pathogenesis of cerebral ischemia. Cytokines exacerbate brain ischemic injury by several mechanisms and they activate the synthesis of acute-phase reactants. We evaluated the association between cytokine-induced inflammation and functional outcome in 41 patients with acute ischemic stroke. Blood samples for interleukin-1 receptor antagonist (IL-1ra), erythrocyte sedimentation rate (ESR), c-reactive protein (CRP) and polymorphonuclear leukocyte (PMNL) count were taken within 48 h from stroke onset. Functional outcome was assessed at six months with the Modified Rankin Scale. Patients with a Rankin score > or = 3 were classified as dependent outcome. The effect of inflammatory variables on outcome was analyzed by logistic regression. Mathew score <75 on admission, atrial fibrillation, non-lacunar infarct size, ESR>13 mm/h in men or >20 mm/h in women, PMNL count >8 x 10(9)/l, CRP>0.8 mg/dl and IL-1ra>500 pg/ml were associated with dependent outcome. On multiple logistic regression, severe stroke on admission, non-lacunar infarct size and ESR remain in the predictive model of outcome with a sensitivity and specificity of 76 and 80%, respectively. This study suggests that in addition to clinical evaluation and neuroimaging, measurement of ESR may be useful for the early detection of stroke patients with poor long-term functional outcome.

Aged↗
PubMed1999

Heparin in acute stroke with atrial fibrillation: clinical relevance of very early treatment.

BACKGROUND: The risk-benefit ratio of early vs late heparinization for acute stroke with nonvalvular atrial fibrillation remains unsettled. OBJECTIVE: To clarify the relationship between timing to heparinization and functional outcome in acute cardioembolic stroke. DESIGN: Consecutive case series. SETTING: Referral center. PATIENTS: In 231 patients with stroke and nonvalvular atrial fibrillation, intravenous or subcutaneous heparin administered with the goal of achieving an activated partial thromboplastin time (APTT) 1.5 to 2.0 times control values. Delay to the initiation of heparin therapy was less than 6 hours from the onset of symptoms in 74 patients and between 6 and 48 hours in 157 patients. Functional outcome (Rankin scale) was assessed 9 +/- 3 (mean +/- SD) days from stroke onset using multivariate analysis and including in the model treatment delay, risk factors (eg, age, hypertension, diabetes, hypercholesterolemia, previous stroke, and heart disease), initial neurological severity, and baseline computed tomographic findings (eg, early signs of infarction and white matter abnormalities). Clinical symptoms on admission (Mathew score) and baseline radiological findings were evaluated in all subjects. The bleeding rate was assessed on subsequent computed tomographic (CT) scans (obtained 7 +/- 2 days after stroke). The relationship between APTT ratios and stroke recurrence or hemorrhagic worsening was also tested. MAIN OUTCOME MEASURES: Functional outcome at hospital discharge and incidence of early recurrent strokes and bleeding complications. RESULTS: Mortality (9%), hemorrhagic worsening (3.4%), and early stroke recurrence (2.1%) occurred in the hospital. Complete recovery was associated with age younger than 70 years (odds ratio [OR], 0.21; 95% confidence interval [CI], 0.05-0.70), a baseline Mathew score higher than 74 (OR, 11.5; 95% CI, 4.95-26.70), normal baseline CT findings (OR, 8.86; CI, 3.99-19.60), and early heparinization (OR, 1.7; 95% CI, 1.10-2.50). Targeted APTT ratios were achieved at 24 hours in fewer than 50% of patients. Whereas stroke recurrence was associated with lower mean APTT ratios, higher mean APTT ratios were observed in patients with symptomatic bleeding, especially on the day of bleeding. Age, admission stroke severity, blood pressure, and baseline CT findings did not predict hemorrhagic worsening. CONCLUSIONS: Delaying anticoagulation in alert patients with stroke and nonvalvular atrial fibrillation is not endorsed by the initial severity of symptoms or the early signs of infarction on CT scan. Functional recovery is improved the sooner heparin is administered. These findings suggest that heparin also has therapeutic properties. However, close APTT monitoring is warranted to lessen the incidence of untoward complications.

Acute Disease↗
PubMed1999

Polymorphonuclear leukocyte elastase in patients with stroke.

INTRODUCTION/OBJECTIVES: Polymorphonuclear leukocytes (PMNL) are involved in the pathogenesis of acute cerebral ischemia and atherosclerosis. Elastase is one of the proteolytic enzymes released by activated PMNL. We evaluated whether plasma levels of elastase-inhibitor complexes (EIC) are related to acute cerebral damage or with extension of carotid atherosclerosis in patients with stroke. METHODS: Plasma levels of EIC were determined in 44 patients during acute and chronic phases of stroke. We recorded in all patients vascular risk factors, clinical severity on admission, infarct volume, and extension of carotid atherosclerosis using B-mode ultrasound exam. RESULTS: EIC levels were not different between acute and chronic phases of stroke. Eleven patients (25%) had increased values of EIC. On multiple regression analysis diabetes, dislipemia, and coronary disease were predictors of abnormal EIC levels. EIC levels were not related to neurological severity on admission, infarct volume, or carotid atherosclerosis. CONCLUSION: EIC levels in stroke patients are associated to the presence of vascular risk factors and may reflect cellular inflammatory aspects of chronic vessel disease. However, whether elastase contributes to the development of carotid atherosclerosis in patients with stroke remains unknown.

Acute Disease↗
PubMed1999

[Heparin in acute cerebral ischemia].

Non fractionated heparin is used in neurovascular disease because of its antithrombolytic action. Therefore, the design of the clinical studies performed to date has emphasized these actions. However, the results obtained in the most recent clinical studies have been discouraging, not only because they have demonstrated its lack of efficacy, but also because the use of this heparin has been followed by an excessive number of complications. This article provides critical comments on the possible causes of these results and underlines the most recent advances obtained in the knowledge of the mechanism of action of this drug. Particularly, its potential antiinflammatory role is emphasized as are the experimental requisites required for this antiinflammatory action to be fully expressed. Based on the results shown it is concluded that it is necessary to prospectively evaluate the role of heparin in acute ischemic ictus.

Acute Disease↗
PubMed1999

[The shadow of ischemia. Therapeutic window].

The mechanisms leading to irreversible ischemic damage are progressively better understood. Hopefully, these major advances will contribute to the design and clinical development of more powerful drugs aimed to combat the tremendous burden of stroke in developed countries. More sensitive neuroimaging techniques able to identify the metabolic and structural state of hypoperfused brain tissue are also available in research centres. Presumably, these techniques will be in the short future accessible to most stroke centres and this could result in the administration of stroke therapies tailored to the individual needs of patients. The review that follows tackles on some of the main advances achieved in recent years in this exciting field.

Brain↗
PubMed1998

[Plasma homocysteine levels in patients with ischemic cerebral infarction].

BACKGROUND: Moderate hyperhomocysteinemia is an independent risk factor for stroke. The relationship between homocysteinemia and stroke and its related factors are unknown in Spain. PATIENTS AND METHODS: We determined plasma homocysteine concentrations in 80 stroke patients and in 48 control subjects without vascular risk factors. Folate, vitamin B12 and creatinine concentrations were also measured in stroke patients. RESULTS: Total plasma homocysteine concentrations were higher in stroke patients compared to controls (11.2 [SD 3.2] mumol/l versus 8.1 [2.6] mumol/l; p < 0.001). Hyperhomocysteinemia was present in 20% of patients and in 2.2% of controls (odds ratio [OR] = 5.75; 95% CI = 1.24-53.4; p < 0.01). Homocysteine values were related to vitamin B12 (r = 0.28; p < 0.05) and creatinine concentrations (r = 0.24; p < 0.05). Multiple regression analysis showed that about 15% of the variation in plasma homocysteine concentrations could be predicted by the values of vitamin B12 (p < 0.001) and creatinine (p < 0.05). Homocysteine values were unrelated to age, sex, folate concentrations, atherosclerotic subtype or to the presence of vascular risk factors. CONCLUSIONS: Moderate hyperhomocysteinemia was present in about 20% of stroke patients in our series. Homocysteine plasma level was not related with other stroke risk factors or with the atherosclerotic subtype of stroke, but it was partially related with the renal function parameters and the serum levels of vitamin B12.

Brain Ischemia↗
PubMed1998

Sympathetic skin response in patients with lateral medullary syndrome.

We have carried out a prospective study of the sympathetic skin response (SSR) in 21 patients with lateral medullary syndrome (LMS), with the aim of identifying the most common pattern of SSR abnormalities and its possible correlation with clinical and radiological findings. The amplitude of the SSR recorded in the ipsilateral hand to the infarct was abnormally reduced in the patients as a group. However, using different stimulation and recording sites, and considering only the presence or absence of the response, we identified 5 different patterns of SSR abnormalities: 1. Normal responses; 2. Bilaterally absent responses to stimulation of the ipsilateral supraorbital nerve but not to other stimulation sites; 3. Absent responses in the side ipsilateral to the stroke, with normal responses in the contralateral side; 4. A combination of patterns 2 and 3; and 5. Absent responses to all stimuli. All patients with ipsilateral facial sensory loss had absent SSR to ipsilateral supraorbital nerve stimulation, while there was only a positive correlation between abnormal contralateral facial sensation and preservation of the SSR (Fisher's exact test P=0.003). No correlation was found between the pattern of SSR abnormalities and the infarct topography, assessed with the MRI. Our findings suggest that the damage to the SSR circuits of patients with LMS is not uniform, and follows an heterogeneous distribution independent from the MRI findings, and poorly related to the clinical sensory manifestations.

Adult↗
PubMed1998

Blood pressure and functional recovery in acute ischemic stroke.

BACKGROUND AND PURPOSE: The relevance of elevated blood pressure in acute ischemic stroke and its most appropriate management are unresolved. We aimed to evaluate the rate of functional recovery with relation to early blood pressure management in patients with ischemic stroke. METHODS: Four hundred eighty-one consecutive ischemic stroke patients were admitted to the Neurology Service within 20.9+/-10.5 hours of symptoms onset as part of the Barcelona Downtown Stroke Registry, including 235 patients who received oral antihypertensive agents within <24 hours after stroke onset. Demographic, clinical (Mathew scale), and CT scan findings were collected prospectively. Mean arterial pressure (MAP) was recorded before hospital arrival and at 7 AM on days 1, 2, and 7 of hospitalization. The primary end point was complete functional recovery at day 7 defined as a score of 0 to 1 on the modified Rankin scale. RESULTS: Two hundred fifty-two patients achieved complete recovery on day 7. Using logistic regression, independent predictors of complete recovery included mild impairment at stroke presentation, lack of history of hypertension, and absence of brain edema on CT scan. Also, a 20% to 30% drop in MAP on day 2 after stroke onset almost tripled the odds of full recovery (odds ratio, 2.9; 95% CI, 1.3 to 6.3). MAP tended to normalize after stroke in all subjects, more rapidly if hypotensive agents were administered. Brain edema was also less frequent in patients with a greater drop in blood pressure. Despite the fact that a drop in MAP >30% from baseline was observed in 49 patients, this preceded worsening stroke in only 4 patients. Conversely, worsening stroke occurred in 51 patients despite stable blood pressure. CONCLUSIONS: These results suggest that complete recovery in ischemic stroke is facilitated by a moderate blood pressure reduction when brain edema develops, most likely as the result of a more adequate cerebral perfusion pressure. Conversely, stroke worsening due to pharmacological hypoperfusion is exceptional.

Activities of Daily Living↗
PubMed1997

[Factors associated to aspirin failure for secondary stroke prevention].

BACKGROUND: It is not settled whether aspirin (ASA) failure may be predicted in stroke and transient ischemic attack (TIA) patients. The risk of ASA failure may be predicted by analyzing the epidemiological traits of patients with stroke or TIA. PATIENTS AND METHODS: We evaluated retrospectively 695 stroke or TIA patients admitted to the Downtown Barcelona Stroke Registry, including 54 patients who recurred while on 125-500 mg/day of ASA (group ASA failure), and 178 patients who showed a good clinical response to the same dose of ASA for at least one year of follow-up (group ASA sensitive). Vascular risk factors, stroke subtypes, and clinical and radiological findings were compared in both groups. RESULTS: On multivariate analysis ASA failure was independently correlated with history of myocardial infarction, nonvalvular atrial fibrillation or hypercholesterolemia. A trend toward age older than 65 was also correlated with ASA failure. On the contrary, periventricular lucencies were a protector factor. Stroke severity at clinical onset and at follow-up was unrelated to the intake of ASA at stroke onset. CONCLUSIONS: Males or females older than 65 years, with a history of coronary heart disease or atrial fibrillation, serum cholesterol level > 240 mg/dl, and a CT scan showing no evidence of small vessel disease are, respectively, the characteristics most frequently encountered in patients who suffer an ischemic stroke despite preventive treatment with 125-500 mg/day of ASA. Moreover, this treatment does not reduce initial and long-term stroke severity.

Aged↗