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Biomedical subjects

J Serena

Publications and source records attributed to J Serena.

At least 19 recordsLinked to original sources

New-onset hypertension and inflammatory response/poor outcome in acute ischemic stroke.

OBJECTIVE: To study the association of previously unknown high blood pressure (HBP) during the acute phase of stroke (new-onset hypertension) with the inflammatory response and clinical outcome. METHODS: We classified 844 patients with hemispheric ischemic stroke into three groups according to history of hypertension and presence of HBP within the first 24 hours after symptom onset: Group I (n = 412), normotensive patients; Group II (n = 265), chronic hypertensive patients; and Group III (n = 167), new-onset hypertensive patients. Interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and metalloproteinase 9 (MMP-9) were measured in blood samples obtained on admission. The influence of new-onset HBP and markers of inflammation on poor neurologic outcome at 3 months was evaluated by logistic regression analysis. RESULTS: New-onset HBP was found in 19.9% of patients. Patients in this group had higher plasma concentrations of IL-6, TNF-alpha, ICAM-1, VCAM-1, and MMP-9 than the other two groups. New-onset HBP was associated with poor outcome at 3 months (odds ratio [OR] 2.10; 95% CI 1.54 to 3.52; p < 0.0001) after adjustment for other prognostic factors. However, when markers of inflammation were included in the model, IL-6 (OR 1.01; 95% CI 1.00 to 1.03; p = 0.020) and MMP-9 (OR 1.01; 95% CI 1.00 to 1.01; p < 0.0001), but not new-onset HBP, were independently associated with poor neurologic outcome. CONCLUSIONS: New-onset high blood pressure in acute ischemic stroke, but not chronic hypertension, is associated with an inflammatory response and poor neurologic outcome.

Aged↗

Micro- and macroalbuminuria predict hemorrhagic transformation in acute ischemic stroke.

BACKGROUND: Hemorrhagic transformation (HT) after cerebral ischemia seems to be related to the endothelial disruption secondary to the ischemic process. Albuminuria has recently been found to be a marker of chronic endothelial damage. OBJECTIVE: To investigate the relationship between albuminuria and HT in patients with acute ischemic stroke. METHODS: We studied 200 patients (51.5% men, age 72.5 +/- 8.5 years) with ischemic stroke within the first 24 hours of evolution. HT development was assessed on CT performed between days 4 and 7 of evolution and classified according to the ECASS II criteria. Urinary samples were collected within the first 3 hours after admission and the presence of albuminuria, which was considered to be present when the ratio albumin-to-creatinine was > or =30 mg/g creatinine, was determined by nephelometry within the first 24 hours of evolution. RESULTS: Forty-nine patients (24.5%) had albuminuria and 36 (18%) had HT on the second CT scan. After adjusting for potential confounders including a previous history of diabetes mellitus, hypertension and atrial fibrillation, stroke severity, the presence of early signs of ischemia and leukoaraiosis on the baseline CT scan, and IV anticoagulant treatment, logistic regression analysis showed that albuminuria was independently associated with HT (OR, 7.45; 95% CI 2.30 to 24.16). Moreover, albuminuria was also a significant and independent predictor of parenchymal hemorrhage type 1 and 2 (OR, 8.30; 95% CI 1.77 to 38.89). CONCLUSION: Albuminuria is an independent predictor of hemorrhagic transformation, and particularly of the most severe bleedings, in patients with acute ischemic stroke. Due to the small number of events, the predictive capacity of albuminuria should be confirmed in larger studies.

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[Patent foramen ovale. What is it and what does it indicate?].

Cryptogenic stroke accounts for up to 40 % of all ischemic strokes and is even more frequent in young patients. The patent foramen ovale (PFO) is found in almost 60% of these young patients and has been suggested as a potential cause of cryptogenic stroke in this age group. However, the pathological relevance of PFO in cryptogenic stroke and the most appropriate therapeutic handling of it have not been established. In this review, the current state of therapeutic handling and ongoing controversies are discussed and the most interesting results in this field, including recent metaanalyses, are presented.

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Outcome in patients with basilar artery occlusion treated conventionally.

BACKGROUND: Most data on the outcome of basilar artery occlusion are from recent case series of patients treated with intra-arterial thrombolysis. The limited knowledge on the outcome after a conventional treatment approach comes from a few small case series of highly selected patients. OBJECTIVE: To provide more data on the outcome of conventional treatment. METHODS: Data were analysed on patients from three centres with symptomatic basilar artery occlusion treated conventionally. Conventional therapy was defined as treatment with antiplatelets, anticoagulation, or both. RESULTS: Data were available on 82 patients. The case fatality was 40%. Among survivors, 65% remained dependent (Rankin score 4-5). Patients younger than 60 years (odds ratio = 3.1 (95% confidence interval, 1.0 to 9.5)) and those with a minor stroke (OR = 3.1 (1.0 to 9.6)) were more likely to have a good outcome (Rankin score 0-3). Patients with a progressive stroke were less likely to have a good outcome (OR = 0.3 (0.08 to 1.2)) than patients with a maximum deficit at onset or fluctuating symptoms at presentation. CONCLUSIONS: Conventional treatment of symptomatic basilar artery occlusion is associated with a poor outcome in almost 80% of patients, which emphasises the importance of the search for a more effective treatment approach.

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The clinical-DWI mismatch: a new diagnostic approach to the brain tissue at risk of infarction.

OBJECTIVE: To evaluate the usefulness of a mismatch between the severity of acute clinical manifestations and the diffusion-weighted imaging (DWI) lesion in predicting early stroke outcome and infarct volume. METHODS: One hundred sixty-six patients with a hemispheric ischemic stroke of <12 hours' duration were studied. The NIH Stroke Scale (NIHSS) score and the volume of DWI lesion were measured on admission and at 72 +/- 12 hours. Infarct volume was measured on T2-weighted or fluid-attenuated inversion recovery images at day 30. Early neurologic deterioration (END) was defined as an increase of > or =4 points between the two NIHSS evaluations. Thirty-eight patients received IV thrombolysis or abciximab. Clinical-DWI mismatch (CDM) was defined as NIHSS score of > or =8 and ischemic volume on DWI of < or =25 mL on admission. The adjusted influence of CDM on END, DWI lesion enlargement at 72 hours, and infarct growth at day 30 was evaluated by logistic regression analysis and generalized linear models. RESULTS: CDM was found in 87 patients (52.4%). Patients with CDM had a higher risk of END than patients without CDM because NIHSS < 8 (odds ratio [OR], 9.0; 95% CI,1.9 to 42) or DWI lesion > 25 mL (OR, 2.0; 95% CI, 0.8 to 4.9). CDM was associated with an increase of 46 to 68 mL in the mean volume of DWI lesion enlargement and infarct growth in comparison with non-CDM. All the effects were even greater and significant in patients not treated with reperfusion therapies. CONCLUSIONS: Acute stroke patients with an NIHSS score of > or =8 and DWI volume of < or =25 mL have a higher probability of infarct growth and early neurologic deterioration. The new concept of CDM may identify patients with tissue at risk of infarction for thrombolytic or neuroprotective drugs.

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Headache as a surrogate marker of the molecular mechanisms implicated in progressing stroke.

The mechanism for headache in patients with acute ischaemic stroke are not completely understood. We analysed the relationship between headache and the early worsening of neurological symptoms in patients with acute ischaemic stroke, and we studied the possible biochemical mechanisms implicated. Headache at the onset of ischaemic stroke predicted progression with a sensitivity, specificity, and positive predictive value of 56%, 99%, and 98%, respectively. CSF concentrations of glutamate, Interleukin-6, and NO-m were significantly greater in patients with progressing stroke than in patients with nonprogressing stroke, and these biochemical markers were also significantly higher in patients with headache than in those without headache. Results of this study suggest that headache at the onset of ischaemic stroke is an independent predictor of neurological worsening and we hypothesize that headache might be a surrogate marker of the molecular mechanisms involved in neurological worsening after acute stroke.

Acute Disease↗

Automatic classification of HITS into artifacts or solid or gaseous emboli by a wavelet representation combined with dual-gate TCD.

BACKGROUND AND PURPOSE: Transcranial Doppler (TCD) can detect high-intensity transient signals (HITS) in the cerebral circulation. HITS may correspond to artifacts or solid or gaseous emboli. The aim of this study was to develop an offline automated Doppler system allowing the classification of HITS. METHODS: We studied 600 HITS in vivo, including 200 artifacts from normal subjects, 200 solid emboli from patients with symptomatic internal carotid artery stenosis, and 200 gaseous emboli in stroke patients with patent foramen ovale. The study was 2-fold, each part involving 300 HITS (100 of each type). The first 300 HITS (learning set) were used to construct an automated classification algorithm. The remaining 300 HITS (validation set) were used to check the validity of this algorithm. To classify HITS, we combined dual-gate TCD with a wavelet representation and compared it with the current "gold standard," the human experts. RESULTS: A combination of the peak frequency of HITS and the time delay makes it possible to separate artifacts from emboli. On the validation set, we achieved a sensitivity of 97%, a specificity of 98%, a positive predictive value (PPV) of 99%, and a negative predictive value (NPV) of 94%. To distinguish between solid and gaseous emboli, where positive refers now to the solid emboli, we used the peak frequency, the relative power, and the envelope symmetry of HITS. On the validation set, we achieved a sensitivity of 89%, a specificity of 86%, a conditional PPV of 89%, and a conditional NPV of 89%. CONCLUSIONS: An automated wavelet representation combined with dual-gate TCD can reliably reject artifacts from emboli. From a clinical standpoint, however, this approach has only a fair accuracy in differentiating between solid and gaseous emboli.

Adult↗

Embolism in acute middle cerebral artery stenosis.

OBJECTIVE: To investigate the frequency of middle cerebral artery (MCA) stenosis in a series of nonselected patients and the coexistence of microembolic signals with stenosis. METHODS: MCA stenosis was sought by transcranial Doppler (TCD) in 387 patients admitted consecutively with acute ischemic cerebrovascular disease within the first 48 hours of the onset of symptoms and again at 6 months. TCD monitoring for microembolic signals was performed on all patients with MCA stenosis. RESULTS: MCA stenoses were found in 29 patients (7%), although in only 20 patients (5%) was the stenosis symptomatic. Microembolic signals were detected in five of 14 symptomatic stenoses (36%) monitored at the acute phase, but none were found in the chronic phase or in asymptomatic stenosis. Despite one third of symptomatic patients having had a further source of emboli, microembolic signals were detected only distally to the MCA stenosis. In the symptomatic group, 25% of stenoses had completely disappeared 6 months after stroke. Microembolic signal detection at the acute phase was associated with the subsequent disappearance of the stenosis. CONCLUSIONS: The frequency of symptomatic MCA stenosis in acute ischemic stroke was 5% in the population studied. Many stenoses are transient, and microembolic signals are often detectable at the poststenotic segment in the acute phase. The origin of at least 25% of symptomatic acute MCA stenoses may be embolic rather than atherosclerotic.

Adult↗

Atherosclerotic aortic arch plaques in cryptogenic stroke: a microembolic signal monitoring study.

BACKGROUND AND PURPOSE: To find out the prevalence of relevant atherosclerotic plaques in the aortic arch and their potential role as a source of embolism in cryptogenic stroke. METHODS: We performed a transoesophageal echocardiography (TEE) on 49 patients with cryptogenic stroke from a total series of 212 non-selected patients with acute ischaemic stroke studied prospectively by cranial computed tomography (CT), colour-duplex and transcranial Doppler (TCD) sonography with micro-embolic signal (MES) monitoring. Cryptogenic stroke was diagnosed in those patients without carotid or intracranial stenosis > 50%, nor lacunar or cardio-embolic strokes. We defined relevant plaques as those > or = 4 mm thick located in the ascending aorta or proximal arch. RESULTS: Twenty-three patients (46.9%) had atherosclerotic aortic plaques (AAP): 3 in the ascending aorta (in 1 > or = 4 mm), 11 in the proximal aortic arch (in 4 > or = 4 mm) and 9 in the descending aorta (in 5 > or = 4 mm). Hence, 5 patients (10.2%) had relevant plaques. Aortic plaques were significantly related to older age (p < 0.001) and male gender (p = 0.042). A carotid artery stenosis < 50% was found in 39% of patients with AAP and in 8% of those without AAP (p = 0.009). MES were detected in 3 patients with plaques > or = 4 mm thick, but not in those without AAP or with AAP < 4 mm thick (p = 0.006). CONCLUSION: Although few patients with cryptogenic stroke had relevant plaques in our non-selected population, our results support the hypothesis that relevant aortic plaques have embolic potential.

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Neurological deterioration in acute lacunar infarctions: the role of excitatory and inhibitory neurotransmitters.

BACKGROUND AND PURPOSE: The mechanisms involved in the neurological deterioration of acute lacunar strokes are unknown. Although accumulating evidence suggests that glutamate release plays a role in the progression of territorial infarctions, it remains to be established whether excitotoxicity also participates in lacunar stroke progression. We investigated whether excitatory and inhibitory amino acid concentrations in blood predict subsequent progressive motor deficits in lacunar infarctions. METHODS: We studied 113 consecutive patients with lacunar infarct, defined by clinical and computed tomography/magnetic resonance imaging criteria, within the first 24 hours after stroke onset. Neurological deterioration was defined as a decrease of >/=1 points in the motor items of the Canadian Stroke Scale in the first 48 hours after admission. Glutamate, glycine, and GABA were determined by high-performance liquid chromatography in plasma samples obtained on admission. Predictive values, sensitivity, specificity, and accuracy of specific glutamate and GABA concentrations and glutamatexglycine/GABA index for progression of lacunar stroke were calculated. RESULTS: Twenty-seven patients (23.9%) had neurological worsening. Plasma concentrations of glutamate (253+/-70 versus 123+/-73 micromol/L, mean+/-SD) were higher and those of GABA (140+/-63 versus 411+/-97 nmol/L) were lower in the progressing group than in the nonprogressing group (both P<0.001). Glutamate concentrations >200 micromol/L and GABA levels <240 nmol/L had a positive predictive value for neurological deterioration of 67% and 84%, respectively. A excitotoxic index >106 had a positive predictive value of 85%. CONCLUSIONS: These findings suggest that an imbalance between the glutamate and GABA concentrations may play a role in the pathophysiology of progressing lacunar infarctions.

Acute Disease↗

Cerebral embolism in a patient with polycythemia rubra vera.

Polycythemia rubra vera (PRV) is a rare haematological disorder that has a high risk of stroke, although the pathophysiological origin of the cerebral ischaemia in this disease is not well known. We report a case of a stroke patient with PRV in whom bilateral embolic signals were detected by transcranial Doppler (TCD). Cerebral computed tomography showed a cortical middle cerebral artery infarction, echocardiography was normal, duplex-scan showed moderate left carotid stenosis and digital angiography disclosed right siphon stenosis. TCD examinations in the acute phase repeatedly showed a great number of bilateral microembolic signals (MESs). Four months later magnetic resonance angiography showed no flow signal in the right siphon and a severe stenosis of the proximal right MCA. The detection of bilateral MESs in the absence of cardiac sources of embolism observed in this patient suggests that ischaemic cerebral events in PRV may have an embolic origin favoured by a prothrombotic state.

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[Normal values for transcranial doppler studies in our medium].

OBJECTIVE: Transcranial Doppler is a technique which is being used ever more frequently in the study of intracranial arteries and is very useful in the study of cerebrovascular disease. The typical values of a healthy population in our country are unknown. The aim of this study was determine mean velocity and pulsatility index reference values in a healthy population. PATIENTS AND METHOD: Transcranial Doppler basal examination was carried out on 118 healthy volunteers without prior haematological or cerebrovascular conditions. Those found to have extracranial arterial stenoses were excluded as were those in whom bilateral temporal bone hyperostosis did not permit insonation in either middle cerebral arteries. The nine intracranial arteries were sounded systematically at fixed depths. The mean and standard deviations of each variable were calculated for side, age group and sex. RESULTS: 49% were males and average age was of 56 years (range, 21-87 years). A sufficient signal to determine the parameters of the study was obtained in 89% of middle cerebral arteries. Statistically significant differences in mean velocity and pulsatility index were found between age groups and sexes. CONCLUSIONS: Sex and age must be taken into account in establishing typical patterns in transcranial Doppler examination. Our results enable parameters of typical values to be established for the adult population in Spain.

Adult↗

Clusters of microembolic signals: a new form of cerebral microembolism presentation in a patient with middle cerebral artery stenosis.

BACKGROUND: Middle cerebral artery (MCA) stenosis is a rare occlusive disease in western populations, with a high risk of stroke recurrence. An artery-to-artery embolic mechanism has been argued. We report the detection of a new pattern of microembolic signals (MES) in the MCA poststenotic segment in a patient with multiple recurrent transient ischemic attacks. CASE DESCRIPTION: A 75-year-old man was admitted to our hospital with a transient leg monoparesis on the left side. Right MCA stenosis was detected by transcranial Doppler ultrasonography (TCD). In spite of aspirin treatment, the patient had a recurrent right hemispheric transient ischemic attack, and anticoagulant therapy was started. A new, similar event happened after correct anticoagulation. The bigated TCD monitoring study of both MCAs disclosed clusters of MES at the poststenotic MCA segment. Each cluster contained between 12 and 45 embolic signals. The patient became asymptomatic and clusters of MES disappeared, coinciding with the combination of ticlopidine and oral anticoagulants. CONCLUSIONS: We describe a new presentation of MES, ie, grouped in clusters of signals, that may be associated with a high risk of stroke recurrence.

Aged↗

The need to quantify right-to-left shunt in acute ischemic stroke: a case-control study.

BACKGROUND AND PURPOSE: Although right-to-left shunt (RLSh) has been reported to be significantly more frequent in young stroke patients with cryptogenic stroke, its relevance in a nonselected population of acute ischemic stroke is not well known. The aim of this study was to determine the importance of the RLSh magnitude as a risk factor for stroke in nonselected patients. METHODS: Two hundred eight patients hospitalized consecutively with transient ischemic attack or acute cerebral infarction and 100 healthy control subjects were studied. Transcranial Doppler ultrasonography (TCD) was performed in both middle cerebral arteries (MCAs) after intravenous application of agitated saline solution. The magnitude of RLSh was quantified by counting the number of signals in 1 MCA during a Valsalva maneuver. RLSh was classified as "no shunt," "small" (< 10 signals), and "large" (> 10 signals), with the latter including the "shower" (> 25 signals) and "curtain" (uncountable signals) patterns. Extensive investigations, including contrast transesophageal echocardiography, were carried out on patients diagnosed as suffering from stroke of an uncertain etiology. The importance of RLSh for stroke was assessed by logistic regression analysis. RESULTS: Contrast TCD detected a large RLSh in 40 (19.7%) patients and in 21 (21%) control subjects, all with cardiac RLSh characteristics. A large RLSh was present in 4.7% of atherothrombotic strokes, 10.5% of cardioembolic strokes, 15.4% of lacunar strokes, and 45.3% of cryptogenic strokes (P<0.001). Although the overall frequency of RLSh was not significantly different between patients and control subjects, the detection of curtain or shower patterns by contrast TCD was associated with a higher risk of stroke (odds ratio, 3.5; 95% confidence interval, 1.29 to 9.87), particularly with cryptogenic stroke (odds ratio, 12.4; 95% confidence interval, 4.08 to 38.09) after adjustment for concomitant vascular risk factors. CONCLUSIONS: It is essential to quantify RLSh by contrast TCD during the Valsalva maneuver given that only those with shower and curtain patterns are associated with a higher risk of ischemic stroke in a nonselected population.

Acute Disease↗

Duration of glutamate release after acute ischemic stroke.

BACKGROUND AND PURPOSE: High levels of glutamate in plasma and cerebrospinal fluid (CSF) have been demonstrated in patients with acute ischemic stroke. The duration of this excitatory amino acid release has not been studied, and therefore the window of opportunity of treatment with glutamate antagonists is unknown. The aim of this investigation was to study the duration of the glutamate increase in patients with stable and progressing ischemic stroke. METHODS: Glutamate in CSF was measured by high-performance liquid chromatography in 184 patients with an acute cerebral infarction of less than 24 hours' duration and in 43 control subjects. RESULTS: Among the 120 patients with stable ischemic stroke, median glutamate levels were significantly lower- and within the reference range of control subjects-in those patients studied 6 to 24 hours from onset of symptoms than in patients studied in the first 6 hours (3 [range, 2 to 10] versus 5 mumol/L [range, 2 to 17]; P < .0001). In 64 patients with progressing ischemic stroke, glutamate concentrations measured at any time interval during the first 24 hours from onset were significantly higher than in the stable stroke and control groups. CONCLUSIONS: The presence of glutamate increase in the CSF cannot be documented for greater than 6 hours in stable ischemic stroke. The sustained elevation of glutamate observed in progressing stroke suggests that the window to prevent neurological deterioration may be wider.

Acute Disease↗