High level of anticardiolipin antibodies is an unusual finding in an unselected stroke population

Anticardiolipin antibodies (ACA) were analysed in 502 consecutive patients admitted to our stroke unit Elevated ACA levels ≥11 units) were found in 20 of 396 patients (5%) with ischemic stroke and TIA, in none of 42 patients with cerebral haematomas and in five of 64 patients (8%) with other diagnoses than stroke. There were no statistically significant differences in occurrence of ACA in these groups. Markedly elevated ACA levels (> 20 units) were found in nine of the 396 patients (2%) with TIA/ischemic stroke. The frequency of ACA was higher in the age group 40–50 years (15%) than in the age group 50–90 years (3.6–6.0%). Re-examination in 18 of the 20 patients with ischemic stroke and elevated ACA levels after 26–395 days (mean 100 days) showed that in 10 patients ACA levels were lower (difference ≥ 6 units = 2 SD), compared to the initial value, whereas eight patients had unchanged ACA levels. The occurrence of previous deep venous thrombosis was significantly more common in patients with elevated ACA levels, otherwise there were no differences concerning earlier stroke, risk factor analysis or other laboratory parameters between patients with and without elevated ACA levels. In conclusion, we found elevated ACA levels in patients with ischemic stroke at a rather low prevalence as compared to most previous studies. The clinical relevance of ACA is uncertain, especially in patients with multiple risk factors. We recommend screening for ACA only in stroke patients < 50 years of age, or when the antiphospholipid syndrome is suspected.     

Do antiphospholipid antibodies increase the long‐term risk of thrombotic complications in young patients with a recent TIA or ischemic stroke?

BACKGROUND: The purpose of our study was to determine the relative risk of thrombotic events in young patients with a recent TIA or ischemic stroke and positive antiphospholipid antibodies (aPL). METHODS: We included 128 consecutive patients aged 18-45 years with a recent TIA or ischemic stroke. All patients underwent computed tomography scanning and were screened for cardiovascular risk factors, cardiac disorders and large vessel disease. Lupus anticoagulant (LA) was screened for by an APTT-based assay and a diluted PT-assay. Anticardiolipin antibodies (aCL) were tested by enzyme-linked immunosorbent assay, using cardiolipin and anti-human IgG and IgM. Thrombotic events could be TIA, stroke, myocardial infarction, deep venous thrombosis or pulmonary embolism. Product limit estimates of the time free of TIA or stroke and of the time free of any thrombotic event were made. The relative risk was estimated by means of a Cox proportional hazards regression model. RESULTS: Of the 128 patients, 22 (17.2%) had aPL. The mean follow-up was 3 years and 3 months (range 41 days to 6 yrs). The incidence of any thrombotic event per 100 patient years of follow-up was 9.0, and the incidence of recurrent stroke or TIA was 7.9. The relative risk of any thrombotic event in patients with aPL was 0.9 (95% CI: 0.3-2.4) and for recurrent ischemic stroke or TIA 0.7 (95% CI: 0.3-2.2). CONCLUSION: In young patients with a recent TIA or ischemic stroke, aPL do not seem to be a strong risk factor for recurrent stroke or TIA, nor for other thrombotic complications.     

Protein S deficiency in middle-aged women with stroke.

We examined the relationship between free protein S deficiency and cerebrovascular disease by reviewing the records of all patients with the diagnoses of cerebral thrombosis, cerebral embolism, and cerebral vascular occlusion who were referred for coagulation studies over a 12-month period. We assayed for free protein S antigen, protein C antigen, and antithrombin III and tested for lupus-like anticoagulant and anticardiolipin antibody. Twenty-two of 267 patients (8.2%) admitted with thrombotic strokes were referred for coagulation studies. Free protein S antigen was significantly lower in women than in men (62 +/- 25% versus 88 +/- 24%, p = 0.03; n = 11 in each group). Six women had free protein S antigen levels below the range recorded for a contemporary group of 24 age-matched normal women (17 to 59% versus 70 to 102%, p less than 0.001); four of these women had cerebral arterial thrombosis and two had venous dural sinus thrombosis. The six women were aged 29 to 55 at the time of their first strokes; two had family members with protein S deficiency, and one of these had died of a stroke at age 52. Other abnormalities in this population included a positive test for lupus-like anticoagulant or anticardiolipin in five patients, a modest decrease in protein S in two men, and one patient with an isolated deficiency of antithrombin III. We conclude that protein S deficiency may be an important risk factor for stroke in middle-aged women but this requires confirmation by prospective studies in unselected patients.     

Stroke in the Lehigh Valley: racial/ethnic differences

We investigated black/white differences in stroke rate (standardized morbidity), severity, and subtype, and the relative frequencies of 5 primary risk factors (hypertension, diabetes, myocardial infarction, other heart diseases, and transient ischemic attack [TIA]) using the Lehigh Valley Stroke Register. Blacks had a statistically significant higher, age-adjusted rate of stroke than whites. We found no differences in stroke severity using our measures but blacks had a statistically higher proportion of lacunar stroke, while whites had a higher proportion of embolic stroke. There were no differences in proportions of thrombotic stroke or intracerebral hemorrhage. The relative frequencies of hypertension, myocardial infarction, other heart diseases, and diabetes were higher for blacks, while the relative frequency of TIA was higher for whites. These observations are consistent with other reports that blacks have a higher frequency of stroke and tend to have more small-vessel cerebrovascular pathology than whites.     

Natural anticoagulants (antithrombin III, protein C, and protein S) in patients with mild to moderate ischemic stroke

BACKGROUND AND PURPOSE: The role of the natural anticoagulants, antithrombin III (AT III), protein C (PC), and protein S (PS), in patients with mild to moderate ischemic stroke remains uncertain. We aimed to find out whether their levels in peripheral blood correlated with the severity of neurological deficit or can predict clinical outcome and recurrence. METHODS: We studied AT III, PC, and free PS levels in 55 consecutive patients likely to survive the study period on admission, 1 week, 1 month and 3 months after a first-ever ischemic stroke. Sex- and age-matched controls were studied once. All patients underwent a full neurological examination and blood sampling at each study time point; comprehensive stroke risk factors were recorded, and the etiology of the ischemic stroke was determined. All patients were contacted 3 years later for possible recurrent ischemic events. RESULTS: AT III level was found to be significantly lower at all time points after stroke; PC level was significantly increased on admission and normal at subsequent measurements, and PS level was normal on admission but significantly decreased later. The levels of the natural anticoagulants did not correlate with the etiology of stroke, any stroke risk factor, or neurological scores, except that the AT III level on admission showed significant correlation with stroke severity and disability at 3 months. Natural anticoagulant levels did not predict recurrence of ischemic stroke. CONCLUSIONS: The measurements of the level of AT III, PC, or PS did not deliver useful information for management of patients with mild or moderate ischemic stroke, expect that AT III level on admission might predict outcome.     

The relationship between protein C, protein S and cytokines in acute ischemic stroke

OBJECTIVE: The role of inflammation in the pathogenesis of acute ischemic stroke is well known, but its association with the clinical picture is as yet unclear. MATERIAL AND METHODS: In our study, we measured the serum levels of the proinflammatory cytokines interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) within the first 50 h of stroke in 60 acute stroke patients, and examined the association with the natural anticoagulants protein C and free protein S. We compared the results with a control group that consisted of 30 volunteers. We also correlated their levels with the clinical outcomes by using the Canadian Neurological Scale (CNS). RESULTS: Neither stroke patients nor the control group had any elevations in IL-1beta serum levels. However, the levels of serum IL-6 were significantly higher in stroke patients (13.7 +/- 19.46 vs. 4.3 +/- 15.88, p = 0.002). In addition, the protein S levels of patients were lower than those of the controls (84.36 +/- 27.97 vs. 95.9 +/- 25.64, p = 0.007). Although IL-6 showed negative correlation with protein S (r = -0.504, p = 0.000), the other studied cytokines TNFalpha and IL-1beta did not correlate with these natural anticoagulants. Another negative correlation was found between IL-6 and CNS scores (r = -0.451, p = 0.000). In addition, both protein C and protein S positively correlated with CNS (r = 0.263, p = 0.042; r = 0.381, p = 0.003). There was also a positive correlation between protein C and protein S (r = 0.408, p = 0.001). CONCLUSIONS: Our results suggest that TNFalpha and IL1beta serum levels are not elevated in the acute phase of stroke and have no correlation with the natural anticoagulants protein C and protein S. However, a decrease in free protein S may be related to elevated IL-6 levels. In addition, increased levels of IL-6 and reduced levels of protein C and protein S may play a role in acute ischemic stroke severity.     

Association Between Troponin Levels and Visceral Infarction in Patients with Acute Ischemic Stroke

BackgroundVisceral infarctions appear to be more common in patients with embolic stroke subtypes, but their relation to troponin elevation remains uncertain.MethodsAmong patients with acute ischemic stroke enrolled in the Cornell AcutE Stroke Academic Registry (CAESAR) from 2011 to 2016, we included those with troponin measured within 24 hours from stroke onset and a contrast-enhanced abdominal computed tomographic scan within 1 year of admission. A troponin elevation was defined as a value exceeding our laboratory's upper limit of normal (.04 ng/ mL) in the absence of a clinically recognized acute ST-segment elevation myocardial infarction. Visceral infarction was defined as a renal or splenic infarction as ascertained by a single radiologist blinded to patients’ other characteristics. Multivariable logistic regression was used to evaluate the association between elevated troponin and visceral infarction.ResultsAmong 2116 patients registered in CAESAR from 2011 to 2016, 153 patients had both a troponin assay and a contrast-enhanced abdominal computed tomographic scan, of whom 33 (21%) had an elevated troponin and 22 (14%) had a visceral infarction. The prevalence of visceral infarction was higher among patients with an elevated troponin (30%; 95% confidence interval [CI], 16%-49%) than among patients without an elevated troponin (10%; 95% CI, 5%-17%) (P = .003). After adjustment for demographics and comorbidities, we found a significant association between elevated troponin and visceral infarction (odds ratio, 3.9; 95% CI, 1.5-10.4).ConclusionsAmong patients with acute ischemic stroke, elevated troponin was associated with visceral infarction. Our results demonstrate that poststroke troponin elevation may indicate the presence of underlying embolic sources.     

Antithrombin, protein C and protein S levels in 127 consecutive young adults with ischemic stroke

Objectives - The aim of our study was to evaluate the prevalence of antithrombin, protein C and protein S deficiencies in consecutive ischemic stroke patients under 45. Material and methods - We studied 127 consecutive patients with a mean age of 34.4 years admitted for an ischemic stroke, over a 2-year period, after exclusion of those with arterial dissection. Antithrombin, protein C and protein S levels were measured in all patients at the acute stage of the ischemic stroke and measurements were repeated in case of abnormality. Results - We found abnormal levels in 9 patients. Seven had an acquired cause of deficiency (pregnancy, oestrogen, acute inflammation). Two had no obvious acquired cause of deficiency but further controls were normal. Conclusions - Hereditary deficiencies of coagulation inhibitors are rare in ischemic stroke patients under 45 and their systematic detection seems to be of poor interest.     

Severe arterial cerebral thrombosis in a patient with protein S deficiency (moderately reduced total and markedly reduced free protein S): a family study

Deficiency of protein S has been associated with an increased risk of thrombotic disease as already shown for protein C deficiency. Deficiencies of any of these two proteins predispose to venous thrombosis but have been only rarely associated with arterial thrombosis. In this study we describe a case of severe cerebral arterial thrombosis in a 44-year old woman with protein S deficiency. The defect was characterized by moderately reduced levels of total and markedly reduced levels of free protein S. C4b-bp level was normal. Protein C, AT III and routine coagulation tests were within the normal limits. In her family two other members showed the same defect. All the affected members had venous thrombotic manifestations, two of them at a relatively young age. No other risk factors for thrombotic episodes were present in the family members. The patient reported was treated with ASA and dipyridamole and so far there were no relapses.     

ABCD2评分结合hs-CRP对短暂性脑缺血发作后发生脑梗死的评估价值

目的 探讨短暂性脑缺血发作（transient ischemic attack,TIA）患者ABCD2评分与血清超敏C反应蛋白（hs-CRP）水平的关系,及ABCD2评分法预测TIA进展为脑梗死的价值.方法 测定79例TIA患者（TIA组）和40例健康体检者（对照组） 血清hs-CRP水平,TIA组按ABCD2评分分为高危组、中危组和低危组,比较3组间hs-CRP水平,并观察其2 d、7 d内脑梗死的发生率.结果 TIA组血清hs-CRP水平高于对照组（P〈0.05）;高、中、低危组间血清hs-CRP水平差异均有统计学意义（P〈0.05）,评分≤3分的TIA患者22例,2 d、7 d发生脑梗死分别为1例（4.5%）、2例（9.1%）;评分为4或5分的患者31例,2 d、7 d进展为脑梗死分别为3例（9.7%）、5例（16.1%）;评分≥6分的患者26例,2 d、7 d进展为脑梗死分别为7例（26.9%）、10例（38.5%）.不同ABCD2评分值的TIA患者,其脑梗死发生率差异均有统计学意义（P均〈0.05）.结论 TIA患者ABCD2评分与血清hs-CRP水平关系密切,两者呈正相关.ABCD2评分值不同,脑梗死的发生率不同,分值越高,发生率越高,联合二者更有助于TIA的指导治疗和风险评估.     

TIA患者高敏C-反应蛋白水平与颈动脉粥样硬化的关系

目的探讨短暂性脑缺血发作（TIA）患者血清高敏C-反应蛋白水平与颈动脉粥样硬化斑块的关系。方法选取62例短暂性脑缺血发作患者为TIA组,同期选择健康体检者30例为对照组,应用颈动脉彩色多普勒超声检查短暂性脑缺血发作患者颈动脉粥样硬化情况,根据颈动脉超声检查,将TIA组分为不稳定斑块组、稳定斑块组,测定血清高敏C-反应蛋白水平含量并进行比较。结果 TIA组血清高敏C-反应蛋白水平显著高于对照组,P〈0.01;TIA组中不稳定粥样斑块组血清高敏C-反应蛋白水平显著高于稳定粥样斑块组,P〈0.01。结论血清高敏C-反应蛋白水平升高对短暂性脑缺血发作患者颈动脉粥样硬化不稳定斑块有显著临床意义,早期测定高敏C-反应蛋白水平有助于评估短暂性脑缺血发作患者的脑卒中风险。     

Enhanced plasma levels of LIGHT in patients with acute atherothrombotic stroke

Objectives – As a member of the tumor necrosis factor superfamily (TNFSF), LIGHT (TNFSF14) was recently found to be associated with platelets and released upon activation. Increased plasma levels of LIGHT have been reported in patients with myocardial infarction and unstable angina. The aim of the study was to analyze plasma levels of LIGHT in acute ischemic atherosclerotic stroke. Materials and methods – The soluble LIGHT protein was analyzed by an enzyme‐linked immunosorbent assay in peripheral blood of patients with acute ischemic atherosclerotic stroke (n = 20), asymptomatic carotid stenosis (n = 19) and normal controls (n = 23). Results – During the initial 24 h after onset, the stroke patients had an increased plasma LIGHT levels as compared with normal controls. Moreover, the plasma LIGHT levels of the stroke patients were correlated with blood platelet count (r = 0.6341, P = 0.0027). Conclusion – The elevated LIGHT levels may reflect a persistent chronic inflammatory response that may have been induced during early stages of the disease. We speculate that this derangement of LIGHT may be important for atherogenetic process of ischemic stroke.     

Analysis of 45 episodes of arterial occlusive disease in Japanese patients with congenital protein C deficiency

Hereditary protein C deficiency is associated with a predisposition to venous thrombosis. It is not clear whether the deficiency is involved in arterial occlusion. In the present study, we screened for protein C amidolytic activity in patients admitted to the National Cardiovascular Center Hospital, and we identified among them 43 probands and 51 relatives with heterozygous protein C deficiency. Among them, 34 patients with heterozygous protein C deficiency had manifested 45 episodes of arterial occlusive disease. Venous thrombotic diseases were less common. In the examination of whether protein C deficiency hastens arterial occlusion, we found a significant difference (p =0.02) in the age at onset of acute myocardial infarction between the patients with protein C deficiency (n=10; 49.4+/-14.8 years) and a group of patients with normal protein C levels (n=42; 60.5+/-10.6 years). Acute myocardial infarction occurred before 40 years of age in a significantly greater proportion of the patients with protein C deficiency (3:10, 30%) as compared with the controls (2:42, 5%) (chi2=5.9, p=0.015). At the onset of atherothrombotic cerebral infarction the patients with protein C deficiency were significantly (p=0.022) younger (n= 11; 57.4+/-12.8 years) than those with normal protein C levels (n=48; 64.6+/-10.1 years). Venous thrombosis was the most frequent clinical manifestation (21 of 31 episodes) in the patients with antithrombin III deficiency (n=26; 68% of the total), who were admitted to our hospital. Thus, our study suggests that congenital protein C deficiency contributes to earlier onset of arterial occlusive diseases, especially acute myocardial infarction, in Japanese subjects.     

Triggered C-reactive protein (CRP) concentrations and the CRP gene −717A>G polymorphism in acute stroke or transient ischemic attack

C-reactive protein (CRP) increases following an acute stroke/transient ischemic attack (TIA), but the increment level varies among patients. We analyzed CRP concentrations during an acute stroke/TIA in relation to the CRP gene −717A>G polymorphism. Six months following an acute ischemic stroke/TIA, basal concentrations of CRP were measured in 507 controls and 219 patients and were found to be unassociated with the CRP −717A>G polymorphism. However, during the acute phase of stroke/TIA, individuals with the AG/GG genotype had significantly elevated CRP concentrations as opposed to those with the AA genotype (2.02 ± 1.59 vs. 1.73 ± 1.69 mg/l, P  = 0.027). In addition, significant 3.22-fold increments in CRP concentrations was noted in individuals carrying the −717G allele when comparing the acute phase with the basal state of each patient and averaging the results. CRP −717A>G polymorphism is associated with triggered CRP concentrations during acute stroke/TIA. These findings might shed more light on the mechanisms of CRP elevation in acute ischemic stroke/TIA.     

Hyperresponsiveness of platelets in ischemic stroke

Platelet activation and aggregation are critical in the pathogenesis of acute ischemic cerebrovascular diseases. The aim of our study was to characterize platelet function in patients with acute ischemic stroke or transient ischemic attack (TIA), and to evaluate the effect of platelet activation on clinical outcome. One hundred thirty-eight consecutive patients with TIA (n = 74) or stroke (n = 64) were enrolled in this study. Platelet aggregation in response to ADP, epinephrine, arachidonic acid, or collagen, and expression of platelet activation receptors (CD62P, CD63, LIBS-1 and PAC-1) in the acute phase and at three months follow-up were evaluated. Platelets derived from stroke patients were more hyperaggregable in response to agonists in the acute phase compared to TIA patients (p[ADP] = 0.002, p[arachidonic acid] = 0.047, p[epinephrine] = 0.020). Platelet activation was enhanced in the acute phase irrespective of the severity of the disease (stroke or TIA) and returned to baseline levels three months later. Persistent elevated platelet activation at three months follow-up (PAC-1) was associated with increased incidence of recurrent stroke (median, [interquartile range] 3.4, [3.0-5.2] versus 2.9, [2.3-4.0], p = 0.048). In conclusion, platelets are hyperactive in acute stroke compared with TIA. A more intensified dual antiplatelet therapy may be of benefit for stroke patients.     

Transient ischemic attack with infarction: A unique syndrome?

It is debated whether transient symptoms associated with infarction (TSI) are best considered a minor ischemic stroke, a subtype of transient ischemic attack (TIA), or a separate ischemic brain syndrome. We studied clinical and imaging features to establish similarities and differences among ischemic stroke, TIA without infarction, and TSI. Eighty-seven consecutive patients with TIA and 74 patients with ischemic stroke were studied. All underwent diffusion-weighted imaging on admission. Symptom duration and infarct volume were determined in each group. Thirty-six patients (41.3%) with TIA had acute infarct(s). Although TIA-related infarcts were smaller than those associated with ischemic stroke (mean, 0.7 vs 27.3 ml; p < 0.001), there was no lesion size threshold that distinguished ischemic stroke from TSI. In contrast, the symptom duration probability density curve was not broad, but instead peaked early with only a few patients having symptoms for longer than 200 minutes. The probability density function for symptom duration was similar between TIA with or without infarction. The in-hospital recurrent ischemic stroke and TIA rate was 19.4% in patients with TSI and 1.3% in those with ischemic stroke. TIA with infarction appears to have unique features separate from TIA without infarction and ischemic stroke. We propose identifying TSI as a separate clinical syndrome with distinct prognostic features.     

急性缺血性脑血管病患者肺炎衣原体感染与血清C反应蛋白的关系

目的:探讨肺炎衣原体感染在急性缺血性脑血管病炎症反应中的作用。方法:检测30例急性缺血性脑血管病患者和30例正常对照者血清中肺炎衣原体特异性抗体IgG和IgM,以及血清C反应蛋白水平。结果:缺血性脑血管病患者血清C反应蛋白水平高于对照者(P<0.01)。血清肺炎衣原体IgG抗体阳性脑血管病患者血清C反应蛋白水平(0.57±0.56mg/dl)高于IgG抗体阴性脑血管病患者(0.42±0.21mg/dl)(P>0.05)。血清肺炎衣原体IgM抗体阳性脑血管病患者血清C反应蛋白水平(0.67±0.73mg/dl)高于IgM抗体阴性脑血管病患者(0.47±0.35mg/dl)(P>0.05)。结论:肺炎衣原体急性和慢性感染均参与急性缺血性脑血管病的炎症反应过程,并与其它卒中因素共同引起血清C反应蛋白水平升高。     

The frequency of type I heterozygous protein S and protein C deficiency in 141 unrelated young patients with venous thrombosis

The frequency of heterozygous protein C and protein S deficiency, detected by measuring total plasma antigen, in a group (n = 141) of young unrelated patients (less than 45 years old) with venous thrombotic disease was studied and compared to that of antithrombin III, fibrinogen, and plasminogen deficiencies. Among 91 patients not receiving oral anticoagulants, six had low protein S antigen levels and one had a low protein C antigen level. Among 50 patients receiving oral anticoagulant therapy, abnormally low ratios of protein S or C to other vitamin K-dependent factors were presented by one patient for protein S and five for protein C. Thus, heterozygous Type I protein S deficiency appeared in seven of 141 patients (5%) and heterozygous Type I protein C deficiency in six of 141 patients (4%). Eleven of thirteen deficient patients had recurrent venous thrombosis. In this group of 141 patients, 1% had an identifiable fibrinogen abnormality, 2% a plasminogen abnormality, and 3% an antithrombin III deficiency. Thus, among the known plasma protein deficiencies associated with venous thrombosis, protein S and protein C deficiencies (9%) emerge as the leading identifiable associated abnormalities.     

Bleeding and subsequent anemia: a precipitant for cerebral infarction

BACKGROUND AND OBJECTIVES: The relationship between bleeding and subsequent anemia (BSA) and the occurrence of stroke has not been sufficiently studied. The purpose of the present study was to elucidate the characteristics of stroke associated with BSA. METHODS: We studied 16 consecutive patients with acute stroke associated with anemia (hemoglobin level on admission < or =9.0 g/dl) and compared their stroke subtypes with those of 32 control subjects. RESULTS: The cause of anemia was upper gastrointestinal bleeding in 11 patients (ulcers in 8; carcinomas in 2, and hemorrhagic gastritis in 1), bleeding from a hemorrhoid in 2, uterine cervical bleeding in 1, ecchymosis probably related to medication in 1, and chronic blood drainage in 1. At least 10 patients had a history of recent (<1 week), active bleeding. Clinical and imaging studies showed that all the patients had infarcts and none had intracerebral hemorrhages. Thirteen patients had infarcts in the region of the middle cerebral artery (MCA) (total MCA region in 2; partial, cortical area in 5; subcortical area in 5, and lenticulostriate artery region in 1), 2 had anterior cerebral artery (ACA) region infarction, and 1 had cerebellar infarction. All 11 patients who underwent vascular imaging studies showed significant stenosis and/or occlusion of the internal carotid artery (ICA) (n = 5), the MCA (n = 4), both the ICA and MCA (n = 1), or the ACA (n = 1). Of the different stroke subtypes (large vessel infarction (LVI), small vessel infarction, cardiogenic embolic infarction, intracerebral hemorrhage), LVI was significantly (p<0.05) more frequent in patients with stroke associated with BSA than in the controls, even though the demographics and risk factors were similar in each group. CONCLUSIONS: The close temporal relationship between the bleeding and the onset of stroke, as well as the predominance of the LVI subtype in the BSA-associated group as compared to controls, suggest that BSA may precipitate atherothrombotic cerebral infarction. A hemodynamic alteration, enhanced thrombosis or a combination of these appears to be the pathogenic mechanism.     

Microembolic signal monitoring in hemispheric acute ischaemic stroke: a prospective study

BACKGROUND AND PURPOSE: There are few data on the occurrence of microembolic signals (MES) in the acute phase of ischaemic stroke. The objective of our work was to systematically study the frequency of MES in non-selected patients with a first-ever hemispheric transient ischemic attack (TIA) or acute cerebral infarction, and to evaluate the clinical usefulness of MES detection. METHODS: 182 consecutive patients with hemispheric TIA or acute cerebral infarction, and 54-age-matched healthy controls were studied. Bilateral transcranial Doppler ultrasound (TCD) monitoring was performed for at least 30 min with a mean time from stroke onset to TCD of 69 h. Stroke severity on admission, early recurrent stroke and dependency on discharge were investigated. RESULTS: MES were detected in 20.5% of patients with arterial sources of embolism, 17. 1% of patients with potential sources of cardioembolism and 5% of patients with cryptogenic stroke. They were not registered, however, in lacunar infarctions (p < 0.001). Stroke severity on admission of patients with MES was greater than that of patients without MES (47. 1 vs. 19.4% with the Canadian Stroke Scale < or =6.5; p = 0.009). Early recurrent stroke was more frequent in patients with MES (11.8%) than in those without MES (4.2%) although the difference was not statistically significant. Multiple logistic regression analysis showed that MES increased the risk of dependency on discharge (odds ratio, 4.2; 95% CI, 1.2-14.9; p = 0.01) independently of age, stroke severity on admission and presence of an arterial or cardiac embolic source. CONCLUSIONS: There is a strong association of MES in the acute phase of stroke with known potential arterial and cardiac embolic sources. MES have an independent predictive value of poor outcome.