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Background and Purpose-There is an overlap between stroke and coronary heart disease, but the exact prevalence of coronary artery disease in patients with nonfatal cerebral infarction is unclear, particularly when there is no known history of coronary heart disease. Methods-We consecutively enrolled 405 patients presenting with acute cerebral infarction documented by neuroimaging who underwent carotid and femoral artery, thoracic, and abdominal aorta ultrasound examinations.Of the 342 patients with no known coronary heart disease, 315 underwent coronary angiography a median of 8 days (interquartile range, 6 -11) after stroke onset. Results-Coronary plaques on angiography, regardless of stenosis severity, were present in 61.9% of patients (95% confidence interval [CI], 56.5-67.3) and coronary stenoses Ն50% were found in 25.7% (95% CI, 20.9 -30.5). The overall prevalence of coronary plaque increased with the number of arterial territories (carotid or femoral arteries) involved, with an adjusted odds ratio of coronary artery disease of 1.25 (95% CI, 0.58 -2.71) for presence of plaque in 1 territory, and 4.31 (95% CI, 1.92-9.68) for presence of plaque in both territories, compared with no plaque in either territory. The presence of plaque in both femoral and carotid arteries had an age-and sex-adjusted positive predictive value of 84% for presence of coronary plaque and a negative predictive value of 44%. Conclusions-There is a high burden of silent coronary artery disease in patients with nonfatal cerebral infarction and no known coronary heart disease, even in the absence of systemic atherosclerosis. The prevalence is even higher in patients with evidence of carotid and/or femoral plaque. (Stroke. 2011;42:22-29.)

Background-Onset-to-reperfusion time has been reported to be associated with clinical prognosis. However, its impact on mortality remained to be assessed. Using a collaborative pooled analysis, we examined whether early mortality after successful endovascular treatment is time dependent. Methods and Results-In a collaborative pooled analysis of 7 endovascular databases, we assessed the impact of onsetto-reperfusion time in large-artery occlusion (internal carotid artery or middle cerebral artery) on outcomes. Successful reperfusion was defined as complete or partial restoration of blood flow within 8 hours from symptom onset. Primary outcome was 90-day all-cause mortality. Secondary outcomes included 90-day favorable outcome (modified Rankin Scale score, 0-2), 90-day excellent outcome (modified Rankin Scale score, 0-1), and occurrence of any intracerebral hemorrhage within 24 to 36 hours after treatment. A total of 480 cases with successful reperfusion (median time, 285 minutes) contributed to the present pooled analysis (120 with internal carotid artery occlusion and 360 with isolated middle cerebral artery occlusion). Increasing onset-to-reperfusion time was associated with an increased rate of mortality and intracerebral hemorrhage and with a decreased rate of favorable and excellent outcomes, without heterogeneity across studies. The adjusted odds ratio for each 30-minute time increase was 1.21 (95% confidence interval, 1.09-1.34; P<0.001) for mortality, 0.79 (95% confidence interval, 0.72-0.87) for favorable outcome, 0.78 (95% confidence interval, 0.71-0.86) for excellent outcome, and 1.21 (95% confidence interval, 1.10-1.33) for intracerebral hemorrhage. Conclusion-Onset-to-reperfusion time affects mortality and favorable outcome and should be considered the main goal in acute stroke patient management. (Circulation. 2013;127:1980-1985 13 A pooled analysis of the 2 IMS trials 3 and a single-center experience study 2 have previously reported the impact of ORT on good clinical outcome, but none has studied associations with 90-day mortality. The methodologies (study period, treatment specificities, baseline characteristics, and outcomes) of the 7 studies are summarized in Table 1. Eligibility, Data Collection, and DefinitionsPatients were eligible for inclusion in this study if they (1) had a largeartery occlusion (intracranial internal carotid artery or middle cerebral artery, M1 or M2) treated by an endovascular approach (thrombolysis or mechanical endovascular therapy) with or without prior use of intravenous thrombolysis; (2) had a successful angiographic reperfusion within 8 hours from symptom onset, defined as a complete or partial restoration of blood flow (Thrombolysis in Myocardial Infarction grade 2-3) 14 ; and (3) had available information on vital status. Data from individual patients were collected on a standardized form with predefined variables and were compiled and analyzed at the coordinating center (University Bichat Hospital, Paris). The following variables were collected: age; sex; initia...

Background and Purpose-The potential detrimental effect of diabetes mellitus and admission glucose level (AGL) on outcomes after stroke thrombolysis is unclear. We evaluated outcomes of patients treated by intravenous and/or intraarterial therapy, according to diabetes mellitus and AGL. Methods-We analyzed data from a patient registry (n=704) and conducted a systematic review of previous observational studies. The primary study outcome was the percentage of patients who achieved a favorable outcome (modified Rankin score ≤2 at 3 months). Results-We identified 54 previous reports that evaluated the effect of diabetes mellitus or AGL on outcomes after thrombolysis. In an unadjusted meta-analysis that included our registry data and previous available observational data, diabetes mellitus was associated with less favorable outcome (odds ratio

Background: Ischemia-modified albumin (IMA)is a new biological marker of ischemia. Previous studies have found increased serum IMA levels after myocardial ischemia, but no study has investigated the possibility that stroke modifies IMA blood levels. Materials and Methods: We studied 118 consecutive patients presenting within 3 h of the onset of an acute neurological deficit [84 brain infarctions (BI), 18 brain hemorrhages (ICH) and 16 transient ischemic attacks lasting less than 1 h or epileptic seizures]. Serum samples were obtained for all patients at initial presentation and repeated only in patients with stroke at 6, 12 and 24 h. IMA was measured by the albumin-cobalt-binding test (Ischemia Technologies, Denver, Colo., USA). Results: The initial median IMA (bootstrap 95% confidence interval, CI) was 83 U/ml (79–86) and 86 U/ml (75–90) in patients with BI and ICH, respectively (p = 0.76), and was 73 U/ml (58–79) in others (p = 0.003 compared with BI, and p = 0.017 with ICH). Baseline IMA levels correlated with the National Institutes of Health Stroke Scale [Spearman correlation coefficient: 0.34 (p = 0.002) in BI, 0.61 (p = 0.008) in ICH]. During the first 24 h, IMA levels increased in BI patients (median, 9.1%; bootstrap 95% CI, 5.2–11.5), whereas no change was observed in ICH patients (median, 1.2%; bootstrap 95% CI, –7.8 to 6.8). Conclusions: IMA blood levels may be a biomarker for early identification of acute stroke. Further studies are required to investigate the role of IMA in the early detection of acute stroke.

IMPORTANCE Treatment with remote ischemic perconditioning has been reported to reduce brain infarction volume in animal models of stroke. Whether this neuroprotective effect was observed in patients with acute ischemic stroke remains unknown.OBJECTIVE To determine whether treatment with remote ischemic perconditioning administered to the leg of patients with acute ischemic stroke can reduce brain infarction volume growth. DESIGN, SETTING, AND PARTICIPANTSThis proof-of-concept multicenter prospective randomized open-label with blinded end point clinical trial was performed from January 12, 2015, to May 2, 2018. Patients were recruited from 11 stroke centers in France. Of the 188 patients who received magnetic resonance imaging within 6 hours of symptom onset and were confirmed to have carotid ischemic stroke, 93 were randomized to receive treatment with lower-limb remote ischemic perconditioning in addition to standard care (the intervention group), and 95 were randomized to receive standard care alone (the control group).INTERVENTIONS Randomization on a 1:1 ratio to receive treatment with remote ischemic perconditioning (4 cycles of 5-minute inflations and 5-minute deflations to the thigh to 110 mm Hg above systolic blood pressure) in addition to standard care or standard care alone. MAIN OUTCOMES AND MEASURESThe change in brain infarction volume growth between baseline and 24 hours, measured by a diffusion-weighted sequence of magnetic resonance imaging scans of the brain.RESULTS A total of 188 patients (mean [SD] age, 67.2 [15.7] years; 98 men [52.1%]) were included in this intention-to-treat analysis. At hospital admission, the median National Institutes of Health Stroke Scale score was 10 (interquartile range [IQR], 6-16) and the median brain infarction volume was 11.4 cm 3 (IQR, 3.6-35.8 cm 3 ); 164 patients (87.2%) received intravenous thrombolysis, and 64 patients (34.0%) underwent mechanical thrombectomy. The median increase in brain infarction growth was 0.30 cm 3 (IQR, 0.11-0.48 cm 3 ) in the intervention group and 0.37 cm 3 (IQR, 0.19-0.55 cm 3 ) in the control group (mean between-group difference on log e -transformed change, -0.07; 95% CI, -0.33 to 0.18; P = .57). An excellent outcome (defined as a score of 0-1 on the 90-day modified Rankin Scale or a score equal to the prestroke modified Rankin Scale score) was observed in 46 of 90 patients (51.1%) in the intervention group and 37 of 91 patients (40.7%) in the control group (P = .12). No significant differences in 90-day mortality were observed between the intervention and control groups (14 of 90 patients; Kaplan-Meier estimate, 15.8% vs 10 of 91 patients; Kaplan-Meier estimate, 10.4%, respectively; P = .45) or with symptomatic intracerebral hemorrhage (4 of 88 patients [4.5%] in both groups; P = .97). CONCLUSIONS AND RELEVANCEIn this study, treatment with remote ischemic perconditioning, during or after reperfusion therapies, had no significant effect on brain infarction volume growth at 24 hours after symptom onset.