Higher mean platelet volume determined shortly after the symptom onset in acute ischemic stroke patients is associated with a larger infarct volume on CT brain scans and with worse clinical outcome

Objective

Mean platelet volume (MPV) determined shortly after the onset of acute ischemic stroke represents the pre-stroke values. Data on its relationship to stroke severity/outcome have been conflicting. We related MPV to infarct volume on CT brain scans and risk of death/dependence 7 days and 3 months post-stroke.

Methods

MPV (within 30 h since stroke onset), infarct volume (13–83 h since stroke onset) and clinical outcomes were evaluated in 81 consecutive patients (32 men, age 52–91 years, 10 small artery occlusion, 10 large artery atherosclerosis, 29 cardioembolic, 32 multiple probable/possible etiology).

Results

Higher MPV was independently associated with larger ln-infarct volume [estimate 0.259, 95% confidence interval (CI) 0.004–0.513, P = 0.046], greater risk of death/dependence 7 days post-stroke [relative risk (RR) = 1.077, 95% CI 1.005–1.115, P = 0.036], and greater risk of death/dependence 3 months post-stroke (RR = 1.077, 95% CI 1.001–1.158, P = 0.048). Considered covariates: stroke etiology, CT scan timing, platelet count and other hematological parameters, demographic variables, history of cerebrovascular, cardiac or cardiovascular diseases, diabetes, serum chemistry, previous antiplatelet and statin use and treatments delivered after the index event.

Conclusions

Data support the view about MPV as a determinant of severity/outcome of the acute ischemic stroke.     

Impact of CYP2C19 polymorphism on clinical outcome following coronary stenting is more important in non-diabetic than diabetic patients

Objective

The aim of this study was to examine the impact of CYP2C19 genotype on clinical outcome in coronary artery disease (CAD) patients with or without diabetes mellitus (DM).

Methods

CYP2C19 polymorphism and DM are associated with increased risk of cardiovascular events during antiplatelet therapy following stent implantation. Platelet reactivity during clopidogrel therapy and CYP2C19 polymorphism were measured in 519 CAD patients (males 70%, age 69 years) treated with stent placement. Patients were divided into two groups; DM (n = 249), and non-DM (n = 270), and clinical events were evaluated according to the carrier state, which included at least one CYP2C19 loss-of-function allele.

Results

The level of platelet reactivity and incidence of cardiovascular events were significantly different between Carriers and non-Carriers of the non-DM (platelet reactivity: 4501 +/− 1668 versus 3691 +/− 1714AUmin, P < 0.01; events, 32/178 versus 2/92, P < 0.01, respectively), however, there was no difference in clinical outcome in the DM group (events, 34/168 versus 14/81, respectively, P = 0.57). Multivariate analysis identified CYP2C19 loss-of-function allele carriage as an independent predictor of cardiovascular events in non-DM, but not in DM (non-DM, HR 7.180, 95% CI, 1.701 to 30.298, P = 0.007; DM, HR 1.374, 95% CI, 0.394 to 4.792, P = 0.618).

Conclusion

The impact of CYP2C19 polymorphism on clinical outcome seems to be more significant in non-DM compared with DM in patients with coronary stents.     

Patent foramen ovale increases the risk of acute ischemic stroke in patients with acute pulmonary embolism leading to right ventricular dysfunction

Background

Patent foramen ovale (PFO) is an established risk factor for ischemic stroke. Since acute right ventricular dysfunction (RVD) observed in patients with PE can lead to right-to-left inter-atrial shunt via PFO, we hypothesized that PFO is a risk factor for ischemic stroke in PE with significant right ventricular dysfunction.

Methods

55 patients (31 F, 24 M), median age 49 years (range 19–83 years) with confirmed PE underwent echocardiography for RVD and PFO assessment. High risk acute PE was diagnosed in 3 (5.5%) patients, while 16 (29%) hemodynamically stable with RVD patients formed a group with intermediate-risk PE. PFO was diagnosed in 19 patients (34.5%). Diffusion-weighted MRI of the brain for acute ischemic stroke (AIS) was performed in all patients 4.91 ± 4.1 days after admission.

Results

AIS was detected by MRI in 4 patients (7.3%). Only one stroke was clinically overt and resulted in hemiplegia. All 4 AIS occurred in the PFO positive group (4 of 19 patients), and none in subjects without PFO (21.0% vs 0%, p = 0.02). Moreover, all AIS occurred in patients with RVD and PFO, and none in patients with PFO without RVD (50% vs 0%, p = 0.038).

Conclusion

Our data suggest that acute pulmonary embolism resulting in right ventricular dysfunction may lead to acute ischemic stroke in patients with patent foramen ovale. However, the clinical significance of such lesions remains to be determined.     

Cilostazol for Primary Prevention of Stroke in Peripheral Artery Disease: A Population-based Longitudinal Study in Taiwan

Background

Clopidogrel, cilostazol, and aspirin were compared in terms of efficacy and safety for primary prevention of stroke in peripheral artery disease (PAD) patients.

Methods

This retrospective cohort study analyzed data contained in the Taiwan National Health Insurance Bureau database for patients treated for PAD but not for stroke during 2002–2008. Patients were stratified according to treatment with aspirin, clopidogrel, cilostazol, or combined therapy. The primary efficacy and safety endpoints were stroke and hemorrhage.

Results

Of the 931 patients enrolled in this study, 479 had received aspirin, 39 had received clopidogrel, 294 had received cilostazol alone, and 33 had received a cilostazol-based combined therapy. Compared to patients treated with aspirin, the patients treated with cilostazol had significantly lower all-stroke risk not only in the overall group (HR = 0.66, 95% CI = 0.48-0.90, p = 0.0086), but also in the subgroup of patients with diabetes (HR = 0.64, 95% CI = 0.42-0.98, p = 0.0394) and in the subgroup of patients with high cardiovascular risk (HR = 0.66, 95% CI = 0.46-0.95, p = 0.0254). Additionally, compared to patients treated with aspirin, those treated with cilostazol did not have significantly more hemorrhagic events in the overall group, in the diabetes subgroup, or in the high cardiovascular risk subgroup. Clopidogrel, cilostazol-based combined therapy and aspirin did not significantly differ in terms of efficacy and hemorrhagic events.

Conclusion

Although this database study indicated that cilostazol therapy is an effective alternative treatment for primary prevention of stroke in PAD, further confirmation is needed in large, prospective, and randomized trials.     

Extracranial carotid artery disease in nasopharyngeal carcinoma patients with post-irradiation ischemic stroke

Objective

Irradiation induced extracranial carotid occlusive disease has been recognized as a potential cause of post-irradiation stroke in nasopharyngeal carcinoma (NPC) patients. Our study aims to investigate the prevalence of extracranial CA disease in post-irradiated Taiwanese NPC ischemic stroke patients.

Methods

Forty-three NPC patients with ischemic stroke were retrospectively selected from the stroke registration of the study hospital and compared with 276 first-ever ischemic stroke patients from the same database, of which 31 patients underwent carotid duplex sonography (CDS). Significant atherosclerotic lesions of the carotid arteries were defined as a >50% stenosis or an occlusion according to CDS.

Results

Significant carotid lesions occurred in 13 of 31 (42%) NPC patients. Stroke was more frequently caused by large artery disease (44% versus 23%; p < 0.01) in NPC patients than in first-ever stroke patients without NPC. Carotid artery disease (odds ratio 7.22, 95% confidence interval 2.51–20.77; p < 0.0001) and absence of diabetes mellitus (odds ratio 0.26, 95% confidence interval 0.07–0.93; p = 0.039) were the strongest independent discriminators between NPC stroke patients and non-NPC stroke patients in a multivariate logistic regression analysis.

Conclusion

Patients who received neck irradiation are at risk for the delayed development of diffused atherosclerosis but also for carotid occlusion within years, although the mechanism remains elusive and probably multifactorial.     

VASP phosphorylation and genetic polymorphism for clopidogrel resistance in Chinese patients with non-cardioembolic ischemic stroke

Background

Clopidogrel resistance(CR)is found in non-cardioembolic ischemic stroke (NCIS) patients. However, it is still largely unknown how to identify CR in NCIS patients by laboratory and genetic characteristics.

Methods

A total of 95 patients with acute NCIS were recruited. Phosphorylation of the vasodilator stimulated phosphoprotein (VASP) was detected using flow cytometry, and genes(CYP2C19,CYP3A4) were detected using the Sanger method. The baseline of platelet reactivity index (BPRI) before clopidogrel treatment and the platelet reactivity index with clopidogrel treatment (CPRI) for 7 days were measured. Laboratory clopidogrel resistance (LCR) was defined as CPRI of ≥ 50%.Clinical clopidogrel resistance (CCR) was defined as the presence of progressive stroke during hospitalization, stroke recurrence or occurrence of other ischemic vascular events within 6 months.

Results

The incidence of LCR was 41.05% and 18.95% developed CCR. The incidence of LCR was significantly higher in GA/AA patients with CYP2C19 (681G > A) (χ2 = 11.16, P = 0.001) and CYP2C19 (636G > A) (χ2 = 4.829, P = 0.028) than in wildtype GG patients. CYP2C19 (681G > A) (OR 6.272, 95%CI 2.162,18.199,P = 0.001) and CYP2C19 (636G > A) (OR: 5.625,95%CI 1.439, 21.583,P = 0.013) were risk factors for LCR. patients with LCR were more likely to develop CCR (χ2 = 6.021, P = 0.014). The probability of CCR was markedly increased in GA/AA patients with CYP2C19 (681G > A) (χ2 = 10.341, P = 0.001). We identified CYP2C19 (681G > A) (OR 7.814, 95%CI 1.816, 33.618 P = 0.006), Essen score (OR 8.351, 95%CI 1.848, 37.745 P = 0.006), and LCR (OR 5.881, 95%CI 1.373, 25.192, P = 0.017) as risk factors for CCR.

Conclusion

In clinical practice,LCR and CYP2C19 gene polymorphism should be assessed in NCIS patients receiving clopidogrel treatment.The Chinese Clinical Trial Registry number: ChiCTR-ONC-13003406     

Genetic determinants of high on-treatment platelet reactivity in clopidogrel treated Chinese patients

Introduction

Cytochrome P450 (CYP), ATP-binding cassette transporters (ABCB1), and paraoxonase-1 (PON1) play crucial roles in clopidogel absorption and bioactivation. Genetic polymorphisms in these genes have been associated with the variability of the response to clopidogrel, however their contribution to high on-treatment platelet reactivity (HPR) in clopidogrel treated Chinese patients is less known.

Materials and methods

Five-hundred Chinese-Han patients treated with clopidogrel for acute coronary syndrome (ACS) were consecutively recruited from the Department of Geriatric Cardiology, General Hospital of Chinese People’s Liberation Army, from September 2010 to September 2012. We assessed the relations of CYP2C19*2 (rs4244285), CYP2C19*3 (rs4986893), CYP2C19*17 (rs12248560), PON1Q129R (rs662) and ABCB1C3435T (rs1045642) to the platelet aggregation after 5 days maintenance dose of clopidogrel administration, and the risk for HPR. The cutoff of HPR was defined as 20 μmol/L adenosine diphosphate (ADP)-induced platelet aggregation > 50%.

Results

Both CYP2C19*2 and *3 alleles were significantly associated with higher platelet aggregation after 5 days maintenance dose of clopidogrel administration (P < 0.00001and P = 0.042, respectively). The platelet aggregation in carriers of at least one CYP2C19 loss-of-function allele (*2 or *3, accounted for 58% of the study population) was obviously higher than that in non-carriers (P < 0.00001). Patients with the CYP2C19*2 allele had a higher risk of HPR than those with the CYP2C19 wild-type genotype [adjusted hazard ratio (HR), 1.56; 95% confidence interval(CI), 1.04–2.33, P = 0.03]. The carriers of at least one CYP2C19 loss-of-function allele could also predict significantly greater risk of HPR compared with non-carriers (adjusted HR1.79,95% CI: 1.33–2.4,P = 0.003). However, the carriage of CYP2C19*3 alone could not predict the risk of HPR significantly (adjusted HR, 1.5; 95% CI: 0.83–3, P = 0.16). Significant relation of CYP2C19*17, PON1Q129R and ABCB1C3435T to the platelet aggregation was not found.

Conclusion

In clopidogrel treated Chinese patients with ACS, carriers of at least one CYP2C19 loss-of-function allele could predict greater risk of HPR, with the impact mainly attributing to CYP2C19*2. Neither ABCB1 nor PON1 genotype could influence the antiplatelet response of clopidogrel in the cohort of Chinese patients.     

Impact of clopidogrel resistance on thrombotic events after percutaneous coronary intervention with drug-eluting stent

Objectives

This study examines whether patient resistance to clopidogrel is associated with long-term thrombotic events after elective coronary drug-eluting stent (DES) implantation.

Methods

We prospectively enrolled 386 patients with stable angina who received elective percutaneous coronary intervention (PCI) with DES. Before the procedure, platelet reactivity was measured by light transmittance aggregometry (LTA) at baseline and approximately 24 h after the 300 mg loading dose of clopidogrel. Clopidogrel resistance was conservatively defined as ≤ 10% absolute difference between baseline and post-treatment platelet aggregation. All patients received chronic dual antiplatelet treatment (aspirin 300 mg and clopidogrel 75 mg daily) for 12 months. Patients were followed for 1 year after coronary stenting for the occurrence of composite thrombotic events, including cardiovascular death, non-fatal myocardial infarction (MI), stent thrombosis or cerebrovascular ischemic accident (CVA).

Results

Clopidogrel resistance was present in 65 patients (16.8%). During follow-up, composite thrombotic events occurred in 16.9% of clopidogrel resistant patients, yet in only 6.2% of non-resistant patients (p = 0.010). The incidence of definite or probable stent thrombosis was 9.2% in clopidogrel resistant patients and 2.5% in non-resistant patients (p = 0.018). After adjustment for other factors that affect cardiovascular outcome, clopidogrel resistance, diabetes, and left ventricular (LV) dysfunction were independently associated with 1-year composite thrombotic events. The hazard ratio (HR) for clopidogrel resistance was 2.44 (95% CI = 1.09 to 5.45; p = 0.031).

Conclusion

This study demonstrates the natural history of clopidogrel resistance among patients with stable cardiovascular disease, and shows that this resistance is an independent predictor of thrombotic events in patients undergoing PCI with DES.     

Local intraarterial tirofiban after formation of anterograde flow in patients with acute ischemic stroke: Preliminary experience and short term follow-up results

Objective

Despite the risk of intracranial hemorrhage, combination therapy with intravenous recombinant tissue plasminogen activator and intraarterial mechanical thrombolysis can be effective for treatment of acute ischemic stroke. We investigated the feasibility and safety of intraarterial tirofiban following formation of anterograde flow after mechanical thrombolysis in acute ischemic stroke.

Methods

We analyzed data from consecutive patients with acute ischemic stroke, who underwent treatment with intraarterial thrombolysis. All patients were evaluated immediately and 7 days later by computed tomography scanning and magnetic resonance imaging scanning with magnetic resonance angiography. For clinical outcome analysis, we followed up the NIHSS score and modified Rankin Scale score during a period of 3 months.

Results

Sixteen patients underwent treatment. The mean baseline NIHSS score was 16.1 ± 4.4 points. 75.1% of patients showed angiographic improvement; 43.8% and 31.3% had complete and partial recanalization, respectively. 53.3% and 56.3% showed clinical improvement and favorable outcome at 24 h and 3 months, respectively. One patient had symptomatic intracranial hemorrhage.

Conclusions

Our results suggest that administration of local intraarterial tirofiban after anterograde flow formation is a viable treatment strategy for patients of acute ischemic stroke for reducing the risk of reocclusion after intraarterial thrombolysis.     

Plasma heart-type fatty acid binding protein level in acute ischemic stroke: Comparative analysis with plasma S100B level for diagnosis of stroke and prediction of long-term clinical outcome

Objectives

Heart-type fatty acid binding protein (H-FABP) is enriched in neuronal cell body as well as myocardium, and is rapidly released from damaged neuron into circulation in cerebral ischemia. We performed a comparative analysis between plasma H-FABP and S100B levels in the acute phase of ischemic stroke.

Methods

The present study included 111 consecutive patients with acute ischemic stroke and 127 control subjects. Measurement of plasma H-FABP and S100B levels was conducted during acute phase (<24 h) of stroke. Clinical severities were evaluated by the use of NIHSS scores at admission and mRS score at 3 months after symptom onset.

Results

Both the plasma H-FABP and S100B levels were significantly higher in stroke group than control group. In multiple logistic regression analysis, statistical significance of both markers remained significant after adjusting the vascular risk factors. In the receiver operator characteristic (ROC) curve analysis, neither H-FABP (area under curve [AUC] = 0.71, P < 0.001, sensitivity: 59.5%, specificity: 79.5%) nor S100B (AUC = 0.70, P < 0.001, sensitivity: 54.0%, specificity: 83.5%) showed a favorable degree of diagnostic value to discriminate stroke from stroke mimic. Plasma H-FABP (r = 0.46, P < 0.01) and S100B (r = 0.45, P < 0.01) were correlated with initial NIHSS score, and both marker were significantly higher in patients with poor clinical outcome.

Conclusion

Although plasma H-FABP is elevated in the acute phase of ischemic stroke, the diagnostic accuracy of H-FABP as a sole marker is not sufficient to be applied in the clinical setting. Plasma H-FABP can be used as a potential marker for stroke prognosis.     

Less favorable neurological recovery after acute stroke in patients with hypercholesterolemia

Objectives

We aimed to investigate the effect of hypercholesterolemia on recovery after acute ischemic stroke.

Methods

Data of 3048 patients admitted for acute ischemic stroke from January to December 2009 were collected from the Stroke Registry in the Chang Gung Healthcare System. Baseline characteristics of patients with and without hypercholesterolemia were compared. The association of hypercholesterolemia with neurological severity and recovery was analyzed using multivariate logistic regression. The patients were then divided on the basis of age for subgroup analysis.

Results

The number of patients with and without a history of hypercholesterolemia was 474 (15.6%) and 2574 (84.4%), respectively. Univariate analysis showed that patients with hypercholesterolemia had a lower National Institutes of Health Stroke Scale (NIHSS) score on admission (p = 0.004). However, during hospitalization, these patients displayed less improvement in their NIHSS score (p = 0.002). These results remained significant in multivariate logistic regression analysis (p < 0.001 and p = 0.002, respectively). Subgroup analysis showed a similar association for hypercholesterolemia in both younger (age < 70) and older (age ≥ 70) age groups.

Conclusions

Acute ischemic stroke in patients with hypercholesterolemia was correlated with reduced severity on admission and less favorable recovery during hospitalization, regardless of age.     

Protease activated receptor-1 (PAR-1) mediated platelet aggregation is dependent on clopidogrel response

Introduction

Clopidogrel inhibits ADP mediated platelet aggregation through inhibition of the P2Y12 receptor by its active metabolite. Thrombin induces platelet aggregation by binding to protease activated receptor-1 (PAR-1), and inhibition of PAR-1 has been evaluated in patients treated with clopidogrel to reduce ischemic events after acute coronary syndromes. Residual PAR-1 mediated platelet aggregation may be dependent on extent of clopidogrel response.

Material and Methods

Platelet aggregation was measured in 55 patients undergoing elective PCI at 16-24 hours after 600 mg clopidogrel loading dose by light transmittance aggregometry using ADP 20 μM and thrombin receptor agonist peptide (TRAP) at 15 μM and 25 μM as agonists. Genomic DNA was genotyped for common CYP2C19 variants.

Results

Increasing quartiles of 20 μM ADP induced platelet aggregation after clopidogrel loading were associated with increasing levels of TRAP mediated platelet aggregation. Patients in the highest quartile (clopidogrel non-responders) of post treatment ADP aggregation had significantly higher TRAP mediated aggregation than the patients in the lowest quartile (clopidogrel responders) [TRAP 15 μM: 79.6 ± 5% vs. 69.5 ± 8%, p < 0.001].

Conclusions

Non-responders to clopidogrel show increased residual platelet aggregation induced by TRAP, whereas clopidogrel responders exhibit attenuated response to TRAP. Addition of PAR-1 antiplatelet drugs may be most effective in patients with reduced clopidogrel response and high residual TRAP mediated platelet aggregation.     

Plasma and Whole Blood Clot Strength Measured by Thrombelastography in Patients Treated with Clopidogrel during Acute Coronary Syndromes

Introduction

Treatment with clopidogrel, a selective platelet P₂Y₁₂ receptor antagonist, reduces risk of recurrent ischemic events in patients with acute coronary syndrome (ACS), by limiting platelet aggregation and activation. Stable whole blood clot formation requires activation of platelets, generation of fibrin and final fibrin crosslinks. In this study we intended to compare plasma and whole blood thrombelastography (TEG) measurements in patients during ACS.

Materials and Methods

Whole blood and plasma samples from 32 patients with non-ST segment elevation myocardial infarction (NSTEMI) were collected after administration of clopidogrel. Whole blood and plasma fibrin clot strength (MA) were determined by TEG. Platelet aggregation was determined by light transmittance aggregometry (LTA) using adenosine 5'-diphosphate (ADP), thrombin receptor activation peptide (TRAP), or collagen as agonists. Fibrinogen and C-reactive protein (CRP) concentrations were measured by ELISA.

Results

Heightened plasma fibrin clot strength was associated with increased platelet reactivity stimulated by ADP (ρ = 0.536; p = 0.002), TRAP (ρ = 0.481; p = 0.007), and collagen (ρ = 0.538; p = 0.01). In contrast to plasma fibrin MA, whole blood MA did not correlate with platelet aggregation. Platelet count was the primary contributor to the difference in thrombin induced whole blood MA and plasma fibrin MA. Increasing levels of CRP were associated with increased plasma fibrin clot strength and platelet reactivity.

Conclusions

Our data suggest that inflammation is associated with increased plasma fibrin clot strength and lower platelet inhibition by clopidogrel during ACS. Platelet count is a main contributor to additional contractile force of whole blood TEG as compared to plasma TEG during treatment with clopidogrel.     

Differences in thrombus structure and kinetics in patients with type 2 diabetes mellitus after non ST elevation acute coronary syndrome

Introduction

Despite optimal secondary prevention therapy following non-ST elevation acute coronary syndrome (NSTE-ACS), recurrent thrombotic events are more frequent in patients with type 2 diabetes mellitus (T2DM).

Materials and Methods

This exploratory study was aimed to evaluate quantitative and qualitative aspects of thrombus. In 28 patients with and without T2DM treated with aspirin and clopidogrel we assessed thrombus quantity using an ex-vivo chamber, platelet reactivity, thrombus ultrastructure and thrombus kinetics one week after NSTE-ACS.

Results

T2DM was associated with increased thrombus [14861 (8003 to 30161) vs 8908 (6812 to 11996), μ²/mm, median (IQR), p = 0.045] and platelet reactivity. In addition, diabetic thrombus showed lower visco-elastic tensile strength [(− 0.2(− 1.7 to 0.7) vs 1.0(− 0.9 to 3.3), p = 0.044)] and was more resistant to autolysis [(27.8(11.7 to 70.7) vs 78.8(68.5 to109.6) mm/min, p = 0.002)]. On SEM, fibrin fibres in diabetes were thinner, with higher lateral interlinkage and mesh-like organisation. Thrombus quantity correlated inversely with thrombus retraction (r = − 0.450 p = 0.016) but not with platelet reactivity (r = 0.153, p = 0.544).

Conclusions

Despite optimal antiplatelet therapy, T2DM patients after NSTE-ACS developed increased thrombus of lower tensile strength and slower retraction. SEM revealed loosely arranged fibrin fibres. Our data showed significant differences in the magnitude as well as structural and mechanistic characteristics of thrombus in patients with T2DM.     

Early superficial temporal artery to middle cerebral artery bypass in acute ischemic stroke

Objective

To evaluate the effects and safety of superficial temporal artery–middle cerebral artery (STA–MCA) anastomosis in the early stage after an acute ischemic event and the improvement of present symptoms in patients with intracranial atherosclerotic occlusive disease with stroke/stroke in progress.

Methods

From 2006 to 2010, 20 patients (15 males and five females) with atherosclerotic cerebrovascular disease were treated with an STA–MCA bypass. All of the patients presented with an acute ischemic stroke or stroke in progress despite maximal medical treatment. The patients underwent an STA–MCA bypass within 7 days from symptom onset. The clinical outcome and hemodynamic study of the 20 patients were preoperatively and postoperatively investigated. A pooled analysis was performed, and the results were compared with those obtained from other delayed STA–MCA bypass studies.

Results

Among the 20 patients who underwent an early STA–MCA bypass, fourteen (70%) patients achieved a good functional outcome (mRS 0, n = 3; mRS 1, n = 9; mRS 2, n = 2). Prior to surgery, the mean basal regional cerebral blood flow (rCBF) and cerebrovascular reserve capacity (CVR) in the symptomatic hemisphere were 37.3 ± 4.3 ml/100 g/min and −1.68 ± 2.9%. The mean basal rCBF and CVR had significantly increased postoperatively, and no reperfusion-induced hemorrhage had occurred. In the pooled analysis, no significant differences were observed in the clinical outcome (P = 0.328) or in the incidence of postoperative complications (P = 0.516) between patients who underwent an early STA–MCA bypass and in patients who underwent a delayed STA–MCA bypass in previous studies.

Conclusions

In this study, which consisted of 20 carefully selected patients with acute ischemic stroke, an early STA–MCA bypass was safely and effectively performed, and in some cases, an early STA–MCA bypass resulted in rapid neurological improvement. An early STA–MCA bypass was beneficial in select patients who had acute ischemic stroke with imaging evidence of a small infarction.     

Frontal lobe atrophy is associated with small vessel disease in ischemic stroke patients

Background

The pathogenesis of frontal lobe atrophy (FLA) in stroke patients is unclear. We aimed to ascertain whether subcortical ischemic changes were more associated with FLA than with parietal lobe atrophy (PLA) and temporal lobe atrophy (TLA).

Methods

Brain magnetic resonance images (MRIs) from 471 Chinese ischemic stroke patients were analyzed. Lobar atrophy was defined by a widely used visual rating scale. All patients were divided into non-severe, mild–moderate, and severe atrophy of the frontal, parietal, and temporal lobe groups. The severity of white matter lesions (WMLs) was rated with the Fazekas’ scale. Clinical and radiological features were compared among the groups. Subsequent logistic regressions were performed to determine the risk factors of atrophy and severe atrophy of the frontal, parietal and temporal lobes.

Results

The frequency of FLA in our cohort was 36.9% (174/471). Severe FLA occurred in 30 (6.4%) patients. Age, previous stroke, and periventricular hyperintensities (PVH) (odds ratio (OR) = 1.640, p = 0.039) were independent risk factors of FLA. Age and deep white matter hyperintensities (DWMH) (OR = 3.634, p = 0.002) were independent risk factors of severe FLA. PVH and DWMH were not independent risk factors of PLA and TLA.

Conclusion

Frontal lobe atrophy in ischemic stroke patients may be associated with small vessel disease. The association between WMLs and FLA was predominant over atrophy of the parietal and temporal lobes, which suggests that the frontal lobe may be vulnerable to subcortical ischemic changes.     

Prehospital transfer medicalization increases thrombolysis rate in acute ischemic stroke. A French stroke unit experience

Objectives

Narrow therapeutic window is a major cause of thrombolysis exclusion in acute ischemic stroke. Whether prehospital medicalization increases t-PA treatment rate is investigated in the present study.

Patients and methods

Intrahospital processing times and t-PA treatment were analyzed in stroke patients calling within 6 h and admitted in our stoke unit. Patients transferred by our mobile medical team (SAMU) and by Fire Department (FD) paramedics were compared.

Results

193 (61.6%) SAMU patients and 120 (38.4%) FD patients were included within 30 months. Clinical characteristics and onset-to-call intervals were similar in the two groups. Mean door-to-imaging delay was deeply reduced in the SAMU group (52 vs. 159 min, p < 0.0001) and was <25 min in 50% of SAMU patients and 14% of FD patients (p < 0.0001). SAMU management was the only independent factor of early imaging (p = 0.0006). t-PA administration rate was higher in SAMU group than in FD group (42% vs. 28%, p = 0.04). Proportion of patients with delayed therapeutic window was higher in FD group than in SAMU group (38% vs. 26%, p < 0.0001).

Conclusion

Prehospital transfer medicalization promotes emergency room bypass, direct radiology room admission and high thrombolysis rate in acute ischemic stroke.     

Association of elevated plasma viscosity with small vessel occlusion in ischemic cerebral disease

Introduction

Elevated plasma viscosity (PV) is observed in patients with vascular risk factors, such as diabetes mellitus or arterial hypertension. In this study we investigated the association of plasma viscosity and the different clinical and radiological entities of cerebral ischemia.

Methods

PV of 465 consecutively admitted patients with clinical symptoms of acute cerebral ischemia without radiological signs of bleeding was measured. Data is expressed as median [range] unless stated otherwise. p < 0.05 was considered statistically significant.

Results

Patients with acute cerebral ischemia (TIA or Stroke) showed increased PV (TIA 1.27mPas [1.07-1.53], stroke 1.27mPas [1.07-1.56]) compared to patients without cerebral ischemia (Mimics) (1.23mPas [1.06-1.42]). The group with radiologically proven small vessel disease (SVD) had a significantly higher mean values of PV (1.29mPas [1.06-1.54]) compared to those with signs of large vessel disease or cardioembolic events (1.22mPas [1.07-1.56], p < 0.001).Patients with chronic heart failure (p = 0.007), arterial hypertension (p < 0.001) and diabetes mellitus (p = 0.002) had higher PV compared to patients without these cardiovascular risk factors. Hyperlipidemia or nicotine abuse showed no relation to PV.

Conclusion

Elevated PV is not only associated TIA and Stroke but is also found in patients with radiological signs of cerebral SVD. High levels of PV could be an underestimated risk for TIA and Stroke and participate in the complex pathophysiology of SVD. Prospective observational and interventional studies are warranted for further evaluation of PV in neurological ischemic diseases.     

Additional value of quantitative EEG in acute anterior circulation syndrome of presumed ischemic origin

Objective

The clinical course of acute stroke can be highly variable and for effective management outcome prediction needs to be refined. We investigated whether EEG parameters are of additional diagnostic and prognostic value in the early phase of acute ischemic anterior circulation stroke.

Methods

Ninety-four patients presenting with acute anterior circulation syndrome (ACS) of presumed ischemic origin were incrementally included. Clinical characteristics were correlated with volume of ischemia and EEG parameters. Predictive values for definite stroke, early neurological deterioration, spontaneous early neurological improvement and death within 1 week after ACS were calculated using ROC curves and logistic regression modelling.

Results

In patients with normal or near normal NIHSS score of 0 or 1, the pairwise derived brain symmetry index (pdBSI) was an independent predictor for definite stroke displaying an overall accuracy of 80%. Early neurological deterioration was independently predicted by pdBSI with a correct classification rate of 95%. In ROC analysis, death was predicted by pdBSI with overall accuracy of 97%. Spontaneous neurological improvement was independently predicted by the delta + theta/alpha + beta – ratio with overall accuracy of 75%. Small-vessel stroke was independently predicted by pdBSI with a correct classification rate of 92%.

Conclusions

EEG may be of prognostic value for spontaneous neurological improvement, early neurological deterioration and death in the acute setting of acute anterior circulation syndrome of presumed ischemic origin.

Significance

These findings may have an impact on stroke care.