Dynamic cross-sectional changes of the middle cerebral artery in atherosclerotic stenosis detected by 3·0-Tesla MRI

Abstract

Objectives:

Atherosclerotic stenosis of the middle cerebral artery (MCA) is one of the causes of ischemic stroke, but aside from investigations using magnetic resonance angiography (MRA), studies evaluating stenosis are rare. The purpose of this study was to assess dynamic changes of MCA cross section between the systolic and diastolic phases in patients with cerebral infarction using 3·0-Tesla magnetic resonance imaging (3T MRI).

Methods:

We assessed 12 stroke patients with M1 stenosis in the MCA and 12 healthy volunteers. We measured MCA cross sections (proximal/distal to stenosis and on the stenosis) in the systolic and diastolic phases by synchronizing imaging with heartbeats, as well as the maximum flow velocity by using cine-phase contrast (PC) MRI. Each patient also underwent conventional MRA.

Results:

Differences in cross sections between systolic and diastolic phases were significantly smaller in the stenosed artery compared to the distal (P < 0·05) and proximal areas (P < 0·01) in stroke patients. The difference in maximal blood velocity between systolic and diastolic phases at the M1 stenosis was significantly larger than that in the area proximal to the stenosis (P < 0·05).

Discussion:

We clearly demonstrated dynamic cross-sectional changes in the stenotic areas by 3T MRI, suggesting hemodynamic shear stress, which may further enhance MCA atherosclerosis.     

Cystatin C as an index of acute cerebral infraction recurrence: one-year follow-up study

Background and purpose: Cystatin C is associated with acute cerebral infarction (ACI). However, the correlation of serum cystatin C level with recurrence of ACI and different subtypes of ACI had not been fully clarified. The aim of this study was to detect the relationship between serum cystatin C level and recurrent ACI in one-year follow-up and different subtypes of ACI.

Methods: A total of 532 consecutive patients with ACI and 339 healthy controls were included. All ACI patients were followed up for one year, the clinical and biochemical characteristics of ACI and ACI recurrent patients were documented and analyzed.

Results: A total of 477 (89.7%) patients completed one-year follow-up study, 64 (13.4%) patients suffered ACI recurrence. The results showed serum cystatin C was 1.04?±?0.19?mg/L and 1.14?±?0.49?mg/L in control and ACI, respectively (p<?.001). The significant risk factors for ACI recurrence were presence of hypertension (p?=?.009, OR =3.32), diabetes (p?=.03, OR =1.87), coronary heart disease (p?=?.01, OR =2.46), and cystatin C (p?=?.003, OR =2.87). The risk of ACI recurrence increased with serum cystatin C level. Additionally, cystatin C level was associated with different subtypes of ACI; large-artery atherosclerosis (LAA) subtype had the highest level of cystatin C in ACI and recurrent ACI group.

Conclusions: Serum cystatin C level is an independent prediction biomarker for ACI recurrence. LAA subtype of ACI and ACI recurrence was more closely related to elevated cystatin C level.     

Electrophysiological profile of the patients with MuSK positive myasthenia gravis

Abstract

Objectives:

To determine the electrophysiological profile of our cohort of patients with muscle-specific tyrosine kinase (MuSK) positive myasthenia gravis (MG).

Methods:

Repetitive nerve stimulation test (RNS) and jitter analysis using concentric needle electrode were performed in 31 MuSK and in 28 acetylcholine receptor (AChR) positive MG patients.

Results:

Pathological RNS was verified in 16 (51·6%) MuSK and 26 (92·9%) AChR MG patients (P < 0·01). Pathological jitter analysis was registered in 28 (90·3%) MuSK and 26 (92·9%) AChR MG patients (P > 0·05). Increased jitter was present in extensor digitorum communis (EDC) in 23 (74·2%) MuSK and in 25 (89·3%) AChR MG patients (P > 0·05) as well as in orbicularis oculi (OO) muscle in 24 (85·7%) MuSK and 22 (81·5%) AChR MG patients (P > 0·05). Lower mean value of mean consecutive difference (MCD) and fewer potential pairs with increased jitter were registered in MuSK MG compared to AChR MG patients only in EDC muscle (P < 0·05). In MuSK MG patients, increased jitter was observed to be more frequent in patients with longer disease duration (P < 0·05) and also in those patients exhibiting more severe disease forms (P < 0·01) only in EDC muscle.

Discussion:

Repetitive nerve stimulation test has low sensitivity in MuSK MG patients, while jitter analysis shows high sensitivity, especially in facial muscles. The EDC muscle in MuSK MG patients usually shows increased jitter in more severe disease forms and later in the course of the disease.     

Influence of internal carotid artery stenosis,blood pressure,glycated hemoglobin,and hemoglobin level on fMRI signals of stroke patients

Abstract

Objectives:

To identify the effect of internal carotid artery (ICA) stenosis, blood pressure (BP), glycated hemoglobin (HbA1c), and hemoglobin level on blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) signals in stroke patients.

Methods:

A total of 18 stroke patients with acute cerebral infarction (13 males and 5 females) and 13 age-matched healthy controls (5 males and 8 females) were recruited. Among 18 stroke patients, 8 had significant ICA stenosis (>50%) and 10 had nonsignificant ICA stenosis (<50%). During handgrip task, stroke patients and normal controls were allowed to use their hands coincided with infarction and right hands, respectively.

Results:

The mean BOLD signals in patients with significant ICA stenosis were significantly less than that in patients with nonsignificant ICA stenosis. Mean arterial pressure (MAP) was significantly correlated with activated voxels of Brodmann area 4 (P < 0·01) and total activated voxels (P = 0·007), whereas hemoglobin and HbA1c showed no significant correlation with activated voxels of Brodmann area 4 or total activated voxels (P > 0·05).

Conclusion:

It is suggested that both ICA stenosis and arterial BP could influence BOLD signal, while HbA1c and hemoglobin level had no effect on BOLD signal.     

急性脑梗死患者血清促动脉硬化指数与颈动脉内膜中层厚度及氧化型低密度脂蛋白水平的研究

目的探讨急性脑梗死(ACI)患者血清氧化型低密度脂蛋白(ox-LDL)、促动脉硬化指数(AIP)水平与颈动脉粥样硬化的关系。方法连续性选取ACI患者120例作为研究对象,选择同期健康体检者60例作为对照组。分别检测两组的ox-LDL水平及血浆脂质代谢水平,后者包括甘油三酯(TG)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C),并计算血浆促动脉硬化指数(AIP)。对ACI组患者进行颈部血管彩超检查,根据检查结果将其分为颈动脉内膜中层厚度(IMT)正常组(11例)、IMT增厚组(25例)和颈动脉粥样斑块形成(CAS)组(84例),比较各组ox-LDL和AIP水平。结果与对照组相比,ACI组斑块检出率、易损斑块检出率明显增高(P0.01);ACI组血清ox-LDL与AIP明显升高(P0.01)。在ACI患者中,CAS组血清ox-LDL及AIP较IMT增厚组明显增高(P0.01);IMT增厚组血清ox-LDL及AIP高于IMT正常组(P0.01,P0.05)。Pearson检验结果显示,ox-LDL水平与IMT水平呈正相关(r=0.720,P0.01);AIP值与IMT水平呈正相关(r=0.717,P0.01);血清AIP与ox-LDL水平之间有相关性(r=0.655,P0.01)。结论 ox-LDL和AIP与颈动脉粥样硬化形成、发展及急性脑梗死发生有密切关系。两者联合测定能够更全面评估缺血性脑卒中发生的风险。     

Vertebral artery dominance,brainstem auditory evoked potential,and vertigo of vascular origin

Abstract

Objective: Vertebral artery dominance (VAD) is defined when there is a significant difference between the diameters of the vertebral arteries (VAs). VAD may be a risk factor for vertigo of vascular origin. The objectives of this study were: (1) to investigate changes of brainstem auditory evoked potential (BAEP) in patients with vertigo caused by VAD through magnetic resonance; and (2) to understand the possible mechanism(s) by which VAD triggers vertigo of vascular origin.

Methods: This prospective study involved 64 patients with vertigo, including 35 patients with VAD (VAD group) and 29 without VAD (non-VAD group) as detected by head magnetic resonance angiography. Age, sex, and other clinical histories were comparable in both groups. The degree of vertigo was graded and BAEP examination was performed in each patient. BAEP changes as well as their correlations of BAEP with the dominant VA and basilar artery (BA) were analyzed in both groups.

Results: The rate of abnormal BA shapes was 60% in the VAD group compared with 34·5% in the non-VAD group (Chi-square?=?4·135, P<0·05). The median BA curvature was higher in the VAD group than that in the non-VAD group, 3·67 and 1·73 mm, respectively (P<0·01). Peak latencies (I, III, and V) in the VAD group were longer than those in the non-VAD group (P<0·01), but the difference in the III did not reach statistical significance (t?=?1·916, P>0·05). Interpeak latencies (III–V and I–V) were longer in the VAD group than those in the non-VAD group (P<0·05); there was no significant difference in the interpeak latencies of I–III (P>0·05). The III–V/I–III ratios were higher in the VAD group than those in the non-VAD group. The vertigo severity level was significantly higher in the VAD group than that in the non-VAD group (3·2±1·0 versus 2·2±0·7). The vertigo severity level correlated with VAD and every major anomaly index of BAEP; its correlations with III–V/I–III were remarkably significant (r?=?0·617, P?=?0·013).

Conclusion: The incidence of abnormal BA shapes and abnormal BAEP, and the vertigo severity level were higher in VAD patients. Moreover, VAD was found to correlate with abnormal BAEP, suggesting that VAD contributed to vertigo of vascular origin.     

Atrophy/hypertrophy cell signaling in muscles of young athletes trained with vibrational-proprioceptive stimulation

Abstract

Objective: To compare the effects of isokinetic (ISO-K) and vibrational-proprioceptive (VIB) trainings on muscle mass and strength.

Methods: In 29 ISO-K- or VIB-trained young athletes we evaluated: force, muscle fiber morphometry, and gene expression of muscle atrophy/hypertrophy cell signaling.

Results: VIB training increased the maximal isometric unilateral leg extension force by 48·1%. ISO-K training improved the force by 24·8%. Both improvements were statistically significant (P0·01). The more functional effectiveness of the VIB training in comparison with the ISO-K training was shown by the statistical significance changes only in VIB group in: rate of force development in time segment 0-50 ms (P<0·001), squat jump (P<0·05) and 30-m acceleration running test (P<0·05). VIB training induced a highly significant increase of mean diameter of fast fiber (+9%, P<0·001), but not of slow muscle fibers (?3%, not significant). No neural cell adhesion molecule-positive (N-CAM⁺) and embryonic myosin heavy chain-positive (MHC-emb⁺) myofibers were detected. VIB induced a significant twofold increase (P<0·05) of the skeletal muscle isoform insulin-like growth factor-1 (IGF-1) Ec mRNA. Atrogin-1 and muscle ring finger-1 (MuRF-1) did not change, but myostatin was strongly downregulated after VIB training (P<0·001). Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) expression increased in post-training groups, but only in VIB reached statistical significance (+228%, P<0·05).

Discussion: We demonstrated that both trainings are effective and do not induce muscle damage. Only VIB-trained group showed statistical significance increase of hypertrophy cell signaling pathways (IGF-1Ec and PGC-1α upregulation, and myostatin downregulation) leading to hypertrophy of fast twitch muscle fibers.     

Cortical N-acetyl aspartate is a predictor of long-term clinical disability in multiple sclerosis

Abstract

Objective:

To evaluate the prognostic value of the cortical N-acetyl aspartate to creatine ratio (NAA/Cr) in early relapsing-remitting multiple sclerosis (RRMS).

Methods:

Sixteen patients with newly diagnosed RRMS were studied by serial MRI and MR spectroscopic imaging (MRSI) once every 6 months for 24 months. Clinical examinations, including the expanded disability status scale (EDSS), were performed at baseline, month 24, and at year 7.

Results:

Baseline cortical NAA/Cr correlated inversely with EDSS at month 24 (r = ?0·61, P < 0·05), and patients with EDSS ≧ 4 had a lower baseline cortical NAA/Cr compared to those with EDSS less than 4 (P < 0·05). Baseline cortical NAA/Cr also correlated inversely with EDSS at the 7-year follow-up (r = ?0·56, P < 0·05), and patients with EDSS ≧ 4 had a lower baseline cortical NAA/Cr compared to those with EDSS less than 4 (P < 0·05).

Baseline brain parenchymal fraction (BPF) correlated inversely with EDSS at month 24 (r = ?0·61, P < 0·05), but not with EDSS at year 7.

Discussion:

Cortical NAA/Cr in early RRMS correlated with clinical disability after 2 and 7 years and may be used as a predictor of long-term disease outcome.     

Bone marrow-derived mesenchymal stem cells expressing the bFGF transgene promote axon regeneration and functional recovery after spinal cord injury in rats

Abstract

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Objective: To investigate neurological effects of transplanting bone marrow-derived mesenchymal stem cells (BMSCs) transfected with the basic fibroblast growth factor (bFGF) gene in spinal cord-injured rats.

Methods: Ninety-six male adult Sprague-Dawley rats were randomized into four groups: (1) pcDNA3·1-bFGF group; (2) pcDNA3·1 group; (3) BMSCs group; and (4) vehicle control (DMEM) group. After the rat model of acute spinal cord injury (SCI) was established, 1×10⁶ BMSCs or cells transfected with pcDNA3·1-bFGF or pcDNA3·1 were injected into rats of groups 1-3. At days 1, 7, 14, and 21 after injection, the Basso-Beattie-Bresnahan (BBB) locomotor rating scale was used to evaluate recovery of motor function. Expression changes of bFGF, myelin basic protein (MBP), and NF200 were examined by immunohistochemistry.

Results: The BBB score of DMEM group was significantly lower than those of groups 1-3 (P<0·05), but the score of pcDNA3·1-bFGF group was significantly higher than that of BMSCs group or pcDNA3·1 group at day 14 or 21 after injection (P<0·01). The number of bFGF-positive neurons in rats of pcDNA3·1-bFGF group was significantly higher than those of groups 1-3 at any time point (P<0·05). The optical density values of NF200-positive neurons and MBP-positive MBP axons in rats of pcDNA3·1-bFGF group were significantly higher than those of groups 1-3 at day 7 or 14 after injection (P<0·05).

Conclusions: bFGF gene-modified BMSCs not only effectively promoted axonal outgrowth but also enhanced recovery of neurological function after SCI in rats, and may be a good candidate to evaluate gene therapy of SCI in man.     

Single parenchymal brain cysticercus: relationship between age of patients and evolutive stage of parasites

Abstract

Background: A recent hypothesis suggested that in many cases cysticercal granulomas represent recently established Taenia solium metacestodes rapidly destroyed by the host’s immune system. Here, we attempted to determine whether patients with cysticercal granulomas are younger than those with other forms of parenchymal brain cysticercosis.

Methods: Series of 185 patients with single parenchymal brain cysticercus, classified according to the stage of the parasite at the moment of diagnosis in cysts without inflammation, cysts with inflammation, granular lesions, and calcifications. We correlated the age of the patients with the parasite evolutive stage.

Results: Patients with cysticercus granulomas were significantly younger than those with vesicular cysts (17·7±12·9 versus 36·8±15·1 years, P<0·005) or calcifications (17·7±12·9 versus 40·8±19·7 years, P<0·0001). There was also a non-significant trend for patients with granulomas to be younger than those with coloidal cysts (17·7±12·9 versus 26·7±15·6 years, P?=?0·367).

Conclusions: Results from this study argued against the classical hypothesis that granulomas are the end result from long-established vesicular cysts destroyed by the host’s immune system. Vesicular (viable) cysticerci must be treated with cysticidal drugs as it is unlikely that they will be spontaneously destroyed.     

Anticonvulsant activity of the ethanolic extract of Punica granatum L. seed

Abstract

Objective:

Various morphological parts of pomegranate (Punica granatum L.) have extensively been used in the folk medicine to treat an array of human ailments. The aim of the present study is to demonstrate the anticonvulsant potential of the ethanolic extract of P. granatum L. seed in chemoconvulsant-induced seizures in mice.

Method:

The anticonvulsant activity of the ethanolic extract was investigated in strychnine (STR)-induced and pentylenetetrazole (PTZ)-induced seizure models in mice. Diazepam was used as reference anticonvulsant drug. Ethanolic extract (150, 300, and 600 mg/kg per os, p.o.), diazepam (1 mg/kg intraperitoneally, i.p.), and distilled water (10 ml/kg, i.p.) were administered before induction of seizures by PTZ (60 mg/kg, i.p.) or STR (2·5 mg/kg, i.p.). The latent time before the onset of convulsions, the duration of convulsions, the percentage of seizure protection, and mortality rate were recorded.

Results:

The seed ethanolic extract did not show any toxicity and did not protect the animals against seizures but demonstrated a significant increase in seizure latency at 300 and 600 mg/kg in both STR and PTZ seizure models (P < 0·001). It also showed a significant reduction in seizure duration at 300 mg/kg (P < 0·05) and 600 mg/kg (P < 0·001) in the STR seizure model and 600 mg/kg (P < 0·01) in the PTZ seizure model compared with the control group.

Conclusion:

Ethanol extract has dose-dependent anticonvulsant activity against STR- and PTZ-induced seizures. This activity might be due to its saponins, flavonoids, triterpenes, and alkaloids ingredients.     

The role of high-sensitivity C-reactive protein levels in functional outcomes in patients with large-artery atherosclerosis and small-artery occlusion

Background: High-sensitivity C-reactive protein (hs-CRP) is an inflammatory marker that is associated with the outcomes of ischemic stroke. However, the role of hs-CRP levels in the functional outcomes after large-artery atherosclerosis (LAA) and small-artery occlusion (SAO) is poorly understood.

Methods: We recruited 1299 patients diagnosed as having LAA and 453 patients diagnosed as having SAO from 1 January 2009 to 31 December 2013, from the Department of Neurology, Tianjin Huanhu Hospital. The hs-CRP values were classified into two groups based on the significant threshold of hs-CRP level in the receiver operating characteristic (ROC) curve (≥3.215 mg/L in LAA and ≥1.72 mg/L in SAO). We examined the relationship between hs-CRP levels on admission and the modified Rankin scale scores using univariate and multivariate analyses.

Results: Patients with LAA had a higher hs-CRP mean value than patients with SAO (7.69 vs. 4.12 mg/L). The ROC curve showed a significant hs-CRP threshold value at 3.215 mg/L in patients with LAA and at 1.72 mg/L in patients with SAO. Logistic regression analyses showed that patients with LAA with hs-CRP levels ≥3.215 mg/L had a significant risk of poor outcome compared with those with hs-CRP levels <3.215 mg/L (odds ratio [OR], 1.545; 95% confidence interval [CI], 1.155–2.067; p = 0.003). Meanwhile, patients with SAO with hs-CRP levels ≥1.72 mg/L had a significant risk of poor outcome compared with those with hs-CRP levels <1.72 mg/L (OR, 1.97; 95% CI, 1.02–3.801; p = 0.043). Moreover, combining hs-CRP with National Institutes of Health Stroke Scale could predict outcome with satisfying clinical accuracy both in LAA and SAO subtype.

Conclusions: Patients with LAA with hs-CRP levels <3.215 mg/L and patients with SAO with hs-CRP levels <1.72 mg/L on admission had favorable functional outcomes at 3 months after stroke onset.     

A simple clinical and MRI scale to predict good outcome in t-PA patients

Abstract

Background and purpose: The frequency of good outcome at 3 months after tissue plasminogen activator (t-PA) therapy is ～35%. The present study aimed to devise a simple scale to predict good outcome using clinical factors and magnetic resonance imaging (MRI) findings before and immediately after t-PA infusion.

Methods: Consecutive patients with acute ischemic stroke treated with t-PA within 3 hours of stroke onset were studied prospectively. We assessed clinical factors independently associated with good outcome [modified Rankin scale (mRS): 0-1] at 3 months after t-PA therapy. We created a simple scale to predict good outcome in t-PA patients using factors selected by multivariate logistic regression analysis.

Results: Subjects comprised 105 patients (69 men; median age, 74 years). Multivariate logistic regression analysis revealed the following independent factors associated with good outcome: baseline National Institutes of Health Stroke Scale (NIHSS) <11 [odds ratio (OR), 13·64; 95% confidence interval (CI), 3·588-51·822; P = 0·0001], glucose <150 mg/dl (OR, 3·76; 95%CI, 1·014-13·963; P = 0·0475), and early recanalization within 1 hour after t-PA infusion (OR, 5·28; 95%CI, 1·179-23·656; P = 0·0296). Those three variables were selected for use in the good outcome scale, with NIHSS <11 as 2 points, glucose <150 mg/dl as 1 point, and early recanalization as 1 point. Frequencies of patients with good outcome for each score were as follows: score 0, 0·0%; score 1, 7·1%; score 2, 43·5%; score 3, 65·4%; and score 4, 71·4%. The C statistic for the score was 0·849 (95%CI, 0·776-0·922).

Conclusion: A simple clinical and MRI scale can predict good outcome in t-PA patients.     

Module modified acute physiology and chronic health evaluation II: predicting the mortality of neuro-critical disease

Abstract

Objectives:

This study aimed to conduct and assess a module modified acute physiology and chronic health evaluation (MM-APACHE) II model, based on disease categories modified-acute physiology and chronic health evaluation (DCM-APACHE) II model, in predicting mortality more accurately in neuro-intensive care units (N-ICUs).

Methods:

In total, 1686 patients entered into this prospective study. Acute physiology and chronic health evaluation (APACHE) II scores of all patients on admission and worst 24-, 48-, 72-hour scores were obtained. Neurological diagnosis on admission was classified into five categories: cerebral infarction, intracranial hemorrhage, neurological infection, spinal neuromuscular (SNM) disease, and other neurological diseases. The APACHE II scores of cerebral infarction, intracranial hemorrhage, and neurological infection patients were used for building the MM-APACHE II model.

Results:

There were 1386 cases for cerebral infarction disease, intracranial hemorrhage disease, and neurological infection disease. The logistic linear regression showed that 72-hour APACHE II score (Wals = 173·04, P < 0·001) and disease classification (Wals = 12·51, P = 0·02) were of importance in forecasting hospital mortality. Module modified acute physiology and chronic health evaluation II model, built on the variables of the 72-hour APACHE II score and disease category, had good discrimination (area under the receiver operating characteristic curve (AU-ROC = 0·830)) and calibration (χ2 = 12·518, P = 0·20), and was better than the Knaus APACHE II model (AU-ROC = 0·778).

Discussion:

The APACHE II severity of disease classification system cannot provide accurate prognosis for all kinds of the diseases. A MM-APACHE II model can accurately predict hospital mortality for cerebral infarction, intracranial hemorrhage, and neurologic infection patients in N-ICU.     

Cognitive impairment and antiphospholipid syndrome: is paradoxical embolism the rule?

Abstract

Objective: Although cognitive decline (CD) is described in antiphospholipid syndrome (APS), its physiopathology is unknown. Paradoxical embolization (PE) is related to CD in Alzheimer disease. The objective of this study was to determine whether PE plays a role in CD in APS patients through a significant right-to-left shunt (sRLS).

Methods: A total of 27 patients diagnosed with APS without a history of stroke were tested for the presence of an sRLS using a contrast-enhanced transcranial Doppler (cTCD) ultrasound. Cognitive decline was assessed using the mini mental state examination (MMSE), the Montreal cognitive assessment (MoCA), and a battery of neuropsychological tests.

Results: Of the 27 patients, 19 (70%) had a non-sRLS condition (≤10 high-intensity transient signs [HITS] on cTCD), and 8 (30%) had an sRLS. Patients with more than 10 years of scholarship performed significantly better on both the MMSE (P = 0·048) and MoCA (P = 0·03). Individuals of the non-sRLS group with more than 10 years of scholarship had better performances on the five-point test (FPT) when compared with the sRLS group (P = 0·01).

Conclusions: Patients without sRLS and with more years of education exhibited a better performance in cognitive tests than sRLS patients.     

Factors predisposing to small lacunar versus large non-lacunar cerebral infarcts: is left ventricular mass involved?

Abstract

Objectives:

To find some specific determinants of lacunar strokes (LS), this study compared LS and non-LS patients using the size and location of cerebral lesions as discriminant between the two groups.

Methods:

The main cardiovascular risk factors and some echocardiographic parameters were assessed in 225 ischemic stroke patients aged 75·1±11·4 (SD) years, including 101 patients with symptoms and lesions of lacunar type (deep hypodensities with diameter ≤ 1·5 cm) and 124 patients with non-lacunar lesions.

Results:

LS patients tended to be younger and had a higher prevalence of smokers than non-LS patients. In a subgroup undergoing echocardiogram, those with LS had a higher left ventricular mass index (LVMI) than non-LS patients (141·6±44·9 vs. 115·1±31·8 g/m², P = 0·005). The prevalence of hypertension, diabetes, and carotid stenoses > 50% was similar in the two groups. In multivariable analysis the ever-smoker status (OR = 1·9, P = 0·02), atrial fibrillation (inverse association, OR = 0·5, P = 0·03), LVMI ≧ 130 g/m² (OR = 6·6, P = 0·001), and age ≤ 72 years (OR = 5·9, P = 0·003) remained independently associated with LS.

Conclusions:

The patients with lacunar cerebral lesions had a greater left ventricular mass than those with non-lacunar lesions, while blood pressure values did not differ. Lacunar lesions were also associated with smoking and a younger age.     

Influence of butyphthalide combined with urinary kallikrein in ACI treatment on neuro-cytokines and vascular endothelial function and its clinical effect

Abstract

Objective: To study the influence of butyphthalide combined with urinary kallikrein in acute cerebral infarction (ACI) treatment on neuro-cytokines and indicators of vascular endothelial function, observe the curative effect and adverse effects, and discuss its safety and feasibility.

Method: 110 ACI patients were chosen as the objects, and classified into observation group (55 cases) and control group (55 cases) according to the method of random number table. Butyphthalide injection combined with urinary kallikrein was adopted for the observation group based on conventional treatment, while cinepazide maleate injection combined with alprostadil injection was applied for the control group based on conventional treatment. The following indicators of both groups were compared before and after treatment: neurotrophic factor (NTF), nerve growth factor (NGF), neuron specific enolase (NSE); content of CXC chemotactic factor ligand 16 (CXCL16), soluble CD ligand (CD40L), Fibulin-5 and high mobility group box B1 (HMGB1); the content of indicators of vascular endothelial function including plasma endothelin ?1 (ET-1) and no therapeutic effects and adverse effects were recorded.

Results: NSE of both groups after treatment decreased obviously, and the content of NTF and NGF increased obviously. NSE content of observation group was lower than that of control group. NTF content and NGF content of observation group were higher than those of control group. The differences had statistical significance (p?<?0.05). The levels of CXCL16, CD40L, Fibulin-5 and HMGB1 declined obviously, compared with pre-treatment, and the levels of observation groups were significantly lower than those of control grip. The differences had statistical significance (p?<?0.05). ET-1 level rose significantly after treatment, and NO level declined obviously after treatment. ET-1 level of observation group was significantly higher than that of control group, and NO level of observation group was significantly lower than that of control group. The difference had statistical significance (p?<?0.05). Clinical effect of observation group was significantly higher than that of control group. The difference had statistical significance (p?<?0.05). The comparison difference of both groups in the occurrence rate of adverse effects had no statistical significance (p?>?0.05).

Conclusion: The application of butyphthalide combined with urinary kallikrein in ACI treatment can effectively inhibit secretion and release of neuro-cytokines, and improve patients’ vascular endothelial function, with significant treatment effect and high safety. Therefore, it deserves to be promoted clinically.     

Lower levels of plasma adiponectin and endothelial progenitor cells are associated with large artery atherosclerotic stroke

Background: Both adiponectin and endothelial progenitor cells (EPCs) have been proposed recently with anti-atherosclerosis effects. However, their impacts on vascular outcomes in patients with large artery atherosclerosis (LAA) are unclear. This study aimed to investigate the relationship between adiponectin, EPCs and stroke with a case-control design. Methods: The study cohort included 127 patients (61.3 ± 11.0 years; 73.2% men) with LAA stroke and 58 control subjects (60.9 ± 9.2 years; 70.7% men) referred for adiponectin and EPCs levels testing. We collected demographic, clinical, angiographical features, and laboratory data. Influence of adiponectin and EPCs levels on cerebral atherosclerosis and LAA stroke was analyzed with regression models. Results: The levels of adiponectin and EPCs in atherosclerotic stroke patients were significantly lower compared with matched controls (p < 0.05). Logistic regression analysis identified that reduced levels of adiponectin and EPCs were closely correlated with cerebral atherosclerosis and LAA stroke. The associations remained significant after adjustment for age, sex and other confounders. Additionally, partial correlation analysis revealed a significant positive association between adiponectin and three subpopulations of EPCs levels (CD34⁺CD133⁺CD309⁺cells: r = 0.510, p = 0.001; CD34⁺ CD133^?CD309⁺cells: r = 0.262, p = 0.004; CD34^?CD133⁺CD309⁺cells: r = 0.348, p < 0.001). Conclusions: Adiponectin is positively correlated with EPCs levels, and both of them are independently associated with LAA stroke.     

HbA1c is associated with increased all-cause mortality in the first year after acute ischemic stroke

Abstract

Objectives:

To assess the association between baseline HbA1c and the poor outcomes within 1 year after acute ischemic stroke.

Methods:

Acute ischemic stroke patients with HbA1c values at baseline (n = 2186) were selected from the abnormal glucose regulation in patients with acute stroke across China study (ACROSS). Logistic regressions were performed to assess the association between HbA1c quartiles (<5·5% [37 mmol/mol], 5·5 to <6·1% [37 to <43 mmol/mol], 6·1 to <7·2% [43 to <55 mmol/mol], and ≥7·2% [≥55 mmol/mol]) and the poor outcomes within 1 year. Poor outcomes were defined as all-cause mortality (modified Rankin scale [mRS] = 6) and poor functional outcome (mRS [2–6]).

Results:

The risk for all-cause mortality was significantly increased in HbA1c level >5·5% [>37 mmol/mol] when compared to HbA1c quartile <5·5% [<37 mmol/mol] and dramatically increased to two to three times higher in the highest HbA1c quartile ≥7·2% [>55 mmol/mol] (1-year all-cause mortality model, odds ratios [ORs] were 1·07, 1·01, and 2·45, P for trend 0·009). After the further analysis with previous diabetes mellitus (DM) and post-stroke insulin use stratified, the risk of mortality was increased across the HbA1c levels (P for trend 0·020) and dramatically augmented in HbA1c ≥7·2% [>55 mmol/mol] in patients without a history of DM and without post-stroke insulin use.

Discussion:

Elevated HbA1c (from 5·5% [37 mmol/mol]) presenting pre-stroke glycemia status has a significant trend in increasing the risk of 1-year all-cause mortality. HbA1c ≥7·2% (>55 mmol/mol) is an independent risk predictor for 1-year all-cause mortality after acute first-ever ischemic stroke. Such an association might be altered by glycometabolism status.