Acute hyperglycemia adversely affects stroke outcome: a magnetic resonance imaging and spectroscopy study

Controversy exists whether acute hyperglycemia is causally associated with worse stroke outcome or simply reflects a more severe stroke. In reversible ischemia models, hyperglycemia is associated with lactic acidosis and conversion of penumbral tissue to infarction. However, the relationship between hyperglycemia, lactic acidosis, and stroke outcome has not been explored in humans. Sixty-three acute stroke patients were prospectively evaluated with serial diffusion-weighted and perfusion-weighted magnetic resonance imaging and acute blood glucose measurements. Patients with hypoperfused at-risk tissue were identified by acute perfusion-diffusion lesion mismatch. As a substudy, acute and subacute magnetic resonance spectroscopy was performed in the 33 most recent patients to assess the relationship between acute blood glucose and lactate production in the ischemic region. In 40 of 63 patients with acute perfusion-diffusion mismatch, acute hyperglycemia was correlated with reduced salvage of mismatch tissue from infarction, greater final infarct size, and worse functional outcome. These correlations were independent of baseline stroke severity, lesion size, and diabetic status. Furthermore, higher acute blood glucose in patients with perfusion-diffusion mismatch was associated with greater acute-subacute lactate production, which, in turn, was independently associated with reduced salvage of mismatch tissue. In contrast, acute blood glucose levels in nonmismatch patients did not independently correlate with outcome measures, nor was there any acute-subacute increase in lactate in this group. Acute hyperglycemia increases brain lactate production and facilitates conversion of hypoperfused at-risk tissue into infarction, which may adversely affect stroke outcome. These findings support the need for randomized controlled trials of aggressive glycemic control in acute stroke.     

Hemostatic markers in ischemic stroke of undetermined etiology

To evaluate the role of the coagulation and fibrinolysis abnormalities in the pathogenesis of ischemic stroke of undetermined etiology, we assayed plasma concentration of fibrinopeptide-A and thrombin-antithrombin III complex, both sensitive markers for thrombin activation and fibrin formation, and D-dimer, a marker of plasmin activity and fibrinolysis. Hemostatic markers were measured in 32 patients with acute stroke and 20 patients with chronic stroke, and compared with 21 normal subjects. Fibrinopeptide-A and thrombin-antithrombin III complex levels were not elevated significantly, whereas the D-dimer level was markedly raised in acute (p<0.001) and chronic (p<0.05) phases of ischemic stroke in comparison with the control group. Prolonged elevation of D-dimer concentration suggests that hemostatic abnormalities have a primary role in the pathogenesis of ischemic stroke. The measurement of D-dimer concentration may help to better decide the indications for therapy of the patients with ischemic stroke of undetermined etiology.     

Hemorheological changes dependent on the time from the onset of ischemic stroke

This work aimed at estimation and comparison of chosen rheological parameters of blood in two group of patients in acute and remote stroke phase. The analysis included the values of shear stress, plasma viscosity, relative blood viscosity, hematocrit value and the parameters of rheological Quemada model of blood flow. The main two groups (30 persons each) consisted of patients after cerebral ischemic episode, remaining under permanent medical control, the first one in the acute and the second in the remote phase. The reference group (20 persons) included the patients who never suffered from any circulatory system disorders and who did not take any drugs affecting the hemorheological parameters. The results suggest that after a distinct increase of most of the hemorheological parameters in the acute stroke phase, a gradual improvement was observed in the remote phase. Since in the latter group the plasma viscosity remained on elevated level, we suggest a creation of a specific feedback mechanism leading to a decrease of the blood viscosity and thus better perfusion of brain. The analysis of Quemada model parameters indicates that the decrease of blood viscosity may result from the increased red cell deformability.     

Aortic atherosclerosis and stroke.

Methods: Studies using transesophageal echocardiography (TEE) suggest aortic atherosclerosis may be a risk factor for stroke, particularly stroke of undetermined mechanism, but controls in prior studies were not balanced for vascular risk factors. We used TEE to evaluate aortic atherosclerosis in 60 patients with stroke compared with a high-risk control population of 46 subjects. We also examined the possible association of plasma viscosity and fibrinogen levels to aortic atherosclerosis. Results: The mean maximal plaque thickness (MMPT) was similar for the control (2.8 +/- 3.6 mm) and the stroke group (3.3 +/- 3.5 mm), but varied with stroke mechanism. The MMPT was similar in stroke of undetermined and atherosclerotic mechanism [3.5 +/- 4 mm (n = 25) and 4.2 +/- 4.3 mm (n = 16), respectively], significantly greater than in stroke of other mechanisms (1.7 +/- 1.2 mm, P < .05, n = 19). Patients with stroke of undetermined mechanism were four times more likely (95% confidence interval [CI] 1.2-12) to have plaques >/=5 mm compared with controls. Ulcerated plaque was associated with plaque thickness (P < .001) and plasma viscosity (P < .001). Conclusions: Aortic atherosclerosis is associated with stroke of undetermined cause suggesting atherosclerosis is a cause of stroke of undetermined etiology. Plaque ulceration was associated with the thickness of aortic plaque and plasma viscosity.     

Increased levels of elastin-derived peptides in cerebrospinal fluid of patients with lacunar stroke

OBJECTIVE: To investigate whether elastin-derived peptides (EDP) are detectable in the cerebrospinal fluid (CSF) of healthy controls and of patients with acute brain ischemia and if so to assess possible trends in EDP levels in different groups of ischemic stroke patients (small-vessel disease vs. other ischemic strokes; first-ever vs. recurrent stroke). PATIENTS AND METHODS: Levels of EDP were determined by ELISA in blood sera and CSF of 80 patients with acute ischemic stroke (mean age 61.5+/-10.8; age range 47-70; 22 women) and in 15 healthy age- and sex-matched controls (mean age 57.3+/-13.4; age range 50-65). The patients were divided into a group with first ever lacunar stroke (27); first ever non-lacunar ischemic stroke (27) and recurrent stroke (26). EDP were measured early (mean 7 days, range 1-15) after stroke onset. RESULTS: Serum EDP levels were mildly higher in recurrent strokes as compared to first ever lacunar lesion and controls. However, in the CSF the concentrations of EDP in stroke patients were strongly elevated (from 2 up to 30 times depending on subgroup) as compared with healthy subjects. The highest level of EDP in CSF and in the serum was found in recurrent strokes. Subgroup analysis revealed a trend for significantly higher EDP concentrations in CSF in lacunar and recurrent stroke as compared with non-lacunar. CONCLUSIONS: This study is the first application of elastin peptide measurement to human CSF and stroke patients. The increased levels of EDP were detected in CSF of patients with lacunar and recurrent strokes.     

TOAST分型的急性缺血性脑卒中患者血糖变异性及其和预后的关系研究

目的 研究TOAST分型的急性缺血性脑卒中患者血糖变异性及其和预后的关系。方法 选取本院2014年2月～2015年2月接诊的112例急性缺血性脑卒中患者作为研究对象,据血糖监测将其分为血糖变异组和非血糖变异组,对所有患者的TOAST分型各亚型血糖变异性、TOAST分型各亚型血糖变异性两两比较情况、NIHSS评分以及Barthel指数、患者预后的多因素进行分析。结果 2组患者的年龄、糖尿病史以及NIHSS评分患者例数具有明显差异(P<0.05)。血糖变异组患者的LAA患者例数明显多于非血糖变异组(P<0.05),LAA组血糖变异性与SAO组和CE组比较有明显差异(P<0.05),而SAO组和CE组的血糖变异性没有明显差异(P>0.05)。入院半个月后血糖变异组患者的NIHSS评分以及Barthel指数没有明显差异(P>0.05),而非血糖变异组患者的NIHSS评分以及Barthel指数均有明显的变化,且2组患者在入院半个月后的NIHSS评分以及Barthel指数有明显差异(P<0.05)。年龄、NIHSS评分以及血糖变异等因素与急性缺血性脑卒中患者预后有关。结论 年龄、糖尿病史、LAA患者等均是影响患者血糖变异性的相关因素,且血糖变异性对急性缺血性脑卒中患者的预后具有一定的影响,是其独立的危险因素,即血糖变异性异常的急性缺血性脑卒中患者的恢复较缓慢,预后情况不良。     

Migrainous stroke

Twenty-two patients with acute migraine-associated stroke were prospectively evaluated; 91% were female, and 23% had a prior history of presumed migrainous stroke. The incidences of major stroke risk factors and mitral valve prolapse were no higher for the study group than for the general population of similar age. Computed tomography, magnetic resonance imaging, or radionucleotide scanning of the brain was performed on all patients, and demonstrated ischemic or hemorrhagic infarction in 12 (55%). Cerebral arteriography revealed abnormalities related to the acute stroke in five (42%) of 12 cases overall, and in four (67%) of six studies performed within 72 hours of stroke onset; one patient (8%) suffered significant complications from arteriography. Although a variety of processes, alone or in combination, may contribute to migrainous stroke, extracranial and/or intracranial vasospasm appears to play a major role in at least some cases.     

Recent advances in stroke management

Major advances in stroke treatment and prevention have occurred over the last several years. Recent studies have documented that appropriate modification of stroke risk factors can lead to a substantial reduction in stroke incidence. In addition, a variety of new risk factors, such as elevated plasma homocysteine levels, antiphospholipid antibodies, and specific genetic factors, are being recognized. The most significant advance in acute stroke therapy is the use of intravenous tissue plasminogen activator (t-PA) for treatment of patients with ischemic stroke within 3 hours of symptom onset. T-PA is currently the only stroke treatment approved by the Federal Drug Administration. There continues to be uncertainty and misunderstanding regarding the risks and benefits of this therapy. A variety of neuroprotective agents have been highly successful for reducing ischemic brain injury in animal stroke models. Recent clinical trials with these agents, however, have not produced beneficial effects in humans. Newer neuroprotective agents with more favorable safety profiles and improvements in clinical trial design may lead to therapeutic successes in the near future. It is apparent that both thrombolytic and neuroprotective treatments for acute stroke must be administered very rapidly after stroke onset. Therefore, acute stroke teams are being developed to facilitate rapid diagnostic evaluation and treatment of stroke patients.     

Higher leukocyte count is associated with higher risk of 3-year mortality in non-diabetic patients with first-ever ischemic stroke

Leukocyte count predicted the risk of first-time myocardial infarction and ischemic stroke. The aim of this study was to determine the role of elevated leukocyte count in non-diabetic patients admitted for acute first-ever ischemic stroke on clinical presentation and 3-year mortality. We studied 462 patients with acute first-ever ischemic stroke without diabetes mellitus or active infection at admission. Patients were classified into 2 groups according to their leukocyte count. A white blood cell (WBC) count ≥ 10,000/μL was defined as an elevated leukocyte count, otherwise as normal. Clinical presentation, risk factors for stroke, laboratory data, co-morbidities, and outcomes were recorded. 64 patients (13.9%) had elevated leukocytes. Multivariate logistic regression showed that an elevated platelet count was positively associated with the elevated leukocyte count, while a low serum sodium level was negatively associated with an elevated leukocyte count (P=0.008, P=0.003, respectively). An elevated leukocyte count was associated with a higher risk of a stroke in evolution (P=0.021). Multivariate Cox regression analysis revealed that an elevated leukocyte count is a significant predictor of 3-year mortality [P=0.010, HR=3.26 (1.33-7.98)]. In conclusion, higher leukocyte counts during the acute stroke stage are associated with increased risk of 3-year mortality in patients with acute, first-ever ischemic stroke.     

前列腺癌相关脑梗死的发病特点

目的 探讨前列腺癌相关脑梗死的发病特点。方法 收集2003年1月-2015年12月在广西医科大学第一附属院住院治疗的前列腺癌合并脑梗死患者的临床表现、实验室及器械检查等资料。结果 本研究共筛查前列腺癌患者2 584例,其中符合前列腺癌合并脑梗死的患者共有34例(1.31%),平均年龄(61.60±6.28)岁。入选的患者中无脑卒中危险因素21例(61.76%)。血液学检查发现D-二聚体水平升高22例(64.71%),总前列腺特异性抗原(Total prostate specific antigen,T-PSA)水平异常升高(>100 ng/mL )19例(55.88%),头颅MRI显示脑内单一梗死灶8例(23.52%),出现累及多个动脉供血区的2个或2个以上梗死灶26例(76.47%),脑梗死发生30 d多数患者预后不良,其中4例(11.77%)死亡。结论 前列腺癌相关脑梗死的患者以缺少常见的脑卒中危险因素、血清D-二聚体水平升高以及T-PSA异常升高、一次发病出现累及多血管分布区的多发性梗死灶以及预后不良等为特点,其发生机制可能与患者血液的凝固性升高有关。     

Investigation of risk factors in children with arterial ischemic stroke

We present data on the known risk factors encountered in children presenting with a first arterial ischemic stroke to a single tertiary center over 22 years. Two hundred twelve patients (54% male; median age, 5 years) were identified. One hundred fifteen (54%) were previously healthy. Cerebral arterial imaging was undertaken in 185 patients (87%) and was abnormal in 79%. Of 104 previously healthy patients investigated with echocardiography, only 8 had abnormal studies. Genetic or acquired conditions causing thrombophilia were rare. Forty percent of patients were anemic, and 21% either had elevated total plasma homocysteine or were homozygous for the t-MTHFR mutation. Trauma and previous varicella zoster infection were significantly more common in the previously healthy group. There was a significant association between cerebral arterial abnormalities and systolic blood pressure greater than 90th percentile and a trend for an association with varicella within the previous year. Clinical history and examination usually identify underlying risk factors and precipitating triggers for arterial ischemic stroke in childhood. Cerebral arterial imaging is usually abnormal, but echocardiography and prothrombotic screening are commonly negative.     

A pilot study regarding knowledge of stroke risk factors in an urban community

Background The premise of the "brain attack" concept is that early intervention may salvage ischemic neurons. Early intervention depends on adequate knowledge of stroke so that patients seek urgent medical attention. Objective: To assess knowledge of stroke risk factors and warning signs in an urban, predominantly black community. Methods: A 20-item questionnaire was administered to two patient groups. Group 1 had a diagnosis of first-ever stroke or transient ischemic attack (TIA). Group 2 (controls) was without a history of cerebral ischemia. Results: Thirty patients in group 1 answered 57.5% of the questions correctly. Thirty patients in group 2 answered 63.1% of the questions correctly (P=.15). Patients showed misperceptions regarding the warning signs of a stroke and were unfamiliar, with the concept of a TIA. Conclusions: Although preliminary because of a limited sample size, the results from our urban medical center suggest that knowledge of stroke is deficient among high-risk individuals who developed cerebral or retinal ischemia. This would mean that opportunities for effective prevention and treatment of stroke are being missed in minority patients. Recruitment of patients for acute stroke trials will also face impediments in urban communities unless a massive educational effort is undertaken.     

Genetic variants of platelet glycoprotein receptors and risk of stroke in young women

BACKGROUND AND PURPOSE: A number of studies have examined the relationship between genetic platelet glycoprotein variants and early-onset atherothrombotic disease, particularly acute myocardial infarction. Data on the association of these genetic susceptibility markers with ischemic stroke are more limited, and their role in hemorrhagic stroke has not been previously examined. METHODS: We performed genotype analysis for 5 common diallelic platelet glycoprotein polymorphisms in a population-based study of 78 white women aged <45 years with arterial stroke (36 ischemic cases and 42 hemorrhagic cases) and 346 demographically similar control subjects. RESULTS: The 807T variant of glycoprotein Ia was associated with a 2-fold increased risk of ischemic stroke (age-adjusted odds ratio [OR]=2.24; 95% CI=0.99 to 5.06). The Met(145) allele of glycoprotein Ibalpha was associated with a trend toward an increased risk of ischemic stroke that was more pronounced in the homozygous state (OR=10.36), but the CI is extremely wide because of the small numbers of subjects (95% CI=1.43 to 79.34). Homozygosity for the Ser(843) allele of the glycoprotein IIb was associated with an approximately 5-fold increased risk of ischemic stroke among subgroups of women who carried a diagnosis of hypertension or diabetes (OR=4.51; 95% CI=1.01 to 20.13) or had elevated plasma homocysteine levels (OR=5.94; 95% CI=1.53 to 23.05). The genotype distributions for all 5 platelet glycoprotein polymorphisms were similar among hemorrhagic stroke cases and controls. CONCLUSIONS: Several inherited platelet glycoprotein variants may be associated with an increased risk of ischemic stroke in young women. These associations seemed to be confined to women with other cardiovascular risk factors. Additional studies involving larger numbers of subjects are needed to confirm these preliminary findings.     

Increased plasma glutamate in stroke patients might be linked to altered platelet release and uptake.

Experimental studies have shown the role of excitotoxicity in the pathogenesis of ischemic brain lesions, and glutamate levels have been found to be elevated in CSF and plasma from patients, early after stroke. In this study, we investigated whether platelets could be involved in the mechanism of altered plasma glutamate levels after stroke. Forty four patients, from 6 hours to 9 months after ischemic stroke, 15 age-related healthy controls and 15 controls with stroke risk factors or previous transient ischemic attack were enrolled. Glutamate plasma levels, platelet glutamate release after aggregation and platelet glutamate uptake were assessed. Plasma glutamate levels were increased up to 15 days after the ischemic event in stroke patients, and the levels at day 3 were inversely correlated with the neurologic improvement between day 3 and 15. Ex vivo platelet glutamate release was decreased by 70% in stroke patients, suggesting previous in vivo platelet activation. Moreover, platelet glutamate uptake in these patients was decreased by 75% up to 15 days and was still reduced 90 days after stroke. Our data show a prolonged increase of glutamate in plasma after stroke, which might presumably be linked to altered platelet functions, such as excessive release of the amino acid or impaired uptake.     

Microalbuminuria in ischemic stroke.

OBJECTIVES: To determine (1) the incidence of microalbuminuria in patients with recent ischemic stroke, (2) its relationship to risk factors for stroke, (3) its prevalence in the major subtypes of ischemic stroke, and (4) its potential for identifying patients at increased risk for recurrent stroke, myocardial infarction, or vascular death. DESIGN: Prospective case-control study. SETTING: Outpatient clinics at the medical centers affiliated with the Department of Veterans Affairs and Oregon Health Sciences University in Portland, Ore. PATIENTS: A total of 186 older men and women (median age, 65 years) who were enrolled in a prospective study of risk factors for recurrent stroke, including 97 patients with recent (6-8 weeks) ischemic stroke, 51 with similar clinical risk factors for stroke, including 24 with a history of remote stroke or transient ischemic attack, and 38 community-dwelling volunteers. RESULTS: Microalbuminuria was 3 times more prevalent in patients with recent stroke (29%) than in those with clinical risk factors for stroke (10%), and was undetectable in healthy elderly controls (P<.001). The presence of microalbuminuria in recent stroke as well as in the combined recent and remote stroke or transient ischemic attack group (n = 121) was predicted by diabetes (odds ratio [OR], 8.4; 95% confidence interval [CI], 2.6-27.0; P<.001; serum albumin levels (OR, 0.12; 95% CI, 0.03-0.50; P<.005); age (OR, 1.1; 95% CI, 1.0-1.2; P<.01), and ischemic heart disease (OR, 3.0; 95% CI, 1.0-9.1; P<.05). Among patients with recent stroke the prevalence of microalbuminuria did not differ among major ischemic stroke subtypes, ie, atheroembolic, 23%; cardioembolic, 30%; and lacunar, 33%. During a mean +/- SD of 1.5 +/- 0.9 years of follow-up, 20% of patients with recent stroke, 14% with risk factors for stroke, and 0% of healthy elderly volunteers had vascular end points (P<.004), with events being as frequent in patients with microalbuminuria (32%) as in patients with macroalbuminuria (33%). After controlling for major clinical risk factors, microalbuminuria remained an independently significant predictor of future stroke in the combined recent stroke and remote stroke or transient ischemic attack group (Cox proportional hazard ratio, 4.9; 95% CI, 1.4-17.6; P<.01). CONCLUSIONS: Microalbuminuria is a common finding in patients with cerebrovascular disease and is associated with increased risk for stroke even after correction for the presence of confounding clinical risk factors. These data suggest that microalbuminuria merits further examination as a potentially inexpensive and easily measured marker of increased risk for stroke.     

A case control study of some hematological and biochemical variables in acute stroke and their prognostic value

Hematocrit, total white cell and platelet counts, plasma urea and creatinine concentrations were estimated in 291 patients (mean age 70 +/- 12 years) admitted consecutively over a 6-month period to a district general hospital with acute stroke. Urinary albumin/creatinine ratio was also determined in a subgroup of patients during a follow-up visit 3 months after ictus. Results were compared with those from age- and sex-matched community controls. Total white cell count was elevated in all types of stroke compared with values from control subjects. Platelet count, plasma urea and creatinine concentrations were higher and the plasma albumin/globulin ratio was lower among patients with ischemic stroke. Elevated total white cell count, urea and creatinine, which were of prognostic significance, were found to be associated with the severity of stroke as indicated by the Glasgow coma score, and did not have any independent prognostic value. Elevated hematocrit was not shown to be a risk factor and did not have any prognostic significance. A low plasma albumin/globulin ratio, an index of plasma viscosity, was a possible risk factor for ischemic strokes. Urinary albumin/creatinine ratios in the highest quintile increased the risk of stroke 13-fold.     

Triaging transient ischemic attack and minor stroke patients using acute magnetic resonance imaging

We examined whether the presence of diffusion-weighted imaging (DWI) lesions and vessel occlusion on acute brain magnetic resonance images of minor stroke and transient ischemic attack patients predicted the occurrence of subsequent stroke and functional outcome. 120 transient ischemic attack or minor stroke (National Institutes of Health Stroke Scale < or = 3) patients were prospectively enrolled. All were examined within 12 hours and had a magnetic resonance scan within 24 hours. Overall, the 90-day risk for recurrent stroke was 11.7%. Patients with a DWI lesion were at greater risk for having a subsequent stroke than patients without and risk was greatest in the presence of vessel occlusion and a DWI lesion. The 90-day risk rates, adjusted for baseline characteristics, were 4.3% (no DWI lesion), 10.8% (DWI lesion but no vessel occlusion), and 32.6% (DWI lesion and vessel occlusion) (p = 0.02). The percentages of patients who were functionally dependent at 90 days in the three groups were 1.9%, 6.2%, and 21.0%, respectively (p = 0.04). The presence of a DWI lesion and a vessel occlusion on a magnetic resonance image among patients presenting acutely with a transient ischemic attack or minor stroke is predictive of an increased risk for future stroke and functional dependence.     

Apolipoprotein A5 gene C56G variant confers risk for the development of large-vessel associated ischemic stroke

OBJECTIVES: Ischemic stroke is a suddenly developing temporary or often permanent damage of the brain. Several candidate genes have been shown to have an impact in the pathogenesis of stroke. The aim of our study was to investigate the possible association between the C56G variant of the apolipoprotein A5 (APOA5) gene and ischemic stroke. METHODS: PCR-RFLP assays were performed to detect the C56G alleles in 403 patients with classified stroke types and 171 controls. RESULTS: Triglyceride levels of subjects carrying 56G allele were elevated compared to the subjects with 56C allele in all stroke subgroups and in the controls. The serum total cholesterol levels did not differ between subjects with C or G alleles in each group. An accumulation of APOA5 56G allele was observed in the large-vessel associated stroke group compared to the healthy controls (10.9 vs. 5.6 %; p < 0.05), while its prevalence did not increase in any other stroke subgroups. Multivariate logistic regression analysis adjusted for differences in age, gender, BMI, serum total cholesterol levels, ischemic heart disease, hypertension, diabetes mellitus, smoking and drinking habits revealed that the APOA5 56G allele represents a susceptibility factor for large-vessel associated stroke (OR = 2.132 at 95 % CI; p < 0.05). CONCLUSION: The data presented here suggest that the 56G allele can confer risk exclusively for development of large-vessel associated stroke. Thereby, the 56G allele differs from the APOA5 T-1131C allelic variant, which has been previously identified as a risk factor for all subgroups of the stroke disease.     

Relationship between ischemic stroke location and autonomic cardiac function

Autonomic cardiac dysfunction is a common complication after acute ischemic stroke (IS). We recruited 75 patients with acute IS with measurements of autonomic cardiac function, including heart rate variability (HRV) and associated parameters, and compared them with 81controls. Of the 75 patients, 28 had right hemispheric infarctions (RH), 29 had left hemispheric infarctions (LH), and 18 had brainstem infarctions (BS). A comparison of HRV in all patients with stroke and in control subjects showed significant differences between IS subgroups and controls in low frequency (LF), high frequency (HF), normalized LF, normalized HF, and LF/HF ranges. A post-hoc comparison identified significant differences between patients with IS with BS infarctions and the control group in LF, HF, and LF/HF ranges. BS infarction may cause a much greater increase in sympathetic modulation and reduced vagal activity compared to RH or LH infarction. Our findings provide evidence that acute IS causes significant damage to the cardiovascular autonomic system, manifesting as abnormalities of HRV. BS stroke might correlate with a significant reduction in parasympathetic and an increase in sympathetic influence on HRV.     

基质金属蛋白酶-9基因多态性与缺血性脑卒中的相关性

目的探讨基质金属蛋白酶-9(matrix metalloproteinases-9,MMP-9)基因多态性与缺血性脑卒中的相关性。方法运用多重小测序技术(multiplex SNa Pshot)分析粤西地区251例缺血性脑卒中患者和96例健康对照组MMP-9基因(rs3787268、rs3918241、rs3918242)的多态性分布,并分析与缺血性脑卒中的相关性。结果 (1)与对照组相比,病例组rs3787268基因型频率有统计学差异(P=0.042),在隐性模型中A/A基因型的个体患病风险升高(OR=2.21,P=0.046);(2)rs3918242基因型频率亦有统计学差异(P=0.007),在显性模型中,携带T基因型的个体患病风险升高(OR=2.14,P=0.009);(3)其中rs3787268在大动脉粥样硬化(large artery atherosclerosis,LAA)亚型组的基因型分布与对照组相比有统计学差异(P=0.039),而非LAA亚型中无统计学差异;rs3918242在LAA亚型组的基因型和等位基因频率与对照组相比分别有统计学差异(P=0.009,P=0.047),在非LAA亚型中无统计学差异。结论 MMP-9基因rs3787268和rs3918242多态位点突变可能与中国粤西地区汉族人群缺血性脑卒中的发病风险相关;并主要可能增加了LAA型脑卒中的发病风险。