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目的 探讨老年人颈动脉狭窄程度及颈动脉斑块的形态学特点与心血管危险因素间的相关性.方法 选择我院行脑血管造影检查的老年患者321例,年龄60~83岁,参考颈动脉彩色超声检查结果,分为颈动脉粥样硬化组(斑块组)和颈动脉正常对照组,分析与年龄、性别、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、尿酸、C-反应蛋白(CRP)、同型半胱氨酸(HCY)、高血压、糖尿病、吸烟、饮酒等心血管病危险因素的相关性.斑块组按颈动脉狭窄程度、斑块表面光顺度等与心血管危险因素进行相关性分析.并随访1年,前瞻性分析各亚组患者心、脑血管事件发生情况.结果 斑块组256例,对照组65例,斑块组TC、LDL-C、尿酸、CRP、吸烟、饮酒、高血压、糖尿病等心血管危险因素均高于对照组;在亚组分析中,年龄、吸烟和糖尿病与颈动脉狭窄程度呈正相关,而CRP、LDL-C、吸烟、糖尿病与颈动脉斑块表面光顺度相关.斑块组46例(18.0%)发生脑血管事件,32例(12.5%)发生心血管事件,颈动脉狭窄程度与脑血管事件呈正相关,而与心血管事件发生差异无统计学意义.颈动脉斑块表面光顺度与心、脑血管事件均呈正相关.结论 老年人颈动脉粥样硬化斑块的发生、发展与心血管危险因素关系密切,颈动脉斑块表面光顺度形态学特点在一定程度上较狭窄程度更能反应老年人动脉粥样硬化水平,并与心、脑血管事件的发生密切相关.  相似文献   

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目的 探讨老年人颈动脉狭窄程度及颈动脉斑块的形态学特点与心血管危险因素间的相关性.方法 选择我院行脑血管造影检查的老年患者321例,年龄60~83岁,参考颈动脉彩色超声检查结果,分为颈动脉粥样硬化组(斑块组)和颈动脉正常对照组,分析与年龄、性别、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、尿酸、C-反应蛋白(CRP)、同型半胱氨酸(HCY)、高血压、糖尿病、吸烟、饮酒等心血管病危险因素的相关性.斑块组按颈动脉狭窄程度、斑块表面光顺度等与心血管危险因素进行相关性分析.并随访1年,前瞻性分析各亚组患者心、脑血管事件发生情况.结果 斑块组256例,对照组65例,斑块组TC、LDL-C、尿酸、CRP、吸烟、饮酒、高血压、糖尿病等心血管危险因素均高于对照组;在亚组分析中,年龄、吸烟和糖尿病与颈动脉狭窄程度呈正相关,而CRP、LDL-C、吸烟、糖尿病与颈动脉斑块表面光顺度相关.斑块组46例(18.0%)发生脑血管事件,32例(12.5%)发生心血管事件,颈动脉狭窄程度与脑血管事件呈正相关,而与心血管事件发生差异无统计学意义.颈动脉斑块表面光顺度与心、脑血管事件均呈正相关.结论 老年人颈动脉粥样硬化斑块的发生、发展与心血管危险因素关系密切,颈动脉斑块表面光顺度形态学特点在一定程度上较狭窄程度更能反应老年人动脉粥样硬化水平,并与心、脑血管事件的发生密切相关.  相似文献   

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目的 探讨老年人颈动脉狭窄程度及颈动脉斑块的形态学特点与心血管危险因素间的相关性.方法 选择我院行脑血管造影检查的老年患者321例,年龄60~83岁,参考颈动脉彩色超声检查结果,分为颈动脉粥样硬化组(斑块组)和颈动脉正常对照组,分析与年龄、性别、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密...  相似文献   

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目的探讨脑微出血(CMB)发生的危险因素及CMB与炎性介质的关系。方法收集非急性缺血性脑血管病患者180例,经头颅MRI磁敏感加权成像(SWI)排除急性脑梗死,根据SWI结果分为2组,CMB组41例,其中深部/幕下型CMB 23例和单纯脑叶型CMB 18例,非CMB组139例。记录临床资料,检测炎性介质高敏C反应蛋白(hs-CRP)、白细胞介素6(IL-6)和基质金属蛋白酶9(MMP-9)水平。采用logistic回归及Spearman相关分析。结果 CMB组hs-CRP、IL-6和MMP-9水平均高于非CMB组(P0.01)。年龄、高血压、收缩压水平、腔隙性脑梗死灶数目、脑白质疏松评分(OR=1.105、8.545、1.617、6.243、1.117,P0.05)及hs-CRP、IL-6、MMP-9(OR=1.575、1.683、1.302,P0.05)是CMB发生的独立危险因素。CMB灶数目与腔隙性脑梗死灶数目、脑白质疏松评分(r=0.382、0.325,P0.05)及hs-CRP、IL-6、MMP-9水平(r=0.507、0.517、0.672,P0.05)呈线性正相关。结论高龄、高血压、腔隙性脑梗死、脑白质病变及炎性介质水平均是CMB发生的独立危险因素。  相似文献   

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BACKGROUND: Aims: to evaluate morphological changes (intima-media thickness, IMT) of the carotid arteries in patients being treated for essential hypertension (EH), and to discover whether this abnormality can be detected in normotensive offspring of subjects with EH (familial trait, FT); and to investigate the interrelationship between IMT and accompanying risk factors. METHODS: Experimental design: cross-sectional study. Setting: angiology department, university teaching hospital. Subjects: the study encompassed 172 subjects, of whom 46 were treated hypertonics aged 40-55 (49) years, and 44 age matched, normotensive volunteers as controls. We also investigated 41 normotensives with FT for essential hypertension aged 20-30 (25) years and 41 age- and sex-matched controls without FT. Interventions: the hypertensive subjects were being treated either with long-acting calcium-channel antagonists or ACE-inhibitors. Measures: using high resolution ultrasound, IMT of the carotid bifurcation and of the common carotid artery was measured. RESULTS: In the hypertensives, the mean IMT was greater than that in the controls (0.92 (0.10) mm vs 0.72 (0.07) mm; p<0.00005). The IMT was independently related to accompanying risk factors: a positive family history of hypertension, age of the patient, duration of EH and the level of systolic/diastolic blood pressure (BP), body mass index and total/LDL-cholesterol. In subjects with FT, IMT was also greater compared to the control group (0.60 (0.05) mm vs 0.55 (0.04) mm; p<0.00005). IMT was not related to BP values. CONCLUSIONS: In treated essential patients with the EH, the IMT was increased. Individuals with FT also had greater IMT in the absence of elevated BP. The IMT in hypertensives was related to accompanying risk factors, which could be pathogenetic determinants of EH and/or its complications.  相似文献   

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OBJECTIVE: To investigate a potential association between occupational risk factors and severity markers of systemic sclerosis (SSc) defined by diffuse cutaneous extent, pulmonary involvement, and immunologic profile, i.e., presence of antitopoisomerase I antibody (anti-topo I). METHODS: Occupational exposures were assessed in 105 patients with SSc from 1998 to 2002. Exposures to silica dust, welding fumes, solvents, and epoxy resins were investigated. A group of 39 exposed SSc patients and a group of 66 unexposed ones were identified and compared according to severity markers of SSc. The stage of cutaneous extent was defined according to the classification of Leroy, as limited scleroderma (lSSc) or diffuse scleroderma (dSSc). Respiratory status was defined by pulmonary function tests and high resolution computed tomography. Immunological profile was determined by the presence of anti-topo I or anticentromere antibodies (ACA). Statistical relationships between occupational exposures and severity markers of SSc were evaluated using a multiple correspondence analysis and Fisher's exact test. RESULTS: Diffuse scleroderma affected mainly patients exposed during their occupational life to toxic agents. There were significant or close to significant associations between toxic exposure and dSSc (p = 0.06), pulmonary involvement (p = 0.10), and negative ACA (p = 0.03). The most incriminated products seemed to be epoxy resins (p = 0.06), white spirit (p = 0.07), aromatic solvents (p = 0.07), and silica coupled to welding fumes (p = 0.10). CONCLUSION: Our results indicate that occupational toxic factors have an influence on the severity of SSc.  相似文献   

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There is a need for blood-based analytic techniques that allow for the detection of patients either with reversible myocardial ischemia or who are at risk for myocardial ischemia. However, given the diverse etiologies of unstable angina and the complex interactions among various cell types, the term “marker for ischemia” should be used with caution (if at all). Unless we find a protein that is released across the diverse pathologic triggers associated with the various stages of progression of atherosclerosis and cellular ischemia, we will be forced to consider a spectrum of proteins (and analytic assays) that are situationally specific. The choice of an appropriate gold standard as we investigate the clinical application of these assays will be one of the most difficult and most important decisions in these studies. It will be critical that conclusions of usefulness in one setting of ischemic heart disease not be generalized in the absence of clinical trials supporting that contention.  相似文献   

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Abstract. Hamrefors V, Hedblad B, Engström G, Almgren P, Sjögren M, Melander O (Lund University, Malmö, Sweden). A myocardial infarction genetic risk score is associated with markers of carotid atherosclerosis. J Intern Med 2012; 271 : 271–281. Objective. To assess whether or not a genetic risk score that was previously shown to be associated with myocardial infarction (MI) and coronary artery disease (CAD) is also associated with markers of carotid atherosclerosis. Design. A total of 4022 middle‐aged subjects from the general Swedish population were genotyped and individually assigned a genetic risk score based on 13 single‐nucleotide polymorphisms (SNPs), previously associated with MI and CAD. The genetic score (Score‐MI) was then related to carotid bulb intima–media thickness (IMT), common carotid artery (CCA) IMT and to the occurrence of carotid plaques in the study population. Results. Score‐MI was associated with IMT of the bulb (P < 0.001) and the CCA (P < 0.001) in unadjusted analyses, and with IMT of the bulb after adjustment for cardiovascular risk factors (P = 0.003). The effect size of Score‐MI on IMT of the bulb was similar to that of LDL cholesterol. After adjustment for cardiovascular risk factors, Score‐MI was also associated with the occurrence of carotid plaques (odds ratio per quintile of Score‐MI = 1.11; 95% confidence interval 1.04–1.18; P = 0.001). In addition to SNPs with known effects on LDL levels, Score‐MI showed nominal associations with increasing systolic blood pressure and decreasing C‐reactive protein levels. Conclusions. This genetic risk score was independently associated with carotid bulb IMT and carotid plaques, providing evidence of an association with early markers of atherosclerosis. This might imply that the genetic MI risk conferred by the score is related to early atherosclerosis and that the risk score may identify at an early stage candidates at risk of developing intermediate phenotypes of atherosclerosis. Further studies should test whether or not assessing the genetic score could be valuable for early treatment decisions in these subjects.  相似文献   

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Hepatocyte growth factor (HGF) has been shown to have a unique stimulating property on the endothelium as well as an anti-apoptotic action on the endothelium. Through these mechanisms, HGF has been shown to have an anti-atherogenic action in animal models. In atherosclerotic disorders, the circulating level of HGF has been shown to be increased to compensate for its decline in tissue. However, whether increased circulating HGF has any influence on the development of atherosclerosis has not been elucidated. In the present study, the association between plasma HGF concentration and the risk factor-carotid atherosclerosis relationship was evaluated. Three hundred and seventeen community-dwelling subjects participated in the study. The plasma concentration of HGF was determined by enzyme-linked immunosorbent assay (ELISA). The subjects were divided into two groups according to the plasma level of HGF: a low HGF group (n=199, plasma HGF < 150 pg/ml) and a high HGF group (n=118, plasma HGF > or = 150 pg/ml). Risk factors for atherosclerosis were evaluated in each subject. Carotid ultrasonography was performed to measure carotid arterial intima-media thickness (IMT) and the presence of plaque. The association between carotid IMT and risk factors was then evaluated in the two HGF groups. The regression lines between age and carotid IMT were significantly different between the low HGF and high HGF groups (F[1,313]=5.98, p=0.015). The regression lines between systolic blood pressure and carotid IMT were also significantly different between the two HGF groups (F[1,313]=5.17, p=0.024). A general linear model showed that the interaction between age and plasma level of HGF was significantly associated with carotid IMT, suggesting that the plasma level of HGF modifies the age-related increase in carotid IMT. In addition, clustering of risk factors was evaluated in subjects with carotid atherosclerosis. The number of total risk factors in carotid atherosclerosis subjects with high plasma HGF was significantly greater than that in those with low HGF, even though the two groups had a similar magnitude of carotid atherosclerosis. In conclusion, these findings indicate that risk factor-dependent augmentation of carotid atherosclerosis could be influenced by circulating HGF.  相似文献   

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Severe carotid stenosis is typically treated with carotid endarterectomy (CEA), but there is debate about the safety of this procedure in patients with occlusion of the contralateral artery, previous CEA in the same artery, and other risk factors. To evaluate the association of these factors with outcomes in standard CEA with Dacron patch angioplasty, we examined the records of 1,609 consecutive isolated CEAs performed at our institution over a 10-year period on 1,400 patients (851 men and 549 women; mean age, 69.5 yr) with symptomatic or high-grade asymptomatic carotid lesions. Twenty-three patients (1.4%) had perioperative strokes, of which 2 were fatal. The overall same-admission mortality was 0.2% (4 patients). Same-admission stroke/death was more likely in patients with any history of tobacco use (odds ratio [OR], 4.6; 95% confidence interval [CI], 1.6-13.6), contralat-eral occlusion (OR, 3.3; 95% CI, 1.2-9.1), angina with a Canadian Cardiovascular Society classification of 2 or greater (OR, 3.2; 95% CI, 1.4-7.6), or transient ischemic attack within the 6 weeks before surgery (OR, 2.4; 95% CI, 1.05-5.3). A total of 9 patients (0.6%) died within 30 days of CEA; our multivariate analysis did not reveal any significant predictors of 30-day mortality. We conclude that standard CEA with patch angioplasty is associated with low rates of death and morbidity for most patients, but patients with any history of tobacco use, substantial angina, contralateral occlusion, or preoperative transient ischemic attack may have an elevated risk of adverse outcomes.  相似文献   

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目的探讨老年高血压患者颈动脉内膜中层厚度(IMT)与心血管危险因素的相关性。方法对75例老年原发性高血压患者行超声测定颈动脉IMT,同时检测患者血压、血脂、空腹血糖(FPG)、肌酐及C-反应蛋白(CRP)。按照颈动脉IMT厚度分为IMT正常组和IMT增厚组,并对2组年龄、病程、血压及生化指标等进行比较。结果IMT增厚组较IMT正常组年龄较大,高血压病程较长,收缩压较高,高密度脂蛋白胆固醇(HDL-C)较低,低密度脂蛋白胆固醇(LDL-C)、FPG、CRP较高; 随着IMT的增厚,高LDL-C、高FPG和高CRP的检出率增加。结论老年高血压患者颈动脉IMT与心血管危险因素的聚集有显著的相关性。  相似文献   

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目的研究老年高血压患者颈动脉粥样硬化、斑块形成与心血管危险因素以及脑卒中发生之间的相关性。方法随机调查204例老年高血压患者,用颈动脉超声检查分析颈动脉硬化、斑块形成与心血管病危险因素及脑卒中的相关性。结果颈动脉硬化、斑块形成与收缩压、脉压呈正相关(r=0.21、0.26,P<0.01),与高血压病程、糖化血红蛋白(HbA1c)亦呈正相关(r=0.17、0.30,P<0.05),与尿酸、胆红素、高密度脂蛋白胆固醇(HDL-C)及脑卒中均有关。结论上述心血管危险因素在老年人颈动脉粥样硬化、斑块形成的发生、发展中起到一定的作用,控制这些危险因素有益于减少脑卒中发生。  相似文献   

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目的探讨原发性高血压(高血压)及相关危险因素与颈动脉内-中膜厚度(intima-media thickness,IMT)的相关性。方法本文收集了2007年6月至2007年12月在贵阳医学院诊治且病历资料较完整的186例高血压患者,按血压水平由低至高分成3组:高血压1级组50例;高血压2级组56例;高血压3级组80例。另外,选择门诊健康体检者50名作为对照组。收集研究对象的一般情况、血生化指标及双侧颈总动脉IMT及斑块的超声测量结果。结果高血压各组的颈动脉IMT,颈动脉斑块发生率明显高于对照组,并随血压等级增加而增加,方差分析及q检验显示差异有统计学意义(P0.05)。Logistic回归分析显示,年龄、男性、吸烟、总胆固醇及低密度脂蛋白胆固醇是颈动脉IMT增加的独立危险因素(P0.05),而脂蛋白(a)、尿酸、肌酐与颈动脉IMT无明显相关性(P0.05)。结论高血压可使颈动脉IMT增加,其程度和颈动脉斑块发生率均随血压分级增高而增加;年龄、男性、吸烟、总胆固醇及低密度脂蛋白胆固醇是颈动脉IMT增加的独立危险因素;脂蛋白(a)、肌酐、尿酸与颈动脉IMT无明显相关性。  相似文献   

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目的 研究血清可溶性肿瘤坏死因子受体 I(s TNFRI)水平与颈动脉粥样硬化的关系。方法 采用超声诊断仪将 82例中老年患者分为斑块形成组与无斑块组 ,分析两组 s TNFRI水平变化及与多种颈动脉粥样硬化危险因素的相关性。结果 斑块形成组冠心病、高血压、糖尿病及脑梗死的发生率较无斑块组显著增高 ,斑块形成组s TNFRI水平显著高于无斑块组 ,s TNFRI升高组比正常组颈动脉内膜 -中层厚度 (IMT)显著增加。多元逐步回归分析示 s TNFRI水平与年龄相关。结论  s TNFRI水平与颈动脉 IMT相关。降低血清 s TNFRI浓度 ,抑制炎症反应不仅可能阻止颈动脉粥样硬化的进展 ,而且对于预防心、脑血管事件具有重要意义  相似文献   

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目的研究血清可溶性肿瘤坏死因子受体I(sTNFRI)水平与颈动脉粥样硬化的关系.方法采用超声诊断仪将82例中老年患者分为斑块形成组与无斑块组,分析两组sTNFRI水平变化及与多种颈动脉粥样硬化危险因素的相关性.结果斑块形成组冠心病、高血压、糖尿病及脑梗死的发生率较无斑块组显著增高,斑块形成组sTN-FRI水平显著高于无斑块组,sTNFRI升高组比正常组颈动脉内膜-中层厚度(IMT)显著增加.多元逐步回归分析示sTNFRI水平与年龄相关.结论sTNFRI水平与颈动脉IMT相关.降低血清sTNFRI浓度,抑制炎症反应不仅可能阻止颈动脉粥样硬化的进展,而且对于预防心、脑血管事件具有重要意义.  相似文献   

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