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肥胖对高血压病患者颈动脉粥样硬化的作用心肺血管病杂志,2005,24(1):16-17.肥胖是心脑血管病的危险因素,而关于肥胖与颈动脉粥样硬化的关系尚不清楚。方法:通过多普勒超声检查高血压病患者颈动脉粥样硬化的方法,选择82例高血压病患者血压一直控制较好,其中男性66例,女性16例,年龄52～80岁,不伴冠心病、糖尿病、脑血管疾病,总胆固醇<5.7mmol/L,甘油三酯<1.7mmol/L,低密度脂蛋白<3.1mmol/L。观察体重指数与颈动脉粥样硬化斑块的发生率及内中膜厚度的相互关系。结果:体重指数高的患者其颈动脉粥样硬化斑块的发生率及内中膜的厚度也高(P<0.05…     

血管活性剂对高血压患者肠系膜动脉平滑肌细胞钙激活钾通道活性的调控作用

肥胖是心脑血管病的危险因素，而关于肥胖与颈动脉粥样硬化的关系尚不清楚。方法：通过多普勒超声检查高血压病患者颈动脉粥样硬化的方法，选择82例高血压病患者血压一直控制较好，其中男性66例，女性16例，年龄52～80岁，不伴冠心病、糖尿病、脑血管疾病，总胆固醇〈5．7mmol／L，甘油三酯〈1．7mmol／L，低密度脂蛋白〈3．1mmol／L。观察体重指数与颈动脉粥样硬化斑块的发生率及内中膜厚度的相互关系。结果：体重指数高的患者其颈动脉粥样硬化斑块的发生率及内中膜的厚度也高（P〈0．05，P〈0．01）。结论：体重指数与颈动脉粥样硬化斑块和内中膜厚度相关。肥胖可能参与动脉粥样硬化的形成和发展。     

脉压差对高血压病患者颈动脉粥样硬化的作用

目的 :高血压病是冠状动脉粥样硬化的危险因素 ,人们普遍关心收缩压与舒张压和动脉粥样硬化与冠心病的关系 ,而对于脉压尚未进行广泛的研究。方法 :本文通过多普勒超声检查高血压病患者颈动脉粥样硬化的方法 ,观察了 64例高血压病患者脉压差与颈动脉粥样硬化斑块的发生率及内中膜厚度的相互关系。结果 :脉压差高的患者其颈动脉粥样硬化斑块的发生率及内中膜厚度也高 (P <0 0 5 ,P <0 0 1)。结论 :脉压差与颈动脉粥样硬化斑块和内中膜厚度相关 ,脉压差可能参与动脉粥样硬化的形成和发展。     

高血压病患者脉压差与颈动脉粥样硬化的相关性研究

目的探讨高血压病患者脉压差与颈动脉粥样硬化斑块的发生率及颈动脉内中膜厚度(IMT)的相关性。方法通过多普勒超声检查70例高血压患者颈动脉粥样硬化斑块及IMT,计算出这些患者的脉压差,观察脉压差与颈动脉粥样硬化斑块的发生率及与颈动脉内中膜厚度(IMT)的相关性。结果脉压差大的患者其颈动脉粥样硬化斑块的发生率及IMT均增高(P<0．05)。结论脉压差与颈动脉粥样硬化斑块和IMT相关,脉压差可促进动脉粥样硬化的形成和发展。     

高血压伴与不伴缺血性脑卒中患者颈动脉内中膜厚度的研究

目的 :用彩色多普勒超声观察高血压伴与不伴缺血性脑卒中患者颈动脉内中膜厚度 ,探讨颈动脉粥样硬化与缺血性脑卒中的关系。方法 :用HDI 30 0 0彩色多普勒超声观察了 36例无缺血性脑卒中的高血压病患者和 36例伴有缺血性脑卒中的高血压病患者双侧颈动脉内中膜厚度 ,并与 2 8名健康对照进行了比较。结果 :1 3组间空腹血糖、血脂和体重指数及平均年龄无显著性差异 (P >0 0 5 ) ;2 单纯高血压病患者和高血压病伴缺血性脑卒中患者颈动脉内中膜厚度明显高于健康对照者 (P <0 0 1) ,且高血压伴缺血性脑卒中患者颈动脉内中膜厚度明显高于无缺血性脑卒中的高血压患者 (P <0 0 1)。结论 :高血压病患者存在有颈动脉粥样硬化 ,且伴有缺血性脑卒中患者颈动脉粥样硬化程度明显加重 ,提示颈动脉粥样硬化程度可作为预测缺血性脑卒中发生的参考指标。     

糖代谢异常和糖尿病患者颈动脉粥样硬化的观察

目的:探讨糖尿病、糖代谢异常患者颈动脉粥样硬化的情况。方法:通过多普勒超声检查颈动脉粥样硬化的方法,观察了糖尿病、糖代谢异常患者颈动脉粥样硬化斑块的发生率及内中膜厚度,并与正常对照组进行比较。结果:糖尿病、糖代谢异常的患者与正常对照组相比其颈动脉粥样硬化斑块的发生率及内中膜厚度显著增加(P<0.01)。结论:糖尿病、糖代谢异常与颈动脉粥样硬化相互关联。     

老年人颈动脉粥样硬化与冠心病的关系

目的探讨老年人颈动脉粥样硬化与冠心病的关系。方法采用高频超声测定颈动脉内中膜厚度和硬化斑块指数,检测80例已施冠脉造影(CAG)者,其中冠心病组(A组)48例,对照组(B组)32例。结果A组中颈动脉内中膜厚度明显高于B组(P<0.001),硬化斑块指数也明显高于B组(P<0.001),动脉硬化检出率在两组中以颈动脉球部为最高,其次颈总动脉和颈内动脉。A组颈动脉粥样硬化发生率明显高于B组(P=0.006)。结论老年人颈动脉粥样硬化严重程度与冠心病发生率成正比。     

陈旧性心肌梗死患者颈动脉粥样硬化与危险因素的关系

为探讨陈旧性心肌梗死患者颈动脉粥样硬化情况,对38例陈旧性心肌梗死患者的颈动脉内中膜厚度及斑块进行超声检测,与32例健康者作对照.结果发现,陈旧性心肌梗死患者的颈动脉内中膜厚度、斑块指数及斑块发生率明显高于对照组.多因素回归分析显示,年龄、总胆固醇、收缩压与颈动脉内中膜厚度密切相关.     

陈旧性心肌梗死患者颈动脉粥样硬化与危险因素的关系

为探讨陈旧性心肌梗死患者颈动脉粥样硬化情况，对38例陈旧性心肌梗死患者的颈动脉内中膜厚度及斑块进行超声检测，与32例健康者作对照。结果发现，陈旧性心肌梗死患者的颈动脉内中膜厚度、斑块指数及斑块发生率明显高于对照组。多因素回归分析显示，年龄、总胆固醇、收缩压与颈动脉内中膜厚度密切相关。     

高血压合并代谢综合征与颈动脉粥样硬化相关性观察

目的探讨高血压合并代谢综合征与颈动脉粥样硬化的相关性。方法选择高血压合并代谢综合征患者52例,单纯高血压病患者42例。全部患者进行颈部动脉血管B超检测,收集临床资料,比较两组颈动脉粥样硬化发生情况。结果观察组与对照组相比较,体重指数(BMI)、空腹血糖(FPG)、餐后2h血糖(2hPG)、胰岛素抵抗指数(HOMA-IR)和总胆固醇(TC)显著升高(P<0.05);高密度脂蛋白(HDL-C)在观察组显著低于对照组(P<0.05);颈总动脉内中膜厚度和颈内动脉内中膜厚度明显增厚(P<0.05);观察组颈总动脉粥样硬化发生率84.0%,高于对照组61.9%(P<0.05);颈总动脉左右侧血管内径及阻力指数均明显增加(P<0.05);两组间收缩期血流峰值无统计学意义。结论高血压合并代谢综合征患者更容易发生颈动脉粥样硬化,代谢综合征可能促进高血压患者颈动脉粥样硬化的形成。     

Increased human urotensin II levels are correlated with carotid atherosclerosis in essential hypertension

BACKGROUND: Circulating blood levels of human urotensin II (U-II), the most potent vasoconstrictor peptide identified to date, are increased in patients with essential hypertension. Our previous studies showed that U-II accelerates human macrophage foam cell formation and vascular smooth muscle cell proliferation, suggesting development of atherosclerotic plaque. In this study, we demonstrated a correlation between plasma U-II level and progression of atherosclerosis in hypertensive patients. METHODS: The intima-media thickness (IMT) and plaque score in the carotid artery, blood pressure (BP), plasma levels of U-II, and atherosclerotic parameters were determined in 50 hypertensive patients and 31 normotensive controls. RESULTS: Plasma U-II level, maximum IMT, plaque score, systolic BP, and homeostasis model assessment for insulin resistance (HOMA-IR) were significantly greater in hypertensive patients than normotensive controls. Age, gender, body mass index, and serum levels of high-sensitive C-reactive protein (CRP), HDL and LDL cholesterols, small dense LDL, triglycerides, lipoprotein(a), insulin, and fasting plasma glucose level were not significantly different between the two groups. In all subjects, plasma U-II level showed significant positive correlations with systolic BP, maximum IMT, plaque score, and HOMA-IR. Multiple logistic regression analysis indicated that the contribution of plasma U-II levels to carotid plaque formation (plaque score >/=1.1) was significantly still greater with a 60% increase than those of established risk factors, such as age, systolic BP, high-sensitive CRP, small dense LDL, and HOMA-IR. CONCLUSIONS: Our results suggest that increased levels of U-II may play a crucial role in the development of carotid atherosclerosis in hypertensive patients.     

Presence and severity of carotid atherosclerosis in asymptomatic hypertension patients with left ventricular hypertrophy]

BACKGROUND AND PURPOSE: Arterial hypertension is associated with structural changes in the cardiovascular system. In hypertensives, a relationship has been found between left ventricular hypertrophy and carotid wall thickness, whereas the association with atherosclerotic plaque is less defined. The aim of this study was to evaluate the occurrence and severity of carotid atherosclerosis in hypertensive patients with or without left ventricular hypertrophy (LVH). MATERIALS AND METHODS: We studied 122 hypertensive subjects (62 men and 60 women), aged 60.1 +/- 12.1. Subjects were considered to have left ventricular hypertrophy if their left ventricular mass index (LVMI) at echocardiography exceeded 110 g/m2 in women and 135 g/m2 in men. Carotid intima-media thickness (IMT), external diameter and atherosclerotic plaques were evaluated by high resolution echo-color Doppler. RESULTS: IMT in both common carotid and bifurcation was significantly greater in hypertensives with LVH (p < 0.01), whereas external diameter did not differ significantly in the two groups. Increased presence (73.4 vs 32.8%) and severity (18.7 vs 5.2% for stenosis > 40%) of atherosclerotic plaque were found in the hypertrophic group. A weak but significant association was present among left ventricular mass index, ventricular wall thicknesses and carotid intima-media thickness, and plaque. CONCLUSIONS: In asymptomatic hypertensive subjects, LVH is associated with an increased risk of plaque formation and progression. Vascular hypertrophy may represent a distinct prognostic factor in hypertension and the association of cardiac and vascular hypertrophy may identify a group at high risk of future cardiovascular events.     

血浆纤维蛋白原对高血压患者颈动脉粥样硬化的作用

目的进一步明确纤维蛋白原(FB)与颈动脉粥样硬化的关系。方法本文通过多普勒超声检查高血压患者颈动脉粥样硬化的方法,观察了118例高血压患者血浆FB与颈动脉粥样硬化斑块的发生率及内膜-中层厚度(IMT)的相互关系。结果不同水平血浆FB组中颈动脉钙化斑发生比例、IMT、高血压病程、年龄和血浆胆固醇均具有显著性差异(P<0.05或P<0.01);FB的多因素Linearregression分析发现IMT和高血压病程是FB的相关因子(P<0.01)。结论血浆FB与颈动脉粥样硬化斑块和IMT相关,FB可能参与动脉粥样硬化的形成和发展。     

C-reactive protein and carotid intimal medial thickness in a community population

BACKGROUND: C-reactive protein (CRP) has been linked to cardiovascular disease and atherosclerosis. Large-scale epidemiological studies have shown a correlation of CRP level with risk of stroke, myocardial infarction and peripheral arterial disease. Nevertheless, the question whether serum CRP itself is an independent indicator of the atherosclerotic process remains unanswered. METHODS: In a community-based sample free of advanced atherosclerotic disease (n = 1018; mean age +/- SD, 54.1 +/- 12.0 years; 49.7% women) we examined the relationship between carotid intimal medial thickness (IMT), conventional vascular risk factors (that is, smoking, obesity, elevated blood pressure, diabetes mellitus, hypercholesterolaemia) and serum CRP. RESULTS: We found an association between increasing IMT values with increasing CRP values for all sites within the carotid system (for example, common carotid artery [CCA-] IMT, beta = 0.174, P < 0.001). The relationship was weakened after accounting for the above-mentioned conventional risk factors (linear regression), particularly body mass index, but remained significant (for example, mean CCA-IMT beta = 0.02, P = 0.042). Including fibrinogen in the regression made the relationship no longer significant (mean CCA-IMT beta = 0.01, P = 0.277). CONCLUSION: It is unlikely that CRP per se is a major independent cause of early arteriosclerosis. Elevations of CRP, or less specifically chronic inflammation, may mediate the effect of certain conventional risk factors on promoting atherogenesis, especially obesity.     

Is cardiovascular reactivity associated with atherosclerosis among hypertensives?

Exaggerated cardiovascular reactivity to behavioral challenges among otherwise healthy individuals has been associated with carotid atherosclerosis. We evaluated whether a similar relationship exists among hypertensives, who are at a heightened atherosclerotic risk. Untreated, hypertensive men (n=251; age range, 40 to 70 years; 197 white, 54 black) completed a standardized battery of behavioral challenges while their blood pressure responses to the battery were measured. Mean and maximum carotid intima-media thickness and the occurrence of carotid plaques were subsequently determined using B-mode ultrasonography. Although greater systolic and diastolic responses to the battery were associated with greater mean and maximum intima-media thickness in univariate analyses (P<0.01), only diastolic reactivity showed a unique association with mean and maximum carotid intima-media thickness after multivariate adjustment for age, race, socioeconomic status, smoking and alcohol use, body mass index, lipid profile, glucose and insulin concentrations, and resting blood pressure (P<0.05). Carotid plaque occurrence was associated with greater systolic reactivity (P=0.05) and was marginally associated with greater diastolic reactivity (P=0.07) in univariate analyses, but neither systolic nor diastolic reactivity was uniquely associated with the presence of carotid plaques after multivariate risk-factor adjustment. Among hypertensives, exaggerated behaviorally evoked cardiovascular reactivity appears to be uniquely associated with greater carotid intima-media thickness but not with carotid plaque occurrence.     

Serum salusin-alpha levels are decreased and correlated negatively with carotid atherosclerosis in essential hypertensive patients.

Salusin-alpha is a new bioactive peptide with mild hypotensive and bradycardic effects. Our recent study showed that salusin-alpha suppresses foam cell formation in human monocyte-derived macrophages by down-regulating acyl-CoA:cholesterol acyltransferase-1, contributing to its anti-atherosclerotic effect. To clarify the clinical implications of salusin-alpha in hypertension and its complications, we examined the relationship between serum salusin-alpha levels and carotid atherosclerosis in hypertensive patients. The intima-media thickness (IMT) and plaque score in the carotid artery, blood pressure, serum levels of salusin-alpha, and atherosclerotic parameters were determined in 70 patients with essential hypertension and in 20 normotensive controls. There were no significant differences in age, gender, body mass index, fasting plasma glucose level, or serum levels of high-sensitive C-reactive protein, high- or low-density lipoprotein (LDL) cholesterol, small dense LDL, triglycerides, lipoprotein(a), or insulin between the two groups. Serum salusin-alpha levels were significantly lower in hypertensive patients than in normotensive controls. The plasma urotensin-II level, maximal IMT, plaque score, systolic and diastolic blood pressure, and homeostasis model assessment for insulin resistance (HOMA-IR) were significantly greater in hypertensive patients than in normotensive controls. In all subjects, maximal IMT was significantly correlated with age, systolic blood pressure, LDL cholesterol, urotensin-II, salusin-alpha, and HOMA-IR. Forward stepwise multiple linear regression analysis revealed that salusin-alpha levels had a significantly independent and negative association with maximal IMT. Serum salusin-alpha levels were significantly lower in accordance with the severity of plaque score. Our results suggest that the decrease in serum salusin-alpha, an anti-atherogenic peptide, may be associated with carotid atherosclerosis in hypertensive patients.     

Abdominal obesity is associated with accelerated progression of carotid atherosclerosis in men

Abdominal obesity increases the risk of clinical atherosclerotic diseases, but whether it accelerates the progression of preclinical atherosclerosis is unknown. We studied whether waist-to-hip ratio (WHR) and waist circumference are associated with 4-year increase in indicators of common carotid atherosclerosis, assessed by B-mode ultrasonography, in 774 Finnish men aged 42-60 years without atherosclerotic diseases. Men with WHR of <0.91, 0.91-0.96 and >0.96 (thirds) had increase in maximal intima-media thickness (IMT) of 0.230, 0.255 and 0.281 mm/4 years (P=0.007 for linear trend; P=0.025 for difference) and plaque height of 0.241, 0.254 and 0.291 mm/4 years (P=0.005, P=0.013) adjusting for age, body mass index and technical covariates. Men with waist circumference of <85, 85-93 and >93 cm (thirds) had increase in maximal IMT of 0.227, 0.251 and 0.290 mm/4 years (P=0.011, P=0.035) and plaque height of 0.229, 0.263 and 0.296 mm/4 years (P=0.003, P=0.013). These associations were stronger in men with high (> or =3.8 mmol/l) than lower serum LDL cholesterol (P<0.05 for interaction). This is the first documentation that abdominal obesity is associated with accelerated progression of atherosclerosis, and supports the view that it is an important cardiovascular risk factor. This study emphasizes the role of avoiding abdominal obesity to prevent atherosclerotic diseases.