瘦素与冠心病

瘦素是肥胖基因编码的一种蛋白质产物,通过与其受体结合发挥抑制食欲、减少能量摄入、增加能量消耗的生物学作用。近来的大量研究显示瘦素与冠心病发生、发展相关,现就近年来发现的瘦素在冠心病中的作用机理作一综述,以期进一步了解冠心病发病机理,为临床治疗冠心病提供帮助。     

瘦素与冠心病发病关系研究进展

自瘦素发现以来,人们对体内脂肪组织进行了大量的基础及临床研究,血清瘦素与冠心病的关系也受到广泛关注。大多数人的研究都支持高血清瘦素与冠心病的发生有密切关系,瘦素可通过多种途径参与,影响冠心病的发生和发展。现就瘦素与冠心病的发病关系作一综述。     

瘦素与冠心病的关系及其机制的研究进展

瘦素 (Leptin)又称“消脂素” ,是肥胖基因 (ob)的产物 ,由哺乳动物体内的白色脂肪细胞分泌 ,在血液中有游离态、结合态两种存在形式 ,其血液浓度与机体脂肪含量成正比。瘦素分泌受到体脂含量、脂肪细胞大小的影响 ,随体内脂肪储存增加而增加。它将脂肪组织中能量储存状况的信息传递至神经中枢 ,使机体适当调整食欲 ,维持机体能量平衡 ,诱导体重下降。瘦素需要与特异的瘦素受体结合方能发挥生物学效应。瘦素及其受体基因发生突变可导致肥胖、不育和胰岛素抵抗等症状。瘦素与肥胖、胰岛素抵抗的密切关系已从大量研究中得到证实。以下就瘦素…     

肥胖患者瘦素水平与冠心病的相关性研究

目的：探讨肥胖患者瘦素水平与冠心病的关系。方法：选取2018年9月~2019年10月广西医科大学第一附属医院心内科收治的胸痛查因（未有冠心病史）择期做冠状动脉造影的肥胖患者（BMI≥27 kg/㎡）作为研究对象,根据冠脉造影结果将患者分为冠心病组和对照组,对两组进行性别、年龄1：1匹配后,剩下46对作为最终研究对象。结果：在多元线性回归分析显示,瘦素与性别（女性,R2=0.495, β=0.385, P＜0.001）、高密度脂蛋白（R2=0.495, β=0.034, P=0.014）有独立的正向相关性。多变量二元Logistic回归分析显示,血清瘦素水平与冠心病独立相关（OR=2.363,95%CI：1.234-4.524,P=0.009）;当瘦素水平作为分类变量进行分析时,最高三分位数的冠心病风险是最低三分位数的3.865倍（P=0.048）。结论：在肥胖人群中,瘦素水平升高与冠心病独立相关。     

瘦素与心血管疾病

瘦素是由肥胖基因编码、脂肪组织分泌的多肽类激素，研究显示瘦素与多个系统疾病有关系。本文就瘦素与心血管疾病的关系作一综述。     

瘦素与冠心病发病机制的研究进展

瘦素是肥胖基因编码的一种蛋白质产物,主要由白色脂肪组织分泌,通过与其受体结合发挥抑制食欲、减少能量摄入、增加能量消耗的生物学作用.近年来大量临床研究显示瘦素与冠心痛的发生、发展密切相关,现就瘦素在冠心病发病中的作用机制作一综述.     

瘦素水平与冠心病的关系研究进展

随着人民生活水平的不断提高,冠心病已成为威胁人类健康的重要疾病.血压升高、胰岛素抵抗、腹型肥胖、致动脉粥样硬化的血脂异常、促血栓形成状态作为代谢综合征的不同表现,经常相互伴随,在同一个体出现.在代谢综合征的研究过程中发现,瘦素(Leptin)与肥胖、高血压、胰岛素抵抗、血脂异常等冠心病易发因素密切相关,因此,瘦素与冠心病的关系也引起了人们更多的关注.     

瘦素与冠心病关系的研究进展

1994年,Zhang等[1]经过首次利用位点克隆技术成功从小鼠和人的脂肪组织中分离克隆了小鼠的肥胖(ob)基因及人类的同源序列,其编码产物为瘦素(1eptin). Scotland大规模冠心病防治的前瞻性研究中,发病组瘦素水平明显高于对照组,瘦素每增加1个标准差,发生心脏冠脉事件的相对危险增加125%,瘦素独立于年龄、体重指数(BMI)、血压和血脂,成为预示冠心病发病的危险因素[2].     

冠心病患者血浆瘦素与可溶性瘦素受体水平的相关性

目的:探讨冠心病患者血浆瘦素（leptin,Lep）及可溶性瘦素受体(soluble leptin receptor,sLR)水平的变化,并分析Lep与冠心病各危险因素的关系。方法: 选取冠心病患者180例,正常对照组60例。所有患者行冠脉造影检查,冠脉狭窄程度采用Genisin评分,酶联免疫法测定Lep、sLR浓度,同时检测总胆固醇(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)、体质量指数(BMI)、腰围、臀围等指标,分析Lep、sLR与冠心病的的关系。结果: 冠心病患者lep水平显著高于对照组［（12±6） vs.（9±5）μg/L,P<0.01］,sLR水平显著低于对照组［（124±62） vs.（164±70）μg/L,P<0.01］,在调整年龄、血糖和血压后,两组间的差别有显著性意义。多元Logistic回归分析显示冠心病患者μg/L。Lep水平的升高独立于年龄、血压、血脂等危险因素。结论: 冠心病患者Lep水平与冠脉病变的严重程度呈正相关,而sLRs水平与冠脉病变严重程度呈负相关。     

瘦素抵抗研究进展

肥胖症已成为严重的健康问题,其发病机制目前仍不清楚。瘦素是与发病相关的重要激素之一,肥胖症者存在瘦素抵抗的原因也不明确。本文从瘦素及其受体、瘦素抵抗机制、瘦素受体信号传递、肥胖症治疗前景等几个方面近年有关文献作一简要综述。     

Leptin is an endothelial-independent vasodilator in humans with coronary artery disease: Evidence for tissue specificity of leptin resistance.

AIMS: We sought to define the mechanisms and correlates of leptin's vascular actions in humans with coronary artery disease. METHODS AND RESULTS: In 131 patients (age 65.7+/-0.7 years mean+/-SEM), ex vivo vascular reactivity to leptin (10(-13)-10(-7) M) was assessed in saphenous vein (SV) rings. Leptin led to SV relaxation (maximal relaxation 24.5+/-1.6%). In separate experiments, relaxation to leptin was unaffected by L-NMMA (17.4+/-3.4 vs.17.8+/-3.3%, P = 0.9) or endothelial denudation (17.4+/-4.4 vs. 22.5+/-3.0%, P = 0.4). We explored the possibility that leptin's vascular effects are mediated via smooth muscle hyperpolarization. In the presence of KCl (30 mmol/L) to inhibit hyperpolarization, the vasodilator effect of leptin was completely blocked (0.08+/-4.1%, P < 0.001 vs. control). Similar results were demonstrated in internal mammary artery rings. The only independent correlate of leptin-mediated vasodilatation was plasma TNF-alpha (r = 0.25, P < 0.05). Neither body mass index nor waist circumference correlated with leptin-mediated vasorelaxation. This lack of a correlation with markers of total body fat/fat distribution suggests that leptin resistance may not extend to the vasculature. CONCLUSION: Leptin is a vasoactive peptide in human SV and internal mammary artery. Its action is not nitric oxide or endothelial-dependent. Markers of body fat did not correlate with leptin-mediated vasodilatation, raising the intriguing possibility of selective resistance to leptin's actions.     

Leptin and coronary heart disease: A systematic review and meta-analysis

Introduction

Leptin, an adipose tissue-derived hormone, plays a central role in regulating human energy homeostasis. The role of leptin in regulating blood pressure, activating the sympathetic nervous system, insulin resistance, platelet aggregation, arterial thrombosis, angiogenesis, and inflammatory vascular responses suggests that leptin may have a close relationship with the development of coronary heart disease (CHD). However, no conclusive data are available to determine the association between leptin and CHD.

Methods

The PubMed, EMBASE and Cochrane databases were surveyed for original studies describing the association between leptin and CHD outcome from the date of publication of each database through March 2013. The data were extracted by two investigators independently.

Results

The meta-analysis reported here was comprised of eight original articles with a total of 21,064 participants (10,842 men, 10,222 women) and 2053 CHD events. The odds ratio for the sociodemographic-adjusted study reported here was 1.57 (95% confidence interval, 1.14–2.16) and 1.72 (95% confidence internal, 1.03–2.87) in males and females, respectively. Further adjustment for additional cardiovascular risk factors resulted in an odds ratio of 1.36 (95% confidence interval, 0.98–1.88) in males and 1.50 (95% confidence interval, 0.93–2.42) in females. Sensitivity analysis restricted to sociodemographics-adjusted studies with high methodological quality indicated an estimate of 1.47 (95% confidence internal, 1.06–2.04) in males and 1.85 (95% confidence internal, 0.61–5.63) in females. Sensitivity analysis restricted to cardiovascular risk factor-adjusted studies showed no significant differences in both males and females.

Conclusion

The results of the meta-analysis represents the most precise and accurate estimate of the relationship between leptin and CHD. Although the associations of leptin and CHD were not statistically significant both in male and female overall, males with high levels of leptin should be paid more attention to. Our findings highlight the need for additional well-designed and gender-specific prospective studies to evaluate the role of leptin on the development of CHD.     

The use of coronary artery calcium scanning in detection and risk stratification of coronary artery disease

Coronary artery calcium (CAC) scan can be obtained using chest computed tomography, with no use of contrast agents, and with a relatively low radiation exposure. The mere absence of calcium is associated with a good prognosis in asymptomatic subjects and in patients at low to medium risk of coronary artery disease. CAC can be quantified in different ways, with higher scores being associated with a higher cardiovascular risk. CAC carries both diagnostic and prognostic information over and above that determined by classical risk factors. This paper presents the overview of the current use of CAC scanning, its advantages and limitations, as well as potential future applications.     

95例拟诊冠心病心绞痛患者冠状动脉造影分析

目的:总结95例临床拟诊冠心病心绞痛患者的冠状动脉造影结果,分析其临床症状及其心电图ST-T改变与冠状动脉造影确诊冠心病的相关性。方法:从发作性胸痛、胸闷为主诉或伴心电图ST-T改变的患者中,筛选出符合或疑似心绞痛,并经心脏超声、胸片检查排除了其他心脏病患者95例,其中典型心绞痛36例;疑似心绞痛的非典型胸痛59例;伴有ST-T改变者87例(缺血型改变25例、非特异性改变62例)。分别接受选择性冠状动脉造影。血管内径狭窄≥50%为造影阳性,诊断冠心病的依据。结果:95例患者造影阳性的45例,其中36例典型心绞痛造影者阳性34例(伴ST-T典型缺血型改变23例、非特异性改变者10例、无改者1例),阳性率94.44%;59例非典型胸痛造影阳性11例(伴非特异性ST-T改变),阳性率18.64%。两组阳性率有显著差异(P<0.01)。结论:典型心绞痛患者冠脉造影诊断冠心病相关性高,非典型胸痛或心电图非特异性ST-T改变患者冠脉造影诊断冠心病阳性率低。     

颈动脉粥样硬化与冠心病关系的研究

目的:研究颈动脉粥样硬化与冠心病的关系。方法:对301例冠状动脉造影的患者作双侧颈动脉超声检查,根据冠脉造影结果分为正常组及冠心病组,冠心病组根据冠状动脉病变支数再分为一支病变组,二支病变组,三支病变组3个亚组。测量颈总动脉后壁内中膜厚度(IMT),斑块厚度,计算斑块积分及粥样斑块发生率。结果:(1)冠心病组IMT,斑块积分及斑块发生率明显高于正常对照组(P<0.01)。(2)随冠脉病变支数增加,斑块积分及IMT增加,亚组比较有显著性差异(P<0.01)。(3)以IMT>0.85mm和(或)出现粥样斑块预测冠心病,特异性75.3％,敏感性84.6％,阳性预测率88.4％。结论:通过颈动脉超声检查可为冠心病的诊断提供依据。     

老年人冠状动脉疾病的外科治疗

目的探讨老年人冠状动脉疾病外科治疗的疗效。方法３５例老年患者接受了冠状动脉旁路移植术。按ＮＹＨＡ心功能分级,Ⅲ级１７例,Ⅳ级１８例。其中３支血管病变２４例,左主干病变６例;左室射血分数小于５０％者２５例。结果人均移植血管３．１根,无手术死亡。术后所有患者心绞痛均消失,心功能恢复至Ⅰ级者３３例,Ⅱ级２例。随访３～６４个月,平均３７个月,无死亡。结论对于老年冠状动脉疾病患者,冠状动脉旁路移植术是一种安全、有效的治疗方法。     

微量尿蛋白与冠状动脉病变相关性研究

目的：分析微量尿蛋白与冠状动脉病变程度和范围的相关性。方法：入选连续179例冠状动脉造影患者,根据尿白蛋白肌酐比值(UACR)分为微量尿蛋白组(30～300μg/mg,n=43)和对照组(UACR＜30μg/mg,n=136)。比较两组冠状动脉造影结果差异,同时分析微量尿蛋白与冠状动脉病变之间的相关性。结果：与对照组相比,微量蛋白尿组高血压、糖尿病患者多见,且其造影阳性率(46．51%比30．15%,P＜0．05)、多支冠状动脉病变发病率(30．23%比8．82%,P<0．01)显著增高。结论：微量蛋白尿患者更易发生严重的冠状动脉病变。     

绝经与女性冠心病关系研究

目的：研究绝经后冠心病（CAD）女性及无冠心病女性血脂水平是否存在差异．探讨激素、血脂对女性冠心病的影响。方法：以39例经冠脉造影证实有一支以上主要冠状动脉狭窄≥50％的绝经后女性CAD患者为CAD组．40例经造影冠脉无明显狭窄的绝经后女性为正常对照组,测定所有对象的总胆固醇（TC）、甘油三脂（TG）、脂蛋白-a[LP（a）]、低密度脂蛋白胆固醇（LDL—C）、高密度脂蛋白胆固醇（HDL—C）、载脂蛋白（Apo）A、ApoB及B／A比值,以放免法测定雌激素（E2）、雄激素（T）、卵泡刺激素（FSH）、黄体生成素（LH）。对两组结果进行比较．并作Logistic多元回归分析。结果：①CAD组的TG、TC、LDL-C、LP（a）和ApoB水平均高于正常对照组,但无显著差异,CAD组的HDL-C及ApoA水平均显著低于正常对照组[（0．85±0．52）mmol／L：（1.23±0．54）mmol／L．（1．24±0．24）mmol／L：（1．86±0．33）mmol／L．P均〈0．05];②CAD组的E2、LH水平[（11．99±6．81）ng／ml,（22．33±13．45）mIU／ml]显著低于正常对照组[（15．40±5．41）ng／ml,（35．96±23．39）mIU／ml]。P〈0．05～〈0．01;③经Logistic多元回归分析：ApoB、HDL-C、E2和LH是对女性绝经后对冠心病有影响的因素（β=3．592,-1．496,-0．183,-0．056,P均〈0．01）。结论：HDL-C、E2和LH是绝经后女性免于冠心病的保护因素。血脂水平对绝经后女性冠心病的发生有一定影响。     

冠心病合并肾动脉狭窄危险因素及临床意义

目的　探讨冠心病合并肾动脉狭窄发病率及危险因素 ,以及冠状动脉造影同时行肾动脉造影的必要性。方法　对 114例接受冠状动脉造影患者同时行肾动脉造影。结果　 114例患者中 ,肾动脉狭窄发病率 18 4% ,经冠状动脉造影证实的 77例冠心病中肾动脉狭窄发病率 2 6 % ,冠状动脉造影正常的 37例中肾动脉狭窄发病率 2 7% ,冠心病患者中肾动脉狭窄发病率明显高于非冠心病组(P <0 0 1)。结论　冠心病患者有较高的肾动脉狭窄的发生率 ,应该在冠状动脉造影明确冠状动脉病变后 ,常规行肾动脉造影。     

Rheumatoid arthritis,periodontal disease and coronary artery disease

Rheumatoid arthritis (RA), periodontal disease (PD), and coronary artery disease (CAD) are common chronic inflammatory diseases. RA is associated with accelerated vascular risk resulting in an increased prevalence of CAD with attendant early mortality and excess morbidity. RA and PD have a common pathobiology. Accordingly, the aim of this study was to evaluate the association between RA, PD, and CAD and the influence of systemic inflammatory factors. A total of 100 active RA patients of which 50 had established CAD and 50 had no CAD were assessed for PD. All subjects underwent a clinical, cardiac, dental, laboratory, and radiological evaluation. Blood samples were obtained, and the level of high sensitivity C-reactive protein (hs-CRP), total white blood counts (WBC), erythrocyte sedimentation rate (ESR), fibrinogen and tumor necrosis factor (TNF) alpha, total cholesterol (TC), and high density lipoprotein (HDL) were assayed. The findings of this study demonstrated an association between RA, PD, and CAD. The RA patients with CAD had significantly more PD than RA patients without CAD. The inflammatory markers, hsCRP, ESR, WBC, fibrinogen, and TNF-α, were raised in all patients but were significantly higher in RA patients with CAD who also had PD. HDL levels were lower in RA patients with CAD when compared to RA patients without CAD. Evidence from this study shows an association between RA, PD, CAD, and systemic levels of the inflammatory mediators. The implication is that inflammation may be the central link between the chronic inflammatory, autoimmune disorders, and atherosclerosis. An erratum to this article can be found at