H型高血压的研究进展

同型半胱氨酸（homocystein，HCY）是蛋氨酸脱甲基产生的中间代谢物，通常血浆HCY水平在10μmol/L以上称为高同型半胱氨酸血症（ HHCY）。 H型高血压是指血浆HCY水平在10μmol/L以上的原发性高血压。高血压、高HCY双重危险因素显著增加了心脑血管事件风险。该文综述了H型高血压的定义、HCY的代谢途径、HCY在血浆中的存在形式以及H型高血压的临床意义和防控策略的研究进展，以期提高对H型高血压的关注，并最终降低心脑血管事件风险。     

H型高血压的诊疗研究进展

原发性高血压是中老年人的常见病、多发病,是当前心脑血管疾病死亡的主要原因。伴有血浆同型半胱氨酸（Hcy）升高的原发性高血压即H型高血压,约占我国成年人高血压的75％。大量研究表明,高同型半胱氨酸血症是冠状动脉硬化性心脏病、脑卒中等心脑血管疾病的危险因素,从而使H型高血压成为诱发各种心脑血管疾病,尤其是脑卒中疾病的元凶。通过对相关文献研究发现,H型高血压的治疗需降压与降低血浆Hcy相结合,而依那普利叶酸片可起到双重效应,并可减少心脑血管事件的发生,从而为临床治疗H型高血压、预防心脑血管疾病提供了新的理论依据。     

H型高血压研究进展

H型高血压是伴有血浆同型半胱氨酸升高的原发性高血压,约占我国成年人高血压的75％,与脑卒中及其他心血管疾病密切相关。降低高血压患者同型半胱氨酸水平对预防卒中有重要意义。     

解读H型高血压

H型高血压是伴有血浆同型半胱氨酸升高的原发性高血压,约占我国成年人高血压的75%,与脑卒中及其他心血管疾病密切相关,可能是一个重要的、独立的危险因素。治疗H型高血压时应同时降低血压及血浆同型半胱氨酸的水平,目前的循证医学证据支持依那普利叶酸片在治疗H型高血压中的运用,但仍需大规模的前瞻性研究证实其有效性及安全性。     

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同型半胱氨酸升高是心脑血管疾病的独立预测因素,且与脑卒中关系更密切。伴有血浆同型半胱氨酸浓度升高(>10μmol/L)的高血压被定义为H型高血压,约占我国成年高血压患者的75%。H型高血压的治疗应双管齐下,同时降低血压和血浆同型半胱氨酸浓度。降低同型半胱氨酸最有效的方法是补充叶酸,但同型半胱氨酸降低后是否减少了卒中、冠心病等心脑血管事件仍存在着争议,目前倾向于在一级预防人群中可能有益。携带MTHFR-C677TT基因型的H型高血压患者基线血浆同型半胱氨酸高,可能需强化治疗。     

H型高血压与冠心病、脑梗死的关系研究

目的探讨H型高血压与冠心病、脑梗死的关系。方法选取我院2012年10月—2013年9月收治的H型高血压患者136例,根据冠状动脉造影、颅脑MRI检查结果分为4组:H型高血压组62例,冠心病组32例,脑梗死组30例,冠心病并脑梗死组12例。测量各组患者血压,测定其血浆同型半胱氨酸水平、血脂、血糖等。结果单因素分析结果显示,各组血压、血糖及血浆总胆固醇、三酰甘油水平比较,差异均无统计学意义(P0.05);冠心病组、脑梗死组、冠心病并脑梗死组血浆同型半胱氨酸水平高于H型高血压组,冠心病并脑梗死组高于冠心病组、脑梗死组(P0.05)。直线相关性分析结果显示,高血压患者血浆同型半胱氨酸水平与冠状动脉狭窄程度、脑梗死灶大小均呈正相关(r=0.780、0.802,P0.05)。多因素Logistic回归分析结果显示,血浆同型半胱氨酸水平升高是冠心病〔OR=4.235,95%CI(1.386,16.852),P=0.014〕、脑梗死〔OR=3.086,95%CI(1.003,13.206),P=0.047〕的独立危险因素。结论高血压患者血浆同型半胱氨酸水平升高是冠心病、脑梗死的独立危险因素,H型高血压与冠心病、脑梗死密切相关。     

中国H型高血压人群基因型特点

原发性高血压是当前心脑血管疾病发病的重要危险因素.伴有高同型半胱氨酸血症（一般指Hcy≥10μmol/L）的原发性高血压,称为H型高血压.研究表明,高血压和血浆Hcy升高在导致心脑血管疾病上具有协同作用.Hcy是蛋氨酸代谢过程中的重要中间产物,其水平与性别、年龄、人种、营养因素、药物、疾病状态、遗传因素等有关,其中遗传是一个非常重要的因素.     

瘦素、抵抗素与H型高血压患者血管内皮功能的相关性研究

正高同型半胱氨酸血症是冠心病、脑卒中等心血管疾病的危险因素,伴有血浆同型半胱氨酸(homocysteine,Hcy)水平升高的高血压被定义为"H型"高血压~[1]。根据这个标准,我国有75%以上的原发型高血压患者可归于"H型"高血压~[2],针对"H型"     

"H型"高血压与老年复发性脑梗死的关系

高血压、糖尿病等为脑卒中危险因素,高同型半胱氨酸血症(Hhcy)也为脑梗死独立危险因素;我国75%的高血压患者伴血浆同型半胱氨酸(Hcy)水平升高,伴血浆Hcy≥10μmoL/L的原发性高血压被定义为"H型"高血压<'[1]>.本文拟探讨"H型"高血压与老年复发性脑梗死的关系.     

老年H型高血压与认知功能障碍的关系

目的 探讨老年原发高血压伴有血浆同型半胱氨酸增高（H型高血压）与认知功能障碍的关系。方法选择2011年8月～2013年2月在中国医科大学附属第一医院老年病科住院的原发高血压患者150例,根据血浆同型半胱氨酸（Hcy）的检测值分为非H型高血压组（Hcy＜10 μmol/L）40例,H型高血压1组（10 μmol/L≤Hcy＜20 μmol/L）60例,H型高血压2组（Hcy≥20 μmol/L）50例。采用简易精神状态量表（MMSE）,蒙特利尔认知评估中文版（MoCA）和日常生活能力量表对各组患者进行认知功能评定。根据MMSE评分及日常生活能力量表评分,将H型高血压患者分为认知功能正常组22例,轻度认知功能障碍组54例,及认知功能障碍组34例。结果 与非H型高血压组相比较,H型高血压1组及H型高血压2组的空腹血糖、餐后2 h血糖、血浆Hcy及血尿酸水平显著升高,MMSE评分及MoCA评分降低;与H型高血压1组相比较,H型高血压2组的血肌酐、餐后2 h血糖及血浆Hcy水平显著升高,MMSE评分及MoCA评分降低。老年H型高血压患者MoCA评分与餐后2 h血糖及血浆Hcy水平呈显著负相关。结论 老年H型高血压患者更易发生认知功能损害,且认知功能损害的程度与血浆Hcy水平呈正相关。     

高血压患者血浆同型半胱氨酸水平与危险分层的关系

目的观察高血压不同危险分层患者血同型半胱氨酸（homocysteine,HCY）水平的变化情况,以探讨高血压患者血HCY值变化的临床意义。方法选择90例住院的高血压患者,按《中国高血压防治指南》（2005年修订版）的危险分层标准,分为3个组：Ⅰ组（中危组）、Ⅱ组（高危组）、Ⅲ组（极高危组）。分别检测其外周血HCY水平并进行组间比较。结果随着危险程度的增高,血HCY的浓度也逐渐升高,而极高危的患者则明显的升高,Ⅰ组与Ⅲ组、Ⅱ组与Ⅲ组HCY水平间差异均有统计学意义（P〈0．05）。血HCY浓度与高血压的危险程度呈正相关。结论高血压患者血HCY值与高血压患者的危险等级密切相关,血HCY值有助于判断高血压患者发生心、脑、血管意外的危险性及脏器受伤的程度,对高血压的预防、诊断和治疗具有一定的临床指导意义。     

中医药治疗高血压病的作用机制研究概况

从肾素-血管紧张素-醛固酮系统、血浆心钠素与内皮素、降钙素基因相关肽等心血管内分泌因子、血液流变学及血脂、氧自由基、胰岛素抵抗、同型半胱氨酸等方面对中医药防治高血压病的作用机制进行了综述,揭示中医药治疗该病的作用机制是多方面的,以期从基因水平上深入研究中医药防治高血压病的作用机制.     

H型高血压的病因及发病机制

H型高血压在我国发病率很高。其同型半胱氨酸水平与年龄、性别、人种、营养及合并疾病等多个因素有关;发病机制涉及到血管内皮细胞功能障碍、血管平滑肌细胞增殖、血脂异常、凝血系统异常及胰岛素抵抗等多个方面。理解这些基本影响因素,将为H型高血压的防治起到重要作用。     

H型高血压临床研究进展

高血压合并高同型半胱氨酸血症是发生脑卒中的重要危险因素,控制血压的同时降低同型半胱氨酸可减少脑卒中发生率。目前已知降低同型半胱氨酸最安全有效的方法是补充叶酸,早期关注同型半胱氨酸水平并检测基因型进行积极干预,将推动我国高血压个体化防治的发展,降低高危患者脑卒中风险。     

Vitamins,homocysteine and cardiovascular risk

A raised plasma level of the amino acid homocysteine is associated with increased risk of cardiovascular disease. This association may be causal—it is biologically plausible, fairly strong, graded, and an increase in plasma homocysteine preceeds the onset of vascular disease.Plasma homocysteine levels are controlled by genetic and nutritional factors, notably folate, vitamin B12 and vitamin B6 intakes. Folic acid in particular lowers plasma homocysteine levels by about 25%. It is not known if this cheap and safe treatment reduces vascular disease risk. Current randomized control trials are addressing this issue, and proof or otherwise of causality must await their results.Homocysteine may also interact with conventional risk factors such as smoking to substantially increase their effect on risk. Thus meticulous risk factor control may be particulary important in subjects at high total cardiovascular risk who also have a raised plasma homocysteine level, and folic acid supplementation may be considered in such individuals.     

Blood levels of homocysteine and increased risks of cardiovascular disease: causal or casual?

BACKGROUND: Accumulating data from epidemiological studies suggest that individuals with elevated blood levels of homocysteine have increased risks of cardiovascular disease. We reviewed the currently available evidence of an association between homocysteine and cardiovascular disease and examined whether the strength of the evidence varies according to study design. METHODS: We used a computerized MEDLINE literature search, 1966 through September 1998, to identify all epidemiological studies that examined the relationship of homocysteine level with risks of coronary heart or cerebrovascular disease. Two measures of plasma homocysteine level and its association with risk of cardiovascular disease were extracted: mean homocysteine level in cases and controls, and relative risk of cardiovascular disease for elevated homocysteine level. RESULTS: A total of 43 studies were reviewed. Most crosssectional and case-control studies indicated higher mean homocysteine levels (either fasting or after methionine load) and/or a greater frequency of elevated homocysteine level in persons with cardiovascular disease as compared with persons without cardiovascular disease. Results of most prospective studies, however, indicated smaller or no association. The few prospective studies that reported a positive association between homocysteine level and risks of cardiovascular disease included patients with preexisting vascular disease. CONCLUSIONS: In contrast to cross-sectional and case-control studies, results of prospective studies indicated less or no predictive ability for plasma homocysteine in cardiovascular disease. Instead, elevated homocysteine level may be an acute-phase reactant that is predominantly a marker of atherogenesis, or a consequence of other factors more closely linked to risks of cardiovascular disease. Randomized trials are necessary to test reliably whether lowering homocysteine levels will decrease risks of cardiovascular disease.     

Relationship of systolic blood pressure with plasma homocysteine: importance of smoking status

BACKGROUND: Elevated plasma homocysteine is a risk factor for cardiovascular disease. Elevations in plasma homocysteine occur in both smokers and hypertensives, but the combined effect of smoking and hypertension on homocysteine is unknown. METHODS: Resting plasma homocysteine levels and blood pressure were determined in 56 normotensives (12 smokers) and 20 essential hypertensives (10 smokers). RESULTS: Plasma homocysteine was significantly higher in all smokers versus all non-smokers (9.46 +/- 0.5 versus 7.9 +/- 0.5 micromol/l, P = 0.041) by two-way ANOVA, and was also significantly higher in all hypertensives versus all normotensives (9.8 +/- 0.6 versus 7.6 +/- 0.4 micromol/l, P = 0.004). There was no interaction between the effects of hypertension and smoking on plasma homocysteine. Hypertensive smokers had significantly higher plasma homocysteine than either normotensive non-smokers (10.65 +/- 0.84 versus 7.05 +/- 0.26 micromol/l), hypertensive non-smokers (7.88 +/- 0.64 micromol/l) or normotensive smokers (8.36 +/- 0.5 micromol/l). In subjects overall, homocysteine levels were correlated (r = 0.306, P = 0.015) with systolic blood pressure but not with diastolic (r = 0.186). This relationship was also significant in smokers, but not non-smokers. Furthermore, subjects in the highest quintile for plasma homocysteine had significantly higher systolic BP than those in the lowest quintile. This effect was not observed when smokers were removed from the analysis. CONCLUSION: Smoking compounds the modest effect of hypertension on plasma homocysteine. The strong relationship between systolic blood pressure and homocysteine that exists only in smokers suggests that smoking-induced homocysteine elevations may raise systolic blood pressure. We speculate that smoking compounds the risk of cardiovascular disease in hypertensives, in part, by elevating homocysteine.