伴同型半胱氨酸升高的高血压——“H型”高血压

高同型半胱氨酸血症是冠状动脉粥样硬化性心脏病、脑卒中等心脑血管疾病的危险因素,伴有血浆同型半胱氨酸水平升高的高血压被定义为＂H型＂高血压,约占我国成年高血压患者的75%。＂H型＂高血压的治疗应同时降低血压和血浆同型半胱氨酸的水平。降低同型半胱氨酸最有效的方法是补充叶酸,并可能减少心脑血管事件的发生。     

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。     

血管性痴呆患者认知功能障碍严重程度与H型高血压和血尿酸水平的相关性

目的 分析血管性痴呆患者认知功能障碍严重程度与H型高血压和血尿酸水平的相关性。方法 本研究纳入2018年6月-2020年6月就诊于海安市人民医院神经内科的血管性痴呆患者400例及体检中心的认知功能正常对象400人。分析血管性痴呆患者和认知功能正常对象的H型高血压检出率、同型半胱氨酸(Hcy)水平以及血尿酸水平的差异。按照认知功能评分将血管性痴呆患者分为轻度痴呆组(n=140)、中度痴呆组(n=140)以及重度痴呆组(n=120),进一步比较各组的H型高血压检出率、Hcy水平和血尿酸水平的差异,分析各组血尿酸和Hcy水平与认知功能的相关性。采用等级logistic回归模型分析血管性痴呆患者认知功能的影响因素。结果 血管性痴呆患者的H型高血压检出率和血Hcy水平高于认知功能正常者(P<0.05);不同痴呆程度组的H型高血压检出率、Hcy以及血尿酸水平差异有统计学意义(P<0.05)。不同痴呆程度组的简易精神状态量表(MMSE)评分与Hcy水平呈负相关,与血尿酸水平呈正相关;年龄(OR=1.026,95%CI 1.002～1.051)、H型高血压(OR=1.038,95%CI 1...     

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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。     

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。     

2015年心血管领域大事记

<正>1高血压脑卒中预防进展脑卒中是中国居民死亡的最主要原因,也是世界第二死亡原因[1]。研究发现,伴血浆同型半胱氨酸(Hcy)升高/叶酸缺乏的原发性高血压(H型高血压)是脑卒中高发的主要危险因素[2]。独特的遗传背景及其与低叶酸水平的相互作用是我国高血压患者脑卒中高发的重要因素。不同于美国整体人群谷物强化叶酸的公共卫生措施[3],中国在饮食特点、烹饪方式等方面均无强化叶酸饮食,导致叶酸水平普遍偏     

氨氯地平联合叶酸降压、降同型半胱氨酸的疗效观察

<正>心脑血管疾病是目前我国面临的重大公共卫生问题之一,在导致我国脑卒中发生的可控危险因素中,高血压和血浆同型半胱氨酸(Homocysteine,Hcy)升高位居前列,大量研究证实,高血压与血浆Hcy升高在导致心脑血管事件上具有协同作用,Hcy升高是我国高血压患者脑卒中高发的重要原因,因此降压同     

腔隙性脑梗死患者同型半胱氨酸与血管性认知障碍的关系

<正>血管性认知障碍(VCI)指由脑血管病及脑血管病危险因素引起的认知功能障碍~([1]),包括非痴呆性VCl(VCIND)和血管性痴呆(VD)~([2])。早期诊断VCIND并控制其危险因素对于延缓痴呆的进展具有重要意义。腔隙性脑梗死(LI)是脑小血管病(CSVD)的一种常见类型,目前认为皮质下多发性LI是造成认知障碍的重要原因之一~([3])。高同型半胱氨酸血症(HHcy)被认为是脑血管病的独立危险因素,与脑梗死的发生密切相关。本文旨在对LI与VCI的关系及同型半胱氨酸(Hcy)在VCI发生过程     

Vascular dementia: the dubious disease

Vascular dementia is not a disease or even a clearly defined disorder. It is a construct, which brings together very heterogeneous disturbances at the clinical, pathological and etiological levels. Due to the absence of neuropathologic diagnostic criteria, the frequency of associated degenerative pathology (mainly of Alzheimer type), and the heterogeneity of the construct, its clinical diagnosis remains questionable using various diagnostic criteria. The concept of vascular cognitive impairment (VCI) has been proposed as a substitute for vascular dementia to provide some clarification about the relationship between ischemic brain lesions and cognitive dysfunction. Its main interest is to allow diagnosis and treatment of minor cognitive deficits associated with ischemic brain lesions before the occurrence of dementia. Clinical and neuropsychological manifestations of VCI are of fronto-subcortical type, quite distinct from those of Alzheimer's disease. From a practical point of view, the main point is to find out and to treat the vascular risk factors which cause cognitive deficits by themselves or increase those associated with Alzheimer's disease.     

Diabetes mellitus and dementia

Patients with diabetes are at increased risk of developing cognitive impairment in comparison with the general population. Diabetes mellitus increases the risk of dementia (vascular and/or neurodegenerative). Diabetes accelerates the progression from mild cognitive impairment to dementia. It has been estimated that type 2 diabetes or impairment of glucose metabolism might be present in up to 80% of patients with Alzheimer disease. The cognitive dysfunction is associated with poorer ability in diabetes self-care and decreased adherence to antidiabetic treatment.     

皮质下缺血性血管性痴呆的诊断和治疗

皮质下缺血性血管性痴呆主要以小血管疾病为病因,包括腔隙状态、关键部位梗死性痴呆和Binswanger综合征,临床上表现为皮质下综合征和认知障碍.积极诊断和治疗皮质下缺血性血管性痴呆有助于降低老年人认知障碍的发病风险.     

Hypertension and dementia

Hypertension is one of the principal risk factors for cerebrovascular diseases. Several epidemiologic studies have also indicated a positive correlation between cognitive decline or dementia and blood pressure level. Indeed, the results of most longitudinal studies show that cognitive functioning is often inversely proportional to blood pressure values measured 15 or 20 years previously. Cerebral infarcts, lacunae, and white matter changes are implicated in the pathogenesis of vascular dementia, but may also favor the development of Alzheimer’s disease. Microcirculation disorders and endothelial dysfunctions are also advanced to explain the deterioration in cognitive functions in hypertensive subjects. Data from recent therapeutic trials open the way to the prevention of dementia (vascular or Alzheimer’s type) by antihypertensive treatments and must be confirmed by other studies.     

Hypertension, Brain Damage and Cognitive Decline

Loss of cognitive function is one the most devastating manifestations of ageing and vascular disease. Cognitive decline is rapidly becoming an important cause of disability worldwide and contributes significantly to increased mortality. There is growing evidence that hypertension is the most important modifiable vascular risk factor for development and progression of both cognitive decline and dementia. High blood pressure contributes to cerebral small and large vessel disease resulting in brain damage and dementia. A decline in cerebrovascular reserve capacity and emerging degenerative vascular wall changes underlie complete and incomplete brain infarcts, haemorrhages and white matter hyperintensities. This review discusses the complexity of factors linking hypertension to brain functional and structural changes, and to cognitive decline and dementia. The evidence for possible clinical markers useful for prevention of decreased cognitive ability, as well as recent data on vascular mechanism in the pathogenesis of cognitive decline, and the role of antihypertensive therapies in long-term prevention of late-life cognitive decline will be reviewed.     

Hypertension as a risk factor of dementia and cognitive decline in the elderly

Management of dementia and cognitive decline is a major issue in geriatrics. Since the average age of society is advancing and patients of dementia are increasing, it is important to remove risk factors of dementia and cognitive decline in order to maintain quality of life in the elderly and to save cost of medicine and care. While hypertension has been known to be a risk factor of cerebrovascular events and vascular dementia, recent studies show that midlife hypertension is also a risk factor of cognitive decline and Alzheimer's disease in late life. Clinical trials and retrospective observation studies also show that treatment of hypertension decreases the risk of Alzheimer's disease. These issues are also related with the consideration of vascular factors in Alzheimer's disease. The white matter lesion as a consequence of hypertension and its meaning in Alzheimer's disease are also discussed.     

Atrial Fibrillation and Cognitive Function: JACC Review Topic of the Week

Numerous vascular risk factors and vascular diseases contribute to cognitive impairment and dementia. Many studies and registries show an association of atrial fibrillation (AF) with cognitive impairment, cognitive decline, and dementia. This is true for vascular dementia and Alzheimer's disease. The assumed multifactorial mechanisms include ischemic stroke, both apparent and silent, cerebral microinfarcts, cerebral hemorrhage, and reduced cerebral blood flow. A number of retrospective observational and prospective studies support that anticoagulation in patients with AF may reduce the risk of cognitive decline and dementia. This holds for both vitamin K antagonists (e.g., warfarin) and direct oral anticoagulants. However, it still remains unproven if anticoagulation reduces cognitive decline and dementia in AF patients based on randomized trials.     

Heart disease and vascular risk factors in the cognitively impaired elderly: implications for Alzheimer's dementia.

The term "cardiogenic dementia" was introduced a few decades ago to indicate an alteration of consciousness and cognition due to heart disease. Although this term is now disused, the relationship between cardiovascular disease and cognitive impairment is currently of great interest, not only for its potential therapeutic implications. but also for the recently recognized important role that vascular factors appear to play in Alzheimer's disease. The aims of this review are therefore 1) to show data supporting the role of cardiac disease--namely congestive heart failure, myocardial infarction and atrial fibrillation--and other vascular risk factors--i.e., hypertension and diabetes--in the development or worsening of cognitive impairment; 2) to highlight recent observations on the relationship between presence and severity of congestive heart failure/ myocardial infarction/atrial fibrillation and Alzheimer's disease: and 3) to uncover the type of studies needed in this field in order to facilitate a more precise algorithm of dementia prevention as well as intervention in demented patients with cardiovascular disease.     

Hypertension, cognitive decline and dementia

Dementia is one of the most common neurological disorders in the elderly. Aging is associated with a large increase in the prevalence and incidence of degenerative (Alzheimer's disease) and vascular dementia, leading to a devastating loss of independence. In view of increasing longevity of populations worldwide, prevention and treatment of dementia has turned into a major public health challenge. In the past decade, longitudinal studies have shown a close association between high blood pressure in middle age, cognitive decline and dementia, including Alzheimer's disease, in the late life. Pathophysiologically, a summation of cerebrovascular damage, white matter changes and pre-existing asymptomatic Alzheimer's brain lesions may lead to dementia, even when each type of lesion individually is not sufficiently severe to cause it. Longitudinal studies assessing the beneficial role of antihypertensive drugs on cognitive decline and dementia have produced promising results. There are few randomised placebo controlled studies, although some of these have produced positive results. Results of three recent meta-analyses are inconsistent, possibly due to methodological issues. Further long-term randomised trials, designed especially to assess a link between antihypertensive therapy and cognitive decline or dementia are therefore needed.     

Microbleeds in vascular dementia: Clinical aspects

Microbleeds are small dot-like lesions which can be appreciated on gradient echo, T2*-weighted magnetic resonance images as hypointensities. They are considered as an expression of small vessel disease on MRI, next to lacunes and white matter hyperintensities (WMH). Microbleeds are relatively common in vascular dementia, with reported prevalences between 35% and 85%. In the context of vascular dementia, microbleeds are mainly thought to result from hypertensive vasculopathy, but the frequent co-occurrence of lobar microbleeds suggests that neurodegenerative pathology and/or cerebral amyloid angiopathy is also of importance. The presence of multiple microbleeds in vascular dementia or in patients with vascular cognitive impairment is related to worse performance on cognitive tests, mainly in psychomotor speed and executive functioning. They may have some predictive value in terms of predicting development of (vascular) dementia, mortality and disability. Data on the occurrence of stroke and post-stroke dementia in patients with microbleeds are to date not available. New definitions and diagnostic criteria for vascular dementia and vascular cognitive impairment are needed and should take into account microbleeds.