体位性高血压和体位性低血压的诊疗研究新进展

体位性高血压和体位性低血压与很多心血管疾病相关,但目前对其研究较少,发病机制、诊断标准、治疗等缺乏统一标准,需要进一步研究。     

体位性高血压研究进展

体位性血压改变(orthostatic blood pressurechange)是指由卧位变成直立位或者倾斜位时血压的变化[1].虽然目前一些研究观察坐位到立位的血压变化,但是不符合严格的定义.体位变化时,机体会产生一系列的适应性改变,在这一变化过程中,如不能维持血压基本稳定,就可能出现体位性低血压(orthostatic hypoten-sion,OH)或体位性高血压(orthostatic hypertension,OHT).     

体位性高血压调查

随着人们对原发性高血压认识的逐步深入,一些特殊类型的高血压如体位性高血压、神经解剖源性高血压、肥胖性高血压等已引起人们的重视。国外有人报道,体位性高血压约占高血压人群的10％,且多见于轻型与临界高血压者。为掌握体位性高血压在我国人群中的发生特点,进一步探讨其发生机制,进而采取针对性治疗,本所对50例中老年轻型和临界性高血压患者进行了调查,并同时调查150例中老年健康人作为对照。     

面色苍白又发慌,留心白色高血压

说到面色苍白,我们首先想到的就是贫血,因为贫血会导致皮肤因缺血而显得苍白。但同时,苍白的脸色也可能与高血压有关,而这种高血压跟贫血“沾亲带故”,临床上称为白色高血压。贫血和高血压并不矛盾白色高血压,顾名思义是指高血压伴面色苍白,通常是肾血管性和肾性高血压的特征。肾血管性高血压主要是由于一侧或双侧肾动脉主干或分支狭窄、闭塞所造成的高血压;而肾性高血压则是指肾脏疾病,如急、慢性肾小球肾炎,肾盂肾炎,多囊肾等引起的高血压。两种疾病各有不同之处,但均可导致肾功能不全,引起肾源性贫血。     

高血压的阶梯式治疗方案

在最近一项有关简化治疗干预控制高血压（STITCH）的研究中，研究人员RFeldman博士指出，一种简单的、阶梯式治疗方案比依据指导原则治疗更为有效。他认为，高血压容易诊断和可用许多有效的方法治疗，但只有1／3的这类病人成功地达到高血压控制，对治疗的非顺从性是一个关键问题。现有的高血压治疗指导原则的复杂性可能是有效治疗的一个障碍。     

老年人体位性高血压的流行病学研究

流调资料提供,体位性高血压在老年人群中占有一定比例。M.Berkman等人曾对200名平均80岁的老年人在直立状态下的血压升高做了初步研究,国内尚未见到有关报导。笔者在老年病普查中发现,相当一部份老年人在直立状态下血压升高并伴有一定症状。现将1,083名老年人中82例体位性高血压的有关调研资料分析如下。     

老年高血压药物治疗要点

老年高血压和青壮年高血压病在发病因及临床症状均有其不同的特点,治疗上有相应的特殊性,以下就三个问题作重点讨论。 一、老年高血压多由老年前期发病而来。但70岁后的高血压约半数是60岁以后发病。由于动脉硬化和主动脉弹性减退,尤以收缩期血压升高为特征,血压日内变化大,容易引起体位性低血压,常合并心、脑、肾及下肢血流障碍及糖、尿酸、血脂、电解质等代谢紊乱。其次由于动脉硬化可引起肾血管性高血压及伴主动脉关闭不全引起的高血压或者由于其它原因引起的继发性高血压应于治疗前给予鉴别。当55岁以后舒张期血压超过14.10KPa或者对药物治疗有效的高血压变为无反应,甚至联合三种以上降压药治疗仍不能使舒张期血压下降至13.30KPa以下,或     

探究社区高龄老人高血压的治疗现状及体位性高血压的相关因素

目的:研究社区高龄老人高血压的治疗现状及体位性高血压的相关因素。方法:此项研究对象为我院2018年1月至2018年12月高龄老人高血压患者,共计200例,予以高龄老人高血压患者问卷调查,进行随访血压观察、掌握其降压药物使用的状况、体位性低血压(OH)和高血压(OHT)等。结果:200例高龄老人高血压患者使用钙拮抗剂110(55.0%)例,血管紧张素转换酶抑制33(16.5%)例,血管紧张素受体抑制剂34(17.0%)例,利尿剂14(7.0%)例,Β受体阻滞剂7(3.5%)例,其他3(1.5%)例。结论:钙拮抗剂、血管紧张素受体抑制剂等目前普遍应用于高龄老人高血压的治疗中,利尿剂使用并不普及,体位改变会影响冠心病、糖尿病等疾病。     

老年高血压患者体位性低血压的护理风险分析及防范措施

目的探讨护理干预对老年高血压患者体位性低血压的防范作用,提出合理的预防措施以减少体位性低血压带来的危害。方法随机选取收治的老年高血压患者120例为研究对象,分为观察组与对照组,各60例,对观察组患者进行体位性低血压危险因素评估并给予护理干预,对照组给予一般护理,统计两组患者发生体位性低血压的发生率,统计卧位及蹲位起立时平均动脉压以及两组发生头昏目眩、恶心呕吐及摔倒等并发症情况。结果观察组老年高血压病患者体位性低血压发生率为11.7%,而对照组发生率为33.3%,差异具有统计学意义(P<0.05);观察组患者卧位及蹲位起立时平均动脉压均高于对照组,差异具有统计学意义(P<0.05);对照组患者发生头昏目眩、恶心呕吐及摔倒的比率高于观察组,差异具有统计学意义(P<0.05)。结论老年高血压患者发生体位性低血压的概率较高,应对老年高血压患者进行风险评估,采取相应预防护理措施,以降低体位性低血压的发生率,减少体位性低血压引起的并发症。     

住院老年患者体位性低血压发生率及相关危险因素初探

目的观察住院老年患者体位性低血压的发病情况及相关危险因素。方法以2009年7月～2011年12月间入住我科的60岁以上老年患者为研究对象,测定卧、立位血压(休息至少5min后的卧位,站立即刻,站立后3min的血压),并采集病史。结果共收集了112例患者的资料,平均年龄(78.23±16.53)岁,其中男42例,女70例。共有31例患者(27.68%)存在体位性低血压。这31例患者中,合并高血压、饮酒、肾功能衰竭、甲状腺功能减退的比率明显高于无体位性低血压患者,而年龄、性别、糖尿病、冠心病、脑卒中、癌症在体位性低血压与非体位性低血压组无显著差异。Logistic逐步回归分析发现高血压与饮酒患者发生体位性低血压的相对危险度(RR)分别为2.7(95%CI1.0～6.8,P=0.04)和3.3(95%CI0.98～9.47,P=0.02)。结论体位性低血压在住院老年患者中比较常见,高血压、饮酒是发生体位性低血压的相关危险因素。     

Prazosin update. A review of its pharmacological properties and therapeutic use in hypertension and congestive heart failure

Prazosin is an orally active post-synaptic selective alpha 1-adrenoreceptor antagonist that has been widely used in treating hypertension and congestive heart failure (CHF). Its role in the treatment of hypertension has previously been reviewed in this journal. Subsequent reports confirm its efficacy in treating mild to severe hypertension as a single agent or, more frequently, in combination with another antihypertensive agent and/or a diuretic. Recent studies of the metabolic effect of prazosin indicate that the drug may have a favourable effect on plasma lipids in hypertensive patients. Its recent use in treatment of congestive heart failure has shown prazosin to be comparable with nitroprusside in producing balanced arterial and venous dilation with generally sustained haemodynamic and clinical effects during long term therapy. Initial studies in Raynaud's phenomenon and in patients with aortic regurgitation or aortic stenosis or with mitral regurgitation are promising, but require confirmation from wider clinical experience. The drug has generally been well tolerated. The primary side effect of orthostatic hypotension can be largely avoided by beginning treatment with a low dose.     

Drug-induced orthostatic hypotension.

Drug-induced orthostatic hypotension is an important clinical problem. When symptomatic, it is poorly tolerated by the patient, and can be a cause for discontinuing treatment. It may have more serious consequences if it leads to syncope, falls and injury, or to sustained loss of perfusion of vital organs resulting in heart attack or stroke. Orthostatic hypotension is easily detected by procedures available to all physicians, who should maintain a high index of suspicion when prescribing drugs commonly known to cause this condition, especially in the elderly. Since the medical conditions calling for the use of these drugs are extremely prevalent, the screening and monitoring of orthostatic hypotension should be instituted as a routine precaution in appropriate patients. Hypertension affects two-thirds of elderly patients. Orthostatic hypotension is an infrequent adverse effect of most of the drugs in current use in the treatment of hypertension; it is, however, more common with alpha 1-blockers (first dose), adrenergic blockers and centrally acting drugs. Sudden loss of blood volume, or excess diuresis, may precipitate orthostatic hypotension in any hypertensive patient. Drugs used for the treatment of psychiatric illnesses are all associated with a significant incidence of orthostatic hypotension: phenothiazines, tricyclic antidepressants and monoamine oxidase inhibitors. Cardiovascular drugs associated with hypotension include dopamine agonists, antianginals and antiarrhythmics.     

Hypertension in the elderly: a Japanese perspective

Elderly individuals with hypertension show specific characteristics as a result of advancing arteriosclerosis, a high frequency of isolated systolic hypertension, increased pulse pressure and orthostatic hypotension. The necessity to treat hypertension in the elderly, including isolated systolic hypertension, has been demonstrated in many large-scale intervention trials. Young-old (65-74 years of age) hypertensive patients should be treated the same as nonelderly hypertensive patients. In old-old (75-84 years of age) patients with mild hypertension (140-159/90-99 mm Hg), the recommended target blood pressure (BP) is <140/90 mm Hg. In old-old (75-84 years of age) and oldest-old (> or =85 years of age) patients with systolic BP > or =160 mm Hg, cautious treatment is required. An intermediate target BP of <150 mm Hg is appropriate, followed by a final target BP of <140 mm Hg, if tolerated. Nonmedical therapy, such as salt restriction, exercise and weight reduction, is useful in the elderly. However, individualised management of nonmedical therapy is necessary to avoid deterioration of quality of life resulting from strict management of the patient's lifestyle. Diuretics, calcium channel antagonists, ACE inhibitors and angiotensin II type 1 receptor antagonists have been established as first-line antihypertensive drugs in the elderly. Use of combination therapy helps to achieve target BPs. The starting dose of each drug should be half the usual dose for nonelderly patients, and may be increased at intervals of >4 weeks, with achievement of the target BP in 3-6 months or longer. In hypertensive patients with co-morbid diseases, the target BP should be determined individually and antihypertensive drugs selected bearing in mind the patient's clinical circumstances. Avoiding hypoperfusion of target organs is very important in elderly hypertensive patients. When treating hypertension in elderly patients, the approach should be to identify individual pathophysiological characteristics and lower the BP cautiously and slowly.     

Placental nitric oxide formation and endothelium‐dependent vasodilation underlie pravastatin effects against angiogenic imbalance,hypertension in pregnancy and intrauterine growth restriction

Pre‐eclampsia and hypertensive disorders of pregnancy are frequently associated with foeto‐placental growth restriction, and that may be triggered by angiogenic imbalance and endothelial dysfunction. Impaired nitric oxide (NO) bioavailability seems to be involved in these pathophysiological changes observed in hypertensive pregnancy. Pravastatin has shown efficacy and to be safe during hypertension in pregnancy. However, NO involvement in pravastatin effects during maternal hypertension and foeto‐placental development is unclear. Therefore, we aimed to examine pravastatin effects on placental NO formation, endothelium‐dependent vasodilation, systolic blood pressure and foeto‐placental development in hypertensive pregnant rats. Biochemical determinants of angiogenesis and oxidative stress were also assessed. Pregnant rats were distributed into four groups: normal pregnancy (Norm‐Preg), pregnancy+pravastatin (Preg‐Prava), hypertensive pregnancy (HTN‐Preg) and hypertensive pregnancy+pravastatin (HTN‐Preg+Prava). Our results showed that pravastatin treatment blunts hypertension and foeto‐placental growth restriction. Also, increases in placental NO levels were found in the HTN‐Preg+Prava group. Pravastatin prevents impaired endothelium‐dependent acetylcholine‐induced vasodilation, exacerbated contractile response to phenylephrine and increases in oxidative stress in the HTN‐Preg+Prava group. Increased soluble fms‐like tyrosine kinase‐1‐to‐placental growth factor (sFlt‐1/PlGF) ratio is reversed by pravastatin treatment in the HTN‐Preg+Prava group. We conclude that NO formation and endothelium‐dependent vasodilation underlie pleiotropic effects associated with pravastatin treatment against hypertension in pregnancy, intrauterine growth restriction, vascular dysfunction and angiogenic imbalance.     

Pathophysiologic therapeutic targets in hypertension: a cardiological point of view

INTRODUCTION: Treatment of arterial hypertension can be a difficult exercise. Anti-hypertensive treatments need to be administered, keeping in mind the pathophysiological mechanisms and correlates at the base of arterial hypertension in the specific patient. AREAS COVERED: The common pathophysiological mechanisms at the base of hypertension and their undisputed mechanistic relationship with clinical events. Additionally, the mounting evidence showing that, from their changes, it may be possible to predict the clinical outcome of patients. Data was sourced from Medline and the Cochrane library. Which were searched from January 1986 to May 2011 to find relevant papers outlining the relation between hypertension, pathophysiology, medical treatment and side/adverse effects of anti-hypertensive drugs. EXPERT OPINION: It appears that the hypertensive patient in the cardiological context is often a subject with a 'complex' health status (e.g., glucose intolerant/diabetic carrier of serum lipids disorder) and as such, he/she should be treated in a 'holistic' pharmacological way. All the ancillary positive and negative effects of the administered drugs should not be dismissed. From a pathophysiological point of view, inhibitors of the renin-angiotensin-aldosterone system could be considered as the most appropriate drugs for the treatment of arterial hypertension and its correlates, especially in the high-risk patient.     

Clinical implication of morning blood pressure surge in hypertension

Cardiovascular events occur most frequently in the morning. The morning surge in blood pressure may be associated with hypertensive target organ damage and subsequent cardiovascular risk in hypertensive patients. In our prospective study on elderly hypertensive patients, the morning blood pressure surge (defined as the increase from the lowest blood pressure during sleep to the average of the first 2 h after waking) was significantly associated with silent hypertensive cerebrovascular disease and subsequent stroke risk. This association was independent of age and 24-h ambulatory blood pressure levels. In addition, even after controlling for these factors and status of silent cerebrovascular disease, the contribution of the morning blood pressure surge remained significant, and a 10 mmHg increase in systolic morning blood pressure surge increase the stroke risk by 22%. A related factor is orthostatic hypertension, which might be associated with increased sympathetic activity, and which is significantly associated with an increase in morning blood pressure surge and ambulatory blood pressure variability. A possible implication is that, in addition to strict blood pressure control, antihypertensive medication that targets exaggerated morning blood pressure may achieve more effective prevention of cardiovascular events in hypertensive patients.     

Angiogenesis and hypertension: the dual role of anti-hypertensive and anti-angiogenic therapies

Essential hypertension may be a consequence of structural and functional alterations of the microvascular network growth resulting partly from abnormal regulation of vascular endothelial growth factor (VEGF), one of the most potent known angiogenic factors. As data from clinical trials on anti-VEGF drugs are becoming available, it is increasingly recognized that VEGF, in addition to being a proliferation and migration factor, is also a maintenance and protection factor for endothelial cells, whose altered regulation may cause a disturbance of vascular homeostasis. Elevated VEGF levels in hypertensive patients were shown to correlate with cardiovascular risk, early microvascular and target organ damage; accordingly treatment of hypertension significantly reduced VEGF levels. Recently and in agreement with the theory that impaired angiogenesis can contribute to increased peripheral resistance and raised blood pressure (BP), an involvement of VEGF gene promoter polymorphisms in the pathophysiology of hypertension has been hypothesized. In the last decade, anti-VEGF drugs have been used in clinical practice, especially in the oncology field. This review will summarize the present understanding of the contribution of VEGF to neoangiogenesis in hypertension and its possible role as a marker of vascular damage. Given the well established effects that antihypertensive drugs exert on the vasculature beyond BP lowering (pleiotropic effects), we will also discuss the effects of antihypertensive treatment on circulating VEGF levels. The biological mechanism and clinical impact of hypertensive complications during anti-angiogenic treatments will also be reviewed.     

Treatment of acute severe hypertension: current and newer agents

Approximately 72 million people in the US experience hypertension. Worldwide, hypertension may affect as many as 1 billion people and be responsible for approximately 7.1 million deaths per year. It is estimated that approximately 1% of patients with hypertension will, at some point, develop a hypertensive crisis. Hypertensive crises are further defined as either hypertensive emergencies or urgencies, depending on the degree of blood pressure elevation and presence of end-organ damage. Immediate reduction in blood pressure is required only in patients with acute end-organ damage (i.e. hypertensive emergency) and requires treatment with a titratable, short-acting, intravenous antihypertensive agent, while severe hypertension without acute end-organ damage (i.e. hypertensive urgency) is usually treated with oral antihypertensive agents.The primary goal of intervention in a hypertensive crisis is to safely reduce blood pressure. The appropriate therapeutic approach of each patient will depend on their clinical presentation. Patients with hypertensive emergencies are best treated in an intensive care unit with titratable, intravenous, hypotensive agents. Rapid-acting intravenous antihypertensive agents are available, including labetalol, esmolol, fenoldopam, nicardipine and sodium nitroprusside. Newer agents, such as clevidipine and fenoldopam, may hold considerable advantages to other available agents in the management of hypertensive crises. Sodium nitroprusside is an extremely toxic drug and its use in the treatment of hypertensive emergencies should be avoided. Similarly, nifedipine, nitroglycerin and hydralazine should not to be considered first-line therapies in the management of hypertensive crises because these agents are associated with significant toxicities and/or adverse effects.     

Nebivolol: a review of its clinical and pharmacological characteristics

Nebivolol is a cardioselective lipophilic beta-blocker devoid of intrinsic sympathomimetic and membrane-stabilizing actions. The pharmacological profile differs from that of conventional cardioselective beta3-blockers in that it displays nitric oxide- (NO) mediated vasodilator activity. The net hemodynamic effect of nebivolol is the result of a balance between the depressant effects of beta3-blockade and an action that tends to maintain cardiac output, presumably connected with its afterload reducing vasodilator effect. Recent studies suggest that nebivolol may also restore endothelial dysfunction. Long-term follow-up studies indicate that the compound is efficacious and safe both in patients with mild hypertension and those with stable angina. An interesting effect of chronic nebivolol therapy in elderly patients with mild hypertension is the reversal of a depressor effect into a pressor effect on standing. This action indicates that nebivolol has advantages over other antihypertensive drugs and that it may protect elderly hypertensive patients from orthostatic complaints. The observation that nebivolol improves exercise capacity in non-claudicant hypertensives is also of clinical interest. Nebivolol resembles serotonin reuptake inhibitors in that it is metabolized by CYP450 2D6 and, therefore, concomitant treatment with serotonin uptake inhibitors may lead to overdosing. Nebivolol compared to placebo does not significantly reduce the mortality risk in elderly subjects. The effects of biological age and comorbidities may be responsible for this finding. In conclusion, clinical studies suggest that nebivolol is effective and safe in patients with hypertension, angina pectoris and heart failure. The beneficial effects on endothelial function, autonomic control and exercise capacity are of considerable clinical interest.     

Type‐specific orthostatic hemodynamic response of hypertensive diseases in pregnancy

Posture changes may differ between types of hypertensive disease. The aim is to evaluate the orthostatic response of impedance cardiography (ICG) measurements in uncomplicated and hypertensive pregnancies. Measurements were performed in supine and standing position in 202 women: 41 uncomplicated pregnancies (UP), 59 gestational hypertension (GH), 35 early‐onset (EPE, < 34 weeks) and 67 late‐onset (LPE, ≥ 34 weeks) preeclampsia were assessed. Measurements were recorded of heart rate, blood pressure, aortic flow parameters, cardiac output, pre‐ejection period and left ventricular ejection time. Overall, orthostatic shifts were different between all groups (P < 0.001). UP was different from the hypertensive complicated gestations in the orthostatic change of the aortic acceleration. In contrast to patients with preeclampsia, those with GH had an increased blood pressure and Heather index, and stable pre‐ejection period after posture change. EPE differed from LPE by change in blood pressure and aortic flow parameters. In addition to static ICG‐measurements, orthostatic shifts improved group characterization from 57.4% to 65.8%. The orthostatic response is altered in hypertensive pregnancies. ICG measurements in the upright as well as during an orthostatic test might have the potential to improve the discriminative yield between hypertensive diseases in pregnancy.