急性缺血性卒中合并心脏病患者血压管理专家共识

急性缺血性卒中的血压管理不同于陈旧缺血性卒中的血压管理。当急性缺血性卒中合并心脏病(如急性心肌梗死或心力衰竭等)时,对于血压管理的要求就变得更加复杂。本共识围绕急性缺血性卒中合并急慢性冠状动脉综合征、合并心力衰竭等临床复杂情况,对降压时机、降压目标、降压用药及处置流程等进行专家意见的总结。     

急性缺血性卒中患者的血压管理

急性缺血性卒中患者在发病最初24 h内一般会出现血压增高,且血压水平与患者预后相关.在缺血性卒中急性期的血压管理中,无论是试图升压或是降压治疗都存在争议.文章综述了缺血性卒中急性期血压变化以及血压管理与卒中预后的关系.     

急性脑卒中的血压管理

急性脑卒中的最合适动脉血压管理,目前缺乏可靠的临床试验依据,根据不同卒中类型,动脉血压的合适处理存在一定差别。本文拟就急性脑卒中的流行病学情况,脑血流调节以及目前对急性缺血性卒中     

急性卒中时血压升高的预后意义[英]／Willmot M…／／Hypertension

急性卒中时血压升高较为常见，并可能与预后不良有关。然而既往的相关研究结论尚未统一。本文意就急性卒中时血压升高与预后的关系进行了汇总分析。     

急性脑卒中的血压管理

急性脑卒中的最合适动脉血压管理,目前缺乏可靠的临床试验依据,根据不同卒中类型,动脉血压的合适处理存在一定差别[1].本文拟就急性脑卒中的流行病学情况,脑血流调节以及目前对急性缺血性卒中(AIS),颅内出血(ICH)血压管理的认识等问题作简要综述.     

卒中后立刻给予降压药无益

降低血压在卒中一级和二级预防中的益处已得到公认，但在急性缺血性卒中患者中进行抗高血压治疗的效果尚不确定。最近在JAMA发表的中国急性缺血性卒中抗高血压治疗试验（China Antihypertensive Trialin Acute Ischemic Stroke，CATIS）显示，在卒中发病后最初48h给予患者药物降低血压并不能降低死亡或严重残疾风险。     

急性缺血性卒中血管内治疗围手术期血压管理

急性缺血性卒中具有高发病率、高致残率和高死亡率的特点。血管内治疗在急性缺血性卒中治疗的有效性和安全性已得到认可,但有关围手术期血压调控的研究较少,最佳血压调控管理策略仍未达成共识。文章对血管内治疗围手术期血压管理进行了综述。     

血管活性药治疗急性卒中

背景:急性卒中后是否应对血压进行处理?如果应处理,那么升高血压还是降低血压更好?这些都还不清楚。 目的:评价降低或升高急性卒中患者血压的作用,不同血管活性药对急性卒中时血压的影响 检索策略:借助CDSR和CCTR数据库检索了Cochrane图书馆(1999年第1期)、检索Medline(1966-)、Embase(1980-)和BIDS ISI(1981-),以及现有的综述文章,并与该领域的研究者和制药公司进行了联系。     

卒中患者适度降低血压可能有益

据最近的AmJHypertens报道,入院后1周内血压明显增高的急性缺血性卒中患者进行适度降压治疗与近期功能改善有关。为了阐明急性缺血性卒中发病后的血压特征,明确其与近期功能转归的关系,西班牙的Rodriguez Garcia等进行了一项病例研究。监测434例缺血性卒中患者的24h血压,其中腔隙性卒中205例,非腔隙性卒中229例;以178例血压正常受试者作为对照。采用美国国立卫生研究院卒中量表(NIHSS)评价卒中严重程度。对第1天发现血压增高的患者给予卡托普利或氨氯地平治疗。主要转归指标为第7天时的中重度残疾(改良Rankin量表4～6分)或住院期间死亡…     

急性卒中病人入院时血压的预后价值

急性卒中病人入院时常有高血压,因高血压是卒中的重要危险因素,且严重高血压是一种潜在的生命威胁,急性降压治疗似乎是符合逻辑的。另一方面,卒中可因自发性或药物性低血压而引起,曾有报道急性降血压治疗对急性卒中病人是有害的,由此提示急性卒中降压要谨慎。一些急性脑缺血患者降压治疗能降低缺血区脑血流量而有害。急性卒中病人的血压可自然下降,不必治疗。     

急性脑卒中患者血压特点的分析

目的研究急性脑卒中患者血压影响因素及动态血压特点。方法82例发病在7天内的急性脑卒中患者。记录患者住院诊室血压及24 h动态血压。血压≥140/90 mm Hg(1 mm Hg=0.133 kPa)为诊室血压升高;24 h动态血压平均值≥130/80 mm Hg、日间平均值≥135/85 mm Hg、夜间平均值≥125/75 mm Hg为动态血压升高。结果既往高血压病史对急性脑卒中患者诊室血压升高有影响(P<0.05)。有高血压病史者平均诊室血压(146.02±18.89)/(86.36±11.52)mm Hg,无高血压病史者平均诊室血压(136.22±14.63)/(82.61±11.86)mm Hg,二者收缩压水平差异有显著性意义(P<0.05)。急性脑卒中患者动态血压表现为夜间血压负荷增加,24 h平均血压于发病后4~5天明显升高,6~7天降低。诊室血压升高与诊室血压正常比较,血压形态均以非杓形和反杓形为主,2组差异无显著性意义(P>0.05)。结论急性脑卒中诊室血压升高与高血压病史有关,急性脑卒中随发病时间延长,血压呈下降趋势。     

卒中防治中的血压调控

文章探讨了卒中防治中的血压调控问题,包括卒中一级、二级预防以及卒中急性期血压的调控,升压治疗与缺血性脑血管病,颅内外血管狭窄的血压调控,抗凝治疗与血压调控,血压节律、变异性与卒中等。     

人群血压水平对急性心肌梗塞及脑卒中患病率的影响

为了解人血压水平对急性心肌梗塞及脑卒中患病率的影响，就城乡人群的血压水平与ＡＭＩ及脑卒中患病率的关系进行探讨。调查结果显示，人群血压水平的升高，直接影响ＡＭＩ及脑卒中的患病率，提示人群血夺水平与ＡＭＩ及脑卒中患病率呈正相关。认为人群血压水平的升高是ＡＭＩ及脑卒中发病的危险因素，提出应早日开展高血压人群防治，采用切实有效的方法，控制高血压。     

脑出血病人急性期动态血压变化及与预后的关系

目的研究脑出血急性期动态血压变化规律以及血压等因素对预后影响.方法对45例急性脑出血病人监测1周动态血压,分析1周内平均收缩压和舒张压、出血量、出血部位、年龄、性别与预后关系.结果脑出血病人7 d血压变化呈逐渐下降趋势,第7天与第1天动态血压参数比较有统计学意义;低龄、女性、出血量少以及收缩压及舒张压较低者病情预后较好.结论脑出血急性期病人血压变化呈逐渐下降趋势,对急性脑出血高血压的处理要慎重,应采取合理、个体化治疗.     

脑梗死患者急性期血压监测与预后的初步研究

目的探讨脑梗死患者急性期动态血压的变化及血压与预后的相关性。方法本研究为前瞻性地对发病48h内入院的53例脑梗死患者进行24 h动态血压监测,持续10天,记录其他影响预后的危险因素,并在21天、3个月做近远期神经功能评分。结果脑梗死患者急性期高血压常见,有自发下降的趋势。在入院4天时,收缩压和舒张压分别下降(8.8±7.9)mm Hg(、4.5±5.0)mm Hg(1 mm Hg=0.133 kPa,P<0.05),4~10天时血压下降趋势趋于平缓。脑梗死患者急性期血压与远期预后单因素分析显示呈U型曲线关系,血压的最适水平为收缩压140~160mm Hg,舒张压75~80 mm Hg。但在多因素分析中仅收缩压≥160 mm Hg与140~159.9 mm Hg比较是近期(P=0.024)和远期(P=0.046)预后不良的独立危险因素,收缩压每升高10 mm Hg,近期和远期预后不良的危险性分别增加368.2%和137.2%。结论脑梗死患者急性期血压显著升高(收缩压≥160 mm Hg)提示预后不良。     

Problems Related to Short-Term Antihypertensive Therapy in Acute Ischemic Stroke

Hypertension is a common early finding after an acute ischemic stroke, even in previously normotensive patients. But its significance and proper management are a matter of debate, because of the lack of adequately powered randomized clinical trials. A close analysis of observational and interventional trials, published so far, fails to convince that an early antihypertensive therapy is needed and beneficial. During the first 24–48 hr after ischemic stroke, only blood pressure values repeatedly higher than 220/120 mmHg require antihypertensive treatment to keep blood pressure levels in the range of 180–220 mmHg systolic and 100–120 diastolic. Blood pressure reduction should be cautious with the aim of keeping the pressure at relatively high values (180/100–105 in previously hypertensive patients and 160–180/90–100 in previously normotensive patients). The usefulness of increasing blood pressure with vasopressive agents in selected patients with ischemic stroke deserves adequate testing with randomized clinical trials.     

Early treatment of hypertension in acute ischemic and intracerebral hemorrhagic stroke: Progress achieved,challenges, and perspectives

Hypertension is the leading risk factor for ischemic and intracerebral hemorrhagic subtypes of stroke. Additionally, high blood pressure (BP) in the acute cerebrovascular event is associated with poor outcome, and a high percentage of stroke survivors have inadequate control of hypertension. The present is a systematic review of prospective, randomized, and controlled trials carried out on safety and efficacy of antihypertensive treatment of both subtypes of acute stroke. Six trials involving 7512 patients were included, which revealed controversies on the speed and the goals of treatment. These controversies could be due at least in part, from the fact that some studies analyzed the results of antihypertensive treatment in ischemic and intracerebral hemorrhagic subtypes of acute stroke together, and from a different prevalence of past-stroke in the randomized groups. Further research is necessary to establish whether standard antihypertensive treatment provides greater benefit than simple observation in patients with ischemic acute stroke and Stage 2 hypertension of JNC 7, albeit they were not candidates for acute reperfusion. In that case, the target reduction in BP could be 10% to 15% within 24 hours. The recently published INTERACT 2 has provided evidence that patients with hemorrhagic stroke may receive intensive antihypertensive treatment safely with the goal of reducing systolic BP to levels no lower than 130 mm Hg. It is important to take into account that marked BP lowering in acute stroke increases the risk of poor outcome by worsening cerebral ischemia from deterioration of cerebral blood flow autoregulation.     

New treatment options for hypertension during acute ischemic or hemorrhagic stroke

Opinion statement Widespread reluctance to treat hypertension during acute stroke is based on historical accounts of unfavorable outcomes of treatment that were badly done: therapies that cannot be controlled, such as sublingual nifedipine, oral or intramuscular antihypertensive drugs may drop blood pressure precipitously, leading to worsening of ischemia. Case fatality in stroke obeys a U-shaped relationship: blood pressures that are either too low or too high are associated with worse outcomes both in ischemic stroke and in intracerebral hemorrhage. Very high blood pressures should be lowered in acute stroke, and there are some circumstances in which high blood pressure must be treated despite the presence of stroke. To avoid worsening of ischemia by reduction in cerebral blood flow, it is necessary to treat high blood pressure in acute stroke with drugs that can be controlled; this usually means giving drugs by intravenous infusion; however, there is recent evidence that transdermal administration of nitrates, which can be removed if pressure is too low, is a convenient alternative that does not reduce cerebral blood flow in acute stroke.     

Hypoperfusion and its augmentation in patients with brain ischemia

Opinion statement Control of hypertension is a well-established goal of the primary and secondary prevention of stroke. However, management of blood pressure in the setting of acute brain ischemia is complicated by the possible effect of blood pressure changes on cerebral perfusion. In acute stroke, patients may have an ischemic penumbra of brain tissue, which has impaired perfusion but which is not irreversibly damaged. The ischemic penumbra may be salvaged with reperfusion. Lowering of blood pressure in this setting, however, would hasten the progression of the penumbra to infarction. With the exception of patients treated with thrombolytic agents, blood pressure reduction is not recommended in acute ischemic stroke for this reason. Preliminary studies suggest that there may be a role for interventions to elevate blood pressure as a treatment for acute stroke patients. Despite interest in induced hypertension as a treatment of stroke dating back to the 1950s, this practice has not achieved widespread use owing to concerns about potential adverse effects such as intracerebral hemorrhage, cerebral edema, and myocardial ischemia. It is commonly used, however, to treat patients with threatened cerebral ischemia due to vasospasm after subarachnoid hemorrhage. Until future studies clarify the effectiveness of induced hypertension in stroke treatment, maintaining adequate blood pressure and fluid volume is recommended for patients with acute ischemic stroke, particularly if the neurologic deficits are fluctuating or the patient has persistent large-vessel occlusive disease.