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.     

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…     

血压变异性与缺血性卒中

高血压是缺血性卒中等心脑血管疾病最重要的危险因素.不过,平均血压并不能完全解释高血压造成的靶器官损害以及降压治疗带来的获益.一系列研究表明,血压变异性(bloodpressure variability,BPV)是独立于平均血压之外的缺血性卒中危险因素,而且BPV与缺血性卒中的转归也存在显著相关性.近年来,针对BPV的研究逐渐成为缺血性卒中防治领域的热点,但BPV与缺血性卒中的具体关联尚不完全清楚.文章对BPV与缺血性卒中的关系进行了简要综述.     

缺血性脑卒中急性期血压管理

<正>缺血性脑卒中发病在我国呈逐年上升趋势,高血压是最主要的独立危险因素。循证医学证实,降压治疗在缺血性卒中的一级和二级预防中起重要作用。但是,关于缺血性脑卒中急性期的血压管理依然存在争议。各国指南对缺血性脑卒中急性期的血压增高均采取相对谨慎的治疗策略。一、缺血性卒中急性期高血压反应的机制急性高血压反应是指在卒中发病24 h内血压升高超过正常值或发病前的水平,其主要原因可能一是介导血压自主调节的神经系统特定区域因卒中     

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。     

卒中后抑郁的药物治疗

抑郁是卒中后常见和严重的并发症之一。卒中后抑郁(post-stroke depression, PSD)与转归不良和病死率增高相关。美国心脏协会/美国卒中协会急性缺血性卒中早期管理指南推荐应对PSD患者进行药物治疗。文章对PSD的药物治疗进行了综述。     

非心源性缺血性卒中患者急性期短时血压变异性与近期转归的相关性

目的：探讨非心源性缺血性卒中患者急性期短时血压变异性与近期转归的相关性。方法连续纳入2013年1月1日至2015年6月31日期间收治的急性期非心源性缺血性卒中患者,收集人口统计学和临床资料,进行24 h动态血压监测并计算各项血压变异性参数。在患者出院时或住院第14天时采用改良Rankin量表（modified Rankin Scale, mRS ）评价近期神经功能转归,mRS 评分0~2分定义为转归良好,＞2分定义为转归不良。采用多变量logistic回归分析判定血压和短时血压变异指标与近期神经功能转归的相关性。结果总共纳入229例急性期非心源性缺血性卒中患者,40.2％的患者近期功能转归不良。近期功能转归不良组平均收缩压[（147.8±19.6）mmHg对（137.7±19.1）mmHg;t=3.868,P<0.001;1 mmHg=0.133 kPa]和平均收缩压实际变异值（中位数,四分位数间距）[11.7（10.0~14.0）mmHg对10.6（8.2~12.5）mmHg;Z=3.544,P<0.001]显著高于功能转归良好组。多变量logistic回归分析显示,校正其他混杂因素后,平均收缩压水平增高（每增高10 mmHg：优势比1.189,95％可信区间1.013~1.369;P=0.034）和收缩压实际变异增大（每增加1 m m Hg：优势比1.182,95％可信区间1.046~1.336;P=0.008）与近期功能转归不良相关。结论急性期非心源性缺血性卒中患者短时血压变异增大与近期功能转归不良相关。     

缺血性卒中防治中的降压治疗:J曲线现象

心血管病降压治疗中的J曲线现象已有较多理论和试验证据,并已得到大多数学者的认可.而有关缺血性卒中的降压治疗是否存在J曲线现象,相关研究和报道不多,尚未达成共识.文章对该现象进行了综述,期待有助于缺血性卒中的血压管理.     

急性缺血性卒中转归的血清生物标志物

血清生物标志物在预测急性缺血性卒中的严重程度、早期神经功能恶化和转归方面具有重要作用.了解这些血清生物标志物的种类、作用机制以及与急性缺血性脑损伤的相关性,有助于急性缺血性卒中患者的早期转归预测并指导治疗.     

缺血性卒中急性期降压治疗策略的研究进展

正缺血性卒中急性期约有60%~75%的患者血压增高(140/90 mm Hg)~[1]。即使既往无高血压病史的患者,在卒中急性期血压也可能增高~[2]。长期以来,不主张在卒中急性期积极降压,机制在于卒中急性期血压增高是机体维持脑灌注压的代偿反应,此时降低血压有可能导致脑灌注压不足,扩大缺血     

Systemic inflammation, blood pressure, and stroke outcome

Hypertension is the most important modifiable risk factor for ischemic stroke, and antihypertensive treatment is of paramount importance to reduce the incidence of stroke mortality and morbidity. The significance and best management of hypertension during the first hours after stroke onset, however, are still matters of debate. Cerebral ischemia results in a complex inflammatory cascade; inflammatory mechanisms are also important participants in the pathophysiology of hypertension. There has been a convergence of evidence that is important to consider in managing systemic blood pressure after stroke to ensure an optimal outcome. The identification of useful markers will allow progress in our ability to treat blood pressure in the acute phase of a stroke. The determination of levels of C-reactive protein, an acute-phase inflammation marker, may help to guide our approach in the management of blood pressure in acute ischemic stroke. Whether this target will be useful in the development of risk prediction strategies or therapies for the treatment of stroke in humans is far from clear.     

Systemic blood pressure and stroke outcome and recurrence

Although it is clear that hypertension is a primary cause of stroke, there has been controversy concerning blood pressure management after stroke. Recent studies indicate that lowering systemic blood pressure after stroke reduces the risk for recurrent stroke or vascular events, but other studies provide evidence that blood pressure should not be lowered in the first week after stroke onset. Additional investigations have provided preliminary evidence that raising blood pressure in the first few days after stroke may improve outcome in selected patients. However, other studies have recorded the benefit of lowering blood pressure in some patients at the acute stage, whereas still others have identified patients in whom lowering blood pressure even later after stroke may be more harmful than beneficial. The remaining challenge is to identify efficient measures for determining when to lower blood pressure in each case of ischemic stroke.     

Systemic blood pressure and stroke outcome and recurrence

Although it is clear that hypertension is a primary cause of stroke, there has been recent controversy about blood pressure management after stroke. Recent studies indicate that lowering systemic blood pressure after stroke does reduce the risk of recurrent stroke or vascular events, but other studies provide evidence that blood pressure should not be lowered in the first week after stroke onset. Additional investigations have provided preliminary evidence that raising blood pressure in the first few days after stroke may improve outcome in selective patients. However, other studies have recorded benefit of lowering blood pressure in some patients at the acute stage, whereas still others have identified patients in whom lowering blood pressure even later after stroke may be more harmful than beneficial. The remaining challenge is to identify efficient measures for determining when to lower blood pressure in each case of ischemic 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.     

The Management of Hypertension for an Acute Stroke: What Is the Blood Pressure Goal?

Stroke is the 4th leading cause of death in the US and a leading cause of disability among adults. Stroke is broadly classified into ischemic and hemorrhagic subtypes. Although the pathogenesis may differ between ischemic and hemorrhagic stroke subtypes, a unifying feature is that hypertension is a major risk factor for most ischemic and hemorrhagic strokes. Prevention of first and recurrent stroke is substantially dependent on blood pressure control. There is controversy about blood pressure management in acute stroke. In this review we discuss controversies about and guidelines for management of blood pressure in acute stroke. We subdivide our discussion to address important questions about acute blood pressure management in ischemic stroke, intraparenchymal hemorrhage, and subarachnoid hemorrhage. In addition, we address BP control recommendations when tissue plasminogen activator administration is being contemplated for treatment of acute ischemic stroke.     

Management of hypertension in the setting of acute ischemic stroke

The optimal management of blood pressure in the first 24 hours of ischemic stroke remains a controversial topic. Most patients are hypertensive at presentation and subsequently experience a spontaneous decline in blood pressure. Decreasing penumbral blood flow and exacerbating vasogenic edema are significant concerns in whether to treat blood pressure elevations. Although an initially elevated blood pressure has been associated with poor outcome, attempts to acutely lower blood pressure are also associated with worsened outcomes. Thus, the current approach in acute ischemic stroke is permissive hypertension, in which antihypertensive treatment is warranted in patients with systolic blood pressure greater than 220 mm Hg, receiving thrombolytic therapy, or with concomitant medical issues. The use of predictable and titratable medications that judiciously reduce (∼ 10% to 15%) the initial presenting mean arterial pressure is recommended in these situations. Future study must define optimal blood pressure goals, likely on an individual basis.     

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。     

Blood Pressure Goals in Acute Stroke—How Low Do You Go?

Purpose of Review

Elevations in systolic blood pressure (BP) greater than 140 mmHg are reported in the majority (75%) of patients with acute ischemic stroke and in 80% of patients with acute intracerebral hemorrhages (ICH). This paper summarizes and updates the current knowledge regarding the proper management strategy for elevated BP in patients with acute stroke.

Recent Findings and Summary

Recent studies have generally showed a neutral effect of BP reduction on clinical outcomes among acute ischemic stroke patients. Thus, because of the lack of convincing evidence from clinical trials, aggressive BP reduction in patients presenting with acute ischemic stroke is currently not recommended. Although in patients treated with intravenous tissue plasminogen activator, guidelines are recommending BP?<?180/105 mmHg but currently, the optimal BP management after reperfusion therapy still remains unclear. In acute ICH, the evidence from randomized clinical trials supports the immediate BP lowering targeting systolic BP to 140 mmHg, which is now recommended by guidelines.