Acute Hypertensive Response Research Articles

The L-shaped correlation between systolic blood pressure and short-term and long-term mortality in patients with cerebral hemorrhage

BackgroundA large amount of evidence has shown the necessity of lowering blood pressure (BP) in patients with acute cerebral hemorrhage, but whether reducing BP contributes to lower short-term and long-term mortality in these patients remains uncertain.AimsWe aimed to explore the association between BP, including systolic and diastolic BP, during intensive care unit (ICU) admission and 1-month and 1-year mortality after discharge of patients with cerebral hemorrhage.MethodsA total of 1085 patients with cerebral hemorrhage were obtained from the Medical Information Mart for Intensive Care III (MIMIC-III) database. Maximum and minimum values of systolic and diastolic BP in these patients during their ICU stay were recorded, and endpoint events were defined as the 1-month mortality and 1-year mortality after the first admission. Multivariable adjusted models were performed for the association of BP with the endpoint events.ResultsWe observed that patients with hypertension were likely to be older, Asian or Black and had worse health insurance and higher systolic BP than those without hypertension. The logistic regression analysis showed inverse relationships between systolic BP-min (odds ratio (OR) = 0.986, 95% CI 0.983–0.989, P < 0.001) and diastolic BP-min (OR = 0.975, 95% CI 0.968–0.981, P < 0.001) and risks of 1-month, as well as 1-year mortality when controlling for confounders including age, sex, race, insurance, heart failure, myocardial infarct, malignancy, cerebral infarction, diabetes and chronic kidney disease. Furthermore, smooth curve analysis suggested an approximate L-shaped association of systolic BP with the risk of 1-month mortality and 1-year mortality. Reducing systolic BP in the range of 100–150 mmHg has a lower death risk in these patients with cerebral hemorrhage.ConclusionWe observed an L-shaped association between systolic BP levels and the risks of 1-month and 1-year mortality in patients with cerebral hemorrhage, which supported that lowering BP when treating an acute hypertensive response could reduce short-term and long-term mortality.

Arterial hypertension in acute stroke. Current therapeutical indications

Acute stroke (the first hours after its onset) is accompanied in over 70% of cases by rapid and significant increases in blood pressure, above normal values. The acute or reactive hypertensive response occurs both in patients with a history of hypertension and in normotensive patients. The greatly increased BP values, not controlled therapeutically, can be followed by the increase in the volume of the cerebral infarct and hemorrhagic transformation or the expansion of the hematoma and the increase in intracerebral pressure, respectively in ischemic or hemorrhagic stroke. This paper especially refers to the therapeutic control of hypertension in various situations (conditions): 1. Laboratory emergencies; 2. Hospital treatment with out thrombolytics or thrombolysis; 3. Endovascular treatment in acute stroke; 4. BP control in hemorrhagic stroke; 5. Continuation or discontinuation of antihypertensive treatment. The updated recommendations for the treatment of HTN in acute stroke result from clinical studies and recommendations of the recent ESO and AHA/ASA Guidelines.

A case report on sepsis with HTN with pyelonephritis with DM 2

Introduction: Modes: Acute arterial hypertension can arise during acute sepsis in everyday practice. The most recent sepsis campaign recommendations did not include any management instructions on this topic. Arterial hypertension that develops during sepsis may go unnoticed, even though it can have serious hemodynamic effects. This report presents a clinical study of acute hypertensive response in sepsis. It demonstrates that during sepsis, At the same time, arterial hypertension, renal salt loss, and glomerular hyperfiltration can all occur. The mechanisms of sepsis-related arterial hypertension and treatment possibilities are also reviewed. Diabetes mellitus is a common cause of pyelonephritis. Acute arterial hypertension can arise during acute sepsis in everyday practice. The most recent sepsis campaign recommendations did not include any management instructions on this topic. Despite its potential for hemodynamic damage, Severe arterial hypertension that develops as a result of sepsis may be an overlooked ailment. This report presents A clinical study of sepsis-induced acute hypertension. It demonstrates that arterial hypertension, renal salt loss, and glomerular hyperfiltration can all lead to kidney failure. all happen at the same time during sepsis. The mechanisms of sepsis-related arterial hypertension and treatment possibilities are also reviewed. Pyelonephritis is frequently caused by diabetes mellitus. Patients with EPN had a lower treatment outcome than those with NEPN. However, EPN and NEPN patients had the same death rate, although EPN patients require more nephrectomy. Shock and an altered sensorium at the time of presentation were both poor prognostic factors in EPN.Patients Information: A 43-year-old woman was admitted To MICU on February 20, 2022 On fever, the patient has had chills for 5 days, vomiting for 1 day, and generalized weakness for 5 days, with a history of hypertension, sepsis, Diabetes Mellitus 2 pyelonephritis, and no history of tuberculosis.clinical findings: By physician's order, the patient had completed all essential investigations. Therapeutic Interventions: medical management was provided to the patient Iv, fluid RL, and NS were used to treat the patient. RT feed 200ml/2 hourly, pan 40 mg OD, Emmet 4 mg sos, pan 40 mg OD Lantus 8 unit HS, She was taking all treatments and the outcomes were good. The patient was taken medication as per a doctor’s order, for example, antipyretic use to treat fever Nursing Management: conclusion: A 43 -year -old woman was admitted with MICU sepsis with HTN with pyelonephritis with DM2, fever With chills for 5 days, vomiting for 1 day, and generalized weakness for 5 days, The medical treatment had a positive impact on the patient's condition. Now, the patient's symptoms have been reduced, and he was in better condition.

Supine blood pressure normalised by daytime series values is independently associated with ischaemic wake-up stroke

Purpose Wake-up stroke constitutes up to 1/4 of all ischaemic strokes; however, its pathomechanisms remain largely unknown. Although low nocturnal blood flow may be the underlying cause, little is known about blood pressure (BP) characteristic of wake-up stroke patients. The aim of our study was to look for differences in BP variables between wake-up stroke and known-onset stroke patients and to seek BP indices which could distinguish wake-up stroke patients from other stroke patients. Materials and Methods In the study, we included ischaemic stroke patients in whom office BP measurement and Ambulatory BP monitoring (ABPM) were recorded at day 7, after acute hypertensive response. The daytime period was defined as the interval from 6 a.m. to 10 p.m. From ABPM, we obtained parameters of BP variability. Additionally, we calculated the BP percentage differences defined as (supine office BP–average daytime BP)/average daytime BP for systolic, diastolic, and mean blood pressure. We calculated analogous indices for night-time. The univariate and multivariate relationships between BP variables and wake-up stroke were analysed. Results Among the recruited 120 patients (aged 61.6 ± 12.3; 88 [73%] males; the baseline National Institutes of Health stroke scale score 4 [3–8]), 36 (30%) had wake-up stroke. In a univariate analysis, the systolic and mean daytime and night-time BP differences were significantly lower in patients with wake-up stroke [(−1.92 (−11.55 to 3.95) vs 4.12 (−2.48 to 11.31), p = 0.006 and −6.20 (−12.32 to 7.42) vs 2.00 (−6.86 to 11.65), p = 0.029 for daytime, respectively; 0.00 (−9.79 to 11.82) vs 9.84 (0.00 to 18.25), p = 0.003 and 0.51 (−8.49 to 12.08) vs 7.82 (−2.47 to 20.39), p = 0.026, for night-time, respectively]. After adjustment for possible confounders, the systolic BP difference remained significantly associated with wake-up stroke (odds ratio = 0.96, 95% confidence interval = 0.92–1.00, p = 0.039). Conclusion The subacute office-ambulatory BP difference including the dynamic (systolic BP), but not static BP component was independently associated with wake-up stroke.

Acute Hypertensive Response in Patients With Acute Intracerebral Hemorrhage: A Narrative Review.

To review the role of the acute hypertensive response in patients with intracerebral hemorrhage, current treatment options, and areas for further research. Review of the literature to assess 1) frequency of acute hypertensive response in intracerebral hemorrhage; 2) consequences of acute hypertensive response in clinical outcomes; 3) acute hypertensive response and secondary brain injury: hematoma expansion and perihematomal edema; 4) vascular autoregulation, safety data side effects of acute antihypertensive treatment; and 5) randomized clinical trials and meta-analyses. An acute hypertensive response is frequent in patients with acute intracerebral hemorrhage and is associated with poor clinical outcomes. However, it is not clear whether high blood pressure is a cause of poor clinical outcome or solely represents a marker of severity. Although current guidelines recommend intensive blood pressure treatment (<140 mm Hg) in patients with intracerebral hemorrhage, 2 randomized clinical trials have failed to demonstrate a consistent clinical benefit from this approach, and new data suggest that intensive blood pressure treatment could be beneficial for some patients but detrimental for others. Intracerebral hemorrhage is a heterogenous disease, thus, a one-fit-all approach for blood pressure treatment may be suboptimal. Further research should concentrate on finding subgroups of patients more likely to benefit from aggressive blood pressure lowering, considering intracerebral hemorrhage etiology, ultra-early randomization, and risk markers of hematoma expansion on brain imaging.

Impact of Uncontrolled Hypertension at 3Months After Intracerebral Hemorrhage.

BackgroundSurvivors of intracerebral hemorrhage (ICH) are at high risk for recurrent stroke, which is associated with blood pressure control. Because most recurrent stroke events occur within 12 to 18 months of the index ICH, rapid blood pressure control is likely to be crucial. We investigated the frequency and prognostic impact of uncontrolled short‐term hypertension after ICH.Methods and ResultsWe analyzed data from Massachusetts General Hospital (n=1305) and the University of Hong Kong (n=523). We classified hypertension as controlled, undertreated, or treatment resistant at 3 months after ICH and determined the following: (1) the risk factors for uncontrolled hypertension and (2) whether hypertension control at 3 months is associated with stroke recurrence and mortality. We followed 1828 survivors of ICH for a median of 46.2 months. Only 9 of 234 (4%) recurrent strokes occurred before 3 months after ICH. At 3 months, 713 participants (39%) had controlled hypertension, 755 (41%) had undertreated hypertension, and 360 (20%) had treatment‐resistant hypertension. Black, Hispanic, and Asian race/ethnicity and higher blood pressure at time of ICH increased the risk of uncontrolled hypertension at 3 months (all P<0.05). Uncontrolled hypertension at 3 months was associated with recurrent stroke and mortality during long‐term follow‐up (all P<0.05).ConclusionsAmong survivors of ICH, >60% had uncontrolled hypertension at 3 months, with undertreatment accounting for the majority of cases. The 3‐month blood pressure measurements were associated with higher recurrent stroke risk and mortality. Black, Hispanic, and Asian survivors of ICH and those presenting with severe acute hypertensive response were at highest risk for uncontrolled hypertension.

An overview of acute hypertensive response following intracerebral hemorrhage: implifications for clinical practice

Vessel Plus is an open acccess journal, which publishes articles related to vascular diseases, including acute respiratory distress syndrome, aneurysm, atherosclerosis, hypertension, stroke, peripheral vascular or pulmonary vascular diseases, etc.

Prognostic significance of acute hypertensive response in ischemic stroke or transient ischemic attack patients and its relationship with left ventricular myocardial function.

Acute hypertensive response (AHR) in acute stroke is associated with adverse outcomes; however, the underlying pathophysiology of the association is poorly understood and its prognostic impact in ischemic stroke remains unclear. We aimed to investigate the prognostic significance of AHR in patients with ischemic stroke or transient ischemic attack (TIA), and further examined the relationship between AHR and myocardial function, using two-dimensional speckle-tracking echocardiography (2D-STE). A total of 244 consecutive patients with acute ischemic stroke (AIS) (n = 192) or TIA (n = 52), who were evaluated with 2D-STE within 7 days from admission, were retrospectively analysed. The primary endpoint was a composite of major adverse cardiovascular and cerebrovascular events (MACCE), including death, myocardial infraction or recurrent ischemic stroke. Among the study population, AHR was observed in 161 (66%) patients. During a mean follow-up of 21.0 ± 12.5 months, 29 patients (11.9%) [25 (15.5%) AHR vs. 4 (4.8%) No AHR, P = 0.014] reached the primary endpoint. A Kaplan-Meier curve revealed that patients with AHR had a significantly higher incidence of MACCE than those without AHR (log-rank P = 0.013). Multivariate Cox regression analysis demonstrated that AHR [adjusted hazard ratio 4.60, 95% confidence interval (95% CI) 1.31-16.15] was a strong predictor of MACCE. In multivariate logistic regression analysis, left ventricular global longitudinal strain (per 1% decrease) showed a significant relationship with AHR (adjusted odds ratio 1.17, 95% CI 1.02-1.35). AHR in patients with AIS or TIA may be an important poor prognostic marker related to myocardial dysfunction.

Acute Management of Hypertension Following Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is responsible for approximately 15% of strokes annually in the United States, with nearly 1 in 3 of these patients dying without ever leaving the hospital. Because this disproportionate mortality risk has been stagnant for nearly 3 decades, a main area of research has been focused on the optimal strategies to reduce mortality and improve functional outcomes. The acute hypertensive response following ICH has been shown to facilitate ICH expansion and is a strong predictor of mortality. Rapidly reducing blood pressure was once thought to induce cerebral ischemia, though has been found to be safe in certain patient populations. Clinicians must work quickly to determine whether specific patient populations may benefit from acute lowering of systolic blood pressure (SBP) following ICH. This review provides nurses with a summary of the available literature on blood pressure control following ICH. It focuses on intravenous and oral antihypertensive medications available in the United States that may be utilized to acutely lower SBP, as well as medications outside of the antihypertensive class used during the acute setting that may reduce SBP.

A12614 Predictors of severity of hypertensive response in acute intracerebral haemorrhage

Objectives: Early elevation in blood pressure (BP) known as acute hypertensive response is common in patients with spontaneous intracerebral hemorrhage (ICH), and a known predictor of a poor outcome. We aimed to identify the independent predictors. Methods: We pooled Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT1) (n = 404) and INTERACT2 (n = 2839) of acute ICH patients (<6 hrs of onset) with elevated systolic BP (SBP, 150–220 mmHg) who were randomized to intensive (target SBP < 140 mmHg) or guideline-recommended (target SBP < 180 mmHg) management. BP at randomisation was measured at least twice and at least two minutes apart using the non-paretic arm (or right arm in situations of coma or tetraparesis) with the patient supine. Multivariable linear regression was used to determine associations. Results: Among 3233 patients, the mean age was 63.4 (12.8) years, mean SBP 179.3 (17.1) mmHg and 36.8% were female. History of hypertension (estimate 2.295, SE 0.691), admission glycemia > 6.5 mmol/lt (3.132, 0.618), elevated heart rate (1.238, 0.222 per 10-bmp increase), and higher NIHSS (0.154, 0.047 per 1-point increase) were significantly associated with hypertensive response at baseline. The use of antithrombotics (−3.742, 0.954) and time from onset to randomization (−0.992, 0.255 per 1-hour increase) were inversely associated with hypertensive response. Conclusion: For patients with acute ICH, if they are with history of hypertension, elevated blood glucose and heart rate, severe neurological deficit, not on antithrombotics, and presented earlier, more frequent BP measurement is required and more intensive BP treatment may be needed.

Antihypertensive therapy in acute ischemic stroke: where do we stand?

Despite the proven benefits of strict blood pressure (BP) control on primary and secondary prevention of stroke, management of acute hypertensive response in the early post-stroke period is surrounded by substantial controversy. Observational studies showed that raised BP on ischemic stroke onset is prognostically associated with excess risk for early adverse events and mortality. By contrast, randomized controlled trials and recent meta-analyses showed that although antihypertensive therapy effectively controls elevated BP in the acute stage of ischemic stroke, this BP-lowering effect is not translated into improvement in the risk of death or dependency. On this basis, acute and aggressive BP responses within 24 h of stroke onset should be avoided and antihypertensive therapy is recommended only for patients presenting with acute ischemic stroke and BP > 220/120 mmHg or those with BP > 185/110 mmHg who are eligible for therapy with intravenous tissue plasminogen activator. By contrast, recent clinical trials showed that intensive BP lowering to levels < 140 mmHg for systolic BP is safe and lowers the risk of hematoma expansion in patients with acute intra-cerebral hemorrhage and this BP target is recommended by current international guidelines. Herein, we provide an overview of randomized trials and recent meta-analyses on the management of hypertension during the acute stage of ischemic stroke. We discuss several areas of uncertainty and conclude with perspectives for future research.

Therapeutic Approach to Hypertensive Emergencies: Hemorrhagic Stroke.

Arterial hypertension represents the most important risk factor for ischemic and haemorrhagic stroke, and an acute hypertensive response is often observed in patients with intracranial haemorrhage (ICH). Available data indicate that the vast majority (> 70%) of patient with acute ICH have a systolic BP above 140mmHg at the time of presentation in the ED; about 20% have SBP values above 180 mmHg. Severe BP elevation in the presence of ICH represents a hypertensive emergency, and worsening of clinical conditions is not infrequent in the first hours after admission; an aggressive early management is therefore required for these patients. Despite this, appropriate management of BP in acute ICH is still controversial, due to the complex issues involved, and the heterogeneous results obtained in clinical trials. This article will review the available evidence supporting acute BP reduction in acute ICH.

Endothelium-Derived C-Type Natriuretic Peptide Contributes to Blood Pressure Regulation by Maintaining Endothelial Integrity.

We previously reported the secretion of C-type natriuretic peptide (CNP) from vascular endothelial cells and proposed the existence of a vascular natriuretic peptide system composed of endothelial CNP and smooth muscle guanylyl cyclase-B (GC-B), the CNP receptor, and involved in the regulation of vascular tone, remodeling, and regeneration. In this study, we assessed the functional significance of this system in the regulation of blood pressure in vivo using vascular endothelial cell-specific CNP knockout and vascular smooth muscle cell-specific GC-B knockout mice. These mice showed neither the skeletal abnormality nor the early mortality observed in systemic CNP or GC-B knockout mice. Endothelial cell-specific CNP knockout mice exhibited significantly increased blood pressures and an enhanced acute hypertensive response to nitric oxide synthetase inhibition. Acetylcholine-induced, endothelium-dependent vasorelaxation was impaired in rings of mesenteric artery isolated from endothelial cell-specific CNP knockout mice. In addition, endothelin-1 gene expression was enhanced in pulmonary vascular endothelial cells from endothelial cell-specific CNP knockout mice, which also showed significantly higher plasma endothelin-1 concentrations and a greater reduction in blood pressure in response to an endothelin receptor antagonist than their control littermates. By contrast, vascular smooth muscle cell-specific GC-B knockout mice exhibited blood pressures similar to control mice, and acetylcholine-induced vasorelaxation was preserved in their isolated mesenteric arteries. Nonetheless, CNP-induced acute vasorelaxation was nearly completely abolished in mesenteric arteries from vascular smooth muscle cell-specific GC-B knockout mice. These results demonstrate that endothelium-derived CNP contributes to the chronic regulation of vascular tone and systemic blood pressure by maintaining endothelial function independently of vascular smooth muscle GC-B.

Effect of Premedication with Oral Clonidine on Hemodynamic Response during Electroconvulsive Therapy.

Background:Electroconvulsive therapy (ECT) is the most effective treatment available for the acute treatment of depression in patients who do not respond to medications. It is generally used as a second line treatment for many psychological disorders, mainly major depression and schizophrenia where medication is not effective. ECT is often associated with some complications such as hypertension, tachycardia arrhythmia and even myocardial infarction. Various methods have been used for prevention or control of these cardiovascular side effects.Aim:The aim of this study was evaluating the effect of oral clonidine (0.3 mg) with control group to know the effect of oral clonidine on hemodynamic response during ECT.Methods and Material:This prospective randomized crossover clinical trial was performed on 25 patients aged 20-50 years, weight 50-70 kg with ASA I and II who were candidates for ECT. Prior to ECT, each patient received oral doses of clonidine (0.3 mg) or a placebo 90 minutes before ECT. Baseline Heart rate, systolic, diastolic and mean arterial pressures were noted just before securing the intravenous cannula. The same parameters were noted after induction, immediately after seizure cessation following delivery of the electric shock and at 1 minute interval for 10 minutes.Statistical Analysis:Data was analyzed by ANOVA test (analysis of variance). P < 0.05 was considered statistically significant.Results:Attenuation of maximum rise in the heart rate and mean arterial pressure by clonidine (0.3 mg) was evident and statistically significant when compared with control group.Conclusion:Oral clonidine (0.3 mg) decreases the acute hypertensive response after electroconvulsive therapy; however, this antihypertensive effect was achieved by decreasing the blood pressure before the electrical stimulus.

Management of Acute Hypertensive Response in Intracerebral Hemorrhage Patients After ATACH-2 Trial.

Acute hypertensive response is elevation of systolic blood pressure (SBP) in the first 24h after symptom onset which is highly prevalent in patients with intracerebral hemorrhage (ICH). Observational studies suggested association between acute hypertensive response and hematoma expansion, peri-hematoma edema and death and disability, and possible reduction in these adverse outcomes with treatment of acute hypertensive response. Recent clinical trials have focused on determining the clinical efficacy of early intensive SBP reduction in ICH patients. The Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH-2) trial was the latest phase 3 randomized controlled multicenter clinical trial aimed to study the efficacy of early intensive reduction of SBP in ICH patients. In this review article, we summarize the results of recent clinical trials, treatment principles based on the latest guidelines, and the anticipated interpretation and incorporation of ATACH-2 trial results in clinical practice.

Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage

BackgroundLimited data are available to guide the choice of a target for the systolic blood-pressure level when treating acute hypertensive response in patients with intracerebral hemorrhage.MethodsWe randomly assigned eligible participants with intracerebral hemorrhage (volume, <60 cm3) and a Glasgow Coma Scale (GCS) score of 5 or more (on a scale from 3 to 15, with lower scores indicating worse condition) to a systolic blood-pressure target of 110 to 139 mm Hg (intensive treatment) or a target of 140 to 179 mm Hg (standard treatment) in order to test the superiority of intensive reduction of systolic blood pressure to standard reduction; intravenous nicardipine to lower blood pressure was administered within 4.5 hours after symptom onset. The primary outcome was death or disability (modified Rankin scale score of 4 to 6, on a scale ranging from 0 [no symptoms] to 6 [death]) at 3 months after randomization, as ascertained by an investigator who was unaware of the treatment assignments.ResultsAmong 1000 participants with a mean (±SD) systolic blood pressure of 200.6±27.0 mm Hg at baseline, 500 were assigned to intensive treatment and 500 to standard treatment. The mean age of the patients was 61.9 years, and 56.2% were Asian. Enrollment was stopped because of futility after a prespecified interim analysis. The primary outcome of death or disability was observed in 38.7% of the participants (186 of 481) in the intensive-treatment group and in 37.7% (181 of 480) in the standard-treatment group (relative risk, 1.04; 95% confidence interval, 0.85 to 1.27; analysis was adjusted for age, initial GCS score, and presence or absence of intraventricular hemorrhage). Serious adverse events occurring within 72 hours after randomization that were considered by the site investigator to be related to treatment were reported in 1.6% of the patients in the intensive-treatment group and in 1.2% of those in the standard-treatment group. The rate of renal adverse events within 7 days after randomization was significantly higher in the intensive-treatment group than in the standard-treatment group (9.0% vs. 4.0%, P=0.002).ConclusionsThe treatment of participants with intracerebral hemorrhage to achieve a target systolic blood pressure of 110 to 139 mm Hg did not result in a lower rate of death or disability than standard reduction to a target of 140 to 179 mm Hg. (Funded by the National Institute of Neurological Disorders and Stroke and the National Cerebral and Cardiovascular Center; ATACH-2 ClinicalTrials.gov number, NCT01176565.)

OP.3C.06] DIFFERENCE IN SUBACUTE BLOOD PRESSURE BETWEEN OFFICE AND AMBULATORY VALUES PREDICTS FUNCTIONAL OUTCOME AFTER ISCHEMIC STROKE

Objective: Acute hypertensive response after ischemic stroke is a self-limiting phenomenon and is associated with functional outcome. Excessive BP fluctuations may reflect increased sympathetic nervous system activity, which can impair the brain repair after stroke. Whether individual BP variation, based on difference between single office and full ambulatory 24-hour BP measurements, have a distinct long-term significance for stroke outcome remains unknown. We tested the hypothesis that subacute BP difference (BPD) [(office BP – mean daytime BP)/mean daytime BP] is independently associated with stroke outcome. Design and method: In a prospective study, we included 132 patients (age 62.9 + /- 12.9, NIH Stroke Scale score (NIHSS) 7.0 + /- 6.2) with acute ischemic stroke. Office (Omron) and Ambulatory BP monitoring (SpaceLabs) was performed on day 7 after stroke onset. The daytime period was defined as the interval from 6 AM to 10 PM. The relationship between these measures (adjusted for age, sex, admission neurological deficit as assessed by NIHSS score, baseline glucose level, and HR) and the 90-day poor outcome (death or dependency, modified Rankin Scale > 2) was studied using a multivariate logistic regression. Results: At 3 months, 28 (21.2%) patients had moderate to severe functional impairment after stroke. BPD given as a percentage was significantly higher in patients with poor outcome (14.2 + /−20.5 vs 2.0 + /−13.5; p < 0.001). In univariate analysis, high BPD (OR = 1.56; 95% CI, 1.19–2.05; p = 0.001) was significantly associated with poor stroke outcome. Age, sex, baseline neurological deficit and glucose level, thrombolytic treatment and subacute systolic BP and heart rate measured at day 7 also predicted stroke functional outcome. In multivariate analysis, the predictive value of BPD remained significant (OR = 2.01; 95% CI, 1.15–3.53; p = 0.01) after adjustment for covariates. Office BP also slightly predicted stroke outcome (OR = 1.02; 95% CI, 1.00–1.04; p = 0.04). By contrast, ambulatory BP levels had no significant predictive value after adjustment.Conclusions: Difference in BP between subacute office and ambulatory values is an independent predictor of functional outcome in patients after ischemic stroke. Both office and ambulatory BP reading are needed to evaluate stroke prognosis accurately.

Arterial stiffness, central blood pressures, wave reflections and acute hypertensive response in stroke

Arterial stiffness, central blood pressures, wave reflections and acute hypertensive response in stroke

Acute hypertensive response in ischemic stroke is associated with increased aortic stiffness

Background and aimsAcute hypertensive response (AHR) affects more than 60% of patients with ischemic stroke and is associated with poor outcomes. We hypothesized that its development is related to arterial stiffening. “The gold standard” estimate of arterial stiffness is carotid-femoral pulse wave velocity (CF-PWV). We compared CF-PWV and indirect indices of arterial stiffness (central augmentation index (cAIxHR), central systolic (cSBP) and pulse (cPP) pressures) between acute ischemic stroke patients who developed AHR and those who were normotensive in the early phase of stroke. MethodsAHR was assessed through hourly BP measurements within 24 h from admission using an oscillometric device. The stiffness was assessed using applanation tonometry with a SphygmoCor® device (Atcor, Sydney, Australia) 7 ± 2 days after stroke. ResultsAmong 102 patients with acute ischemic stroke, 73(71.5%) met AHR criteria. In an univariate analysis, CF-PWV, cAIxHR, cSBP and cPP were higher in those who developed AHR (10.9 vs. 8.3 m/s, p < 0.001; 30.8 vs. 23.9%, p = 0.004; 138.2 vs. 117.2 mmHg, p < 0.001; 54.6 vs. 44 mmHg, p = 0.005, respectively). In a multivariate logistic regression analysis, CF-PWV was independently associated with AHR after adjustment for age and peripheral mean blood pressure (pMBP) (p = 0.04), for age, pMBP and diabetes mellitus (DM) (p = 0.045), and age, pMBP, DM and hypertension (p = 0.047). ConclusionThis study revealed for the first time that AHR in ischemic stroke is associated with elevated aortic stiffness independently of other clinical factors including age and hypertension preceding stroke. A potential pathophysiological mechanism responsible for this relationship includes impaired baroreceptor function in stiff arteries resulting in impaired BP autoregulation.

Management of Acute Hypertensive Response in Patients With Ischemic Stroke.

High blood pressure (BP) >140/90 mm Hg is seen in 75% of patients with acute ischemic stroke and in 80% of patients with acute intracerebral hemorrhages and is independently associated with poor functional outcome. While BP reduction in patients with chronic hypertension remains one of the most important factors in primary and secondary stroke prevention, the proper management strategy for acute hypertensive response within the first 72 hours of acute ischemic stroke has been a matter of debate. Recent guidelines recommend clinical trials to ascertain whether antihypertensive therapy in the acute phase of stroke is beneficial. This review summarizes the current data on acute hypertensive response or elevated BP management during the first 72 hours after an acute ischemic stroke. Based on the potential deleterious effect of lowering BP observed in some clinical trials in patients with acute ischemic stroke and because of the lack of convincing evidence to support acute BP lowering in those situations, aggressive BP reduction in patients presenting with acute ischemic stroke is currently not recommended. While the early use of angiotensin receptor antagonists may help reduce cardiovascular events, this benefit is not necessarily related to BP reduction.