Purpose-To estimate the prevalence of elevated blood pressure in adult patients with acute stroke in the United States (U.S.).Methods-Stroke patients were classified by initial systolic blood pressure into four categories using demographic, clinical, and treatment data from the National Hospital Ambulatory Medical Care Survey, the largest study of utilization and provision of emergency department services in the U.S. We also compared the age-, sex-, and ethnicity-adjusted rates of elevated blood pressure strata comparable with stages 1 and 2 hypertension in the U.S. population.Results-Of the 563,704 stroke patients evaluated, initial systolic blood pressure was <140 mm Hg in 173,120 patients (31%), 140-184 mm Hg in 315,207 patients (56%), 185-219 mm Hg in 74,586 patients (13%), and ≥220 mm Hg in 791 patients (0.1%). The mean time interval between presentation and evaluation was 40 ± 55, 33 ± 39, 25 ± 27, and 5 ± 1 minutes for increasing systolic blood pressure strata (p=0.009). A 3-and 8-fold higher rate of elevated blood pressure strata was observed in acute stroke than the existing rates of stages 1 and 2 hypertension in the U.S. population. Labetalol and hydralazine were used in 6,126 (1%) and 2,262 (0.4%) patients, respectively. Thrombolytics were used in 1,283 patients (0.4%), but only in those with SBP of 140-184 mm Hg.Conclusions-In a nationally representative large dataset, elevated blood pressure was observed in over 60% of the patients presenting with stroke to the emergency department. Elevated blood pressure was associated with an earlier evaluation, however, the use of thrombolytics was restricted to ischemic stroke patients with systolic blood pressure <185 mm Hg.
Background and Purpose-The Joint National Committee on High Blood Pressure identified a new category of blood pressure in adults termed prehypertension. Our objective was to determine the long-term risk of cardiovascular diseases associated with this new category in a well-defined cohort of adults. Methods-We evaluated the association of prehypertension (120 to 139/80 to 89 mm Hg) and hypertension (Ͼ140/ 90 mm Hg) with the incidence of atherothrombotic brain infarction (ABI), all strokes, myocardial infarction (MI), and coronary artery disease (CAD) using pooled repeated measures and Cox proportional hazards analyses during follow-up after adjusting for age, gender, obesity, diabetes mellitus, hypercholesterolemia, cigarette smoking, and study period in a cohort of 5181 persons who participated in the Framingham Study. Results-Among the 11 116 person observations with a mean follow-up period of 9.9Ϯ1.0 years, prehypertension was not associated with an increased risk for ABI (relative risk [RR], 2.2; 95% CI, 0.5 to 9.3). Among the 11 802 person observations with a mean follow-up period of 9.7Ϯ1.5 years, prehypertension was associated with an increased risk for MI (RR, 3.5; 95% CI, 1.6 to 7.5). Prehypertension was also associated with an increased risk of CADs among the 11 570 person observations (RR, 1.7; 95% CI, 1.2 to 2.4). Conclusions-Prehypertension appears to be associated with an increased risk of MI and CAD but not stroke. Further studies are required to confirm the anticipated benefits of identifying and intervening in persons with prehypertension.
The December 2003 report from the National Institute of Neurological Disorders and Stroke (NINDS) Workshop on priorities for clinical research in intracerebral hemorrhage (ICH) recommended clinical trials for evaluation of blood pressure management in acute ICH as a leading priority. The Special Writing Group of the Stroke Council of the American Heart Association in 1999 and 2007 emphasized the need for clinical trials to ensure evidence-based treatment of acute hypertensive response in ICH. To address important gaps in knowledge, we conducted a pilot study funded by the NINDS, Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) I Trial, during 2004–2008 to determine the appropriate level of systolic blood pressure (SBP) reduction. We now have initiated a multicenter, randomized Phase III trial, the ATACH II Trial, to definitively determine the efficacy of early, intensive, anti-hypertensive treatment using intravenous (IV) nicardipine initiated within 3 h of onset of ICH and continued for the next 24 h in subjects with spontaneous supratentorial ICH. The primary hypothesis of this large (N = 1,280), streamlined, and focused trial is that SBP reduction to ≤140 mm Hg reduces the likelihood of death or disability at 3 months after ICH, defined by modified Rankin scale score of 4–6, by at least 10% absolute compared to standard SBP reduction to ≤180 mm Hg. The ATACH II trial is a natural extension of numerous case series, the subsequent ATACH I pilot trial, and a preliminary, randomized, and controlled trial in this patient population funded by the Australian National Health and Medical Research Council. Both trials recently confirmed the safety and tolerability of both the regimen and goals of antihypertensive treatment in acutely hypertensive patients with ICH, as proposed in the present trial. The underlying mechanism for this expected beneficial effect of intensive treatment is presumably mediated through reduction of the rate and magnitude of hematoma expansion observed in approximately 73% of the patients with acute ICH. The Australian trial provided preliminary evidence of attenuation of hematoma expansion with intensive SBP reduction. The ATACH II trial will have important public health implications by providing evidence of, or lack thereof, regarding the efficacy and safety of acute antihypertensive treatment in subjects with ICH. This treatment represents a strategy that can be made widely available without the need for specialized equipment and personnel, and therefore, can make a major impact upon clinical practice for treating patients with ICH.
The authors performed a multicenter prospective observational study to evaluate the feasibility and safety of intravenous antihypertensive protocol for acute hypertension in patients with intracerebral hemorrhage (ICH). Twenty-seven patients with ICH and acute hypertension (mean age 61.37 +/- 14.27; 10 were men) were treated to maintain the systolic blood pressure (BP) below 160 mm Hg and diastolic BP below 90 mm Hg within 24 hours of symptom onset. Neurological deterioration (defined as a decrease in initial Glasgow Coma Scale score > or = 2) was observed in 2 (7.4%) of 27 patients during treatment. Among patients who underwent follow-up computed tomography, hematoma expansion (more than 33% increase in hematoma size at 24 hours) was observed in 2 (9.1%) of 22 patients. Patients treated within 6 hours of symptom onset were more likely to be functionally independent (modified Rankin scale < or = 2) at 1 month compared with patients who were treated between 6 and 24 hours (8 of 18 versus 0 of 9,P = .03). Aggressive pharmacological treatment of acute hypertension in patients with ICH can be initiated early with a low rate of neurological deterioration and hematoma expansion.
This trial is a multicenter open-labeled pilot trial to determine the tolerability and safety of three escalating levels of antihypertensive treatment goals for acute hypertension in 60 subjects with supratentorial intracerebral hemorrhage (ICH). The pilot trial is the natural development of numerous case series evaluating the effect of antihypertensive treatment of acute hypertension in subjects with ICH. The proposed trial will have important public health implications by providing necessary information for a definitive phase III study regarding the efficacy of antihypertensive treatment of acute hypertension in subjects with ICH. The specific aims of the present pilot study are to: (1) Determine the tolerability of the treatment as assessed by achieving and maintaining three different systolic blood pressure goals with intravenous nicardipine infusion for 18 to 24 hours postictus in subjects with ICH who present within 6 hours of symptom onset; (2) Define the safety, assessed by the rate of neurological deterioration during treatment and serious adverse events, of three escalating systolic blood pressure treatment goals using intravenous nicardipine infusion; and (3) Obtain preliminary estimates of the treatment effect using the rate of hematoma expansion (within 24 hours) and modified Rankin scale and Barthel index at 3 months following symptom onset.
Stroke is the third leading cause of death and the leading cause of long-term disability in the United States. Approximately 80% of all strokes are ischemic and there are limited therapies approved for the treatment of acute ischemic stroke. Understanding the mechanisms of ischemic brain damage is necessary for the development of innovative treatment strategies. In this review, we discuss the hemodynamic and molecular mechanisms of ischemic brain damage and the potential therapeutic strategies, including reperfusion and primary and secondary neuroprotection, and strategies for recovery of function, such as neural plasticity and stem cell transplantation. The effective treatment of ischemic stroke is likely to result from a combination of therapeutic modalities aimed at different mechanisms of ischemic brain damage and delivered at specific times after acute cerebral ischemia.
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