The trial enrolled 495 Black and Hispanic, English and Spanish speaking adults with uncontrolled systolic blood pressure (SBP ≥ 140 mmHg) who had experienced a first-time or recurrent stroke or transient ischemic attack.
After multivariable adjustment, including baseline SBP and mean SBP during the first 12-month follow-up, there was a significantly positive relationship of SD SBP with the risk of subsequent first stroke (per SD increment; odds ratio, 1.41; 95% confidence interval: 1.17-1.69) and first ischemic stroke (odds ratio, 1.55; 95% confidence interval: 1.26-1.90).
SBP and DBP values were higher in patients with emergencies than in those with urgencies (BP 193 ± 15/102 ± 15 vs. 189 ± 13/96 ± 13 mmHg in 2008 and 192 ± 17/98 ± 15 vs. 189 ± 12/94 ± 15 mmHg in 2015, P < 0.001 for both).Among hypertensive emergencies, the different forms of organ damage were 25% acute coronary syndromes and 1% aortic dissection in both periods, 34 and 38% acute heart failure, 40 and 37% stroke.
We hypothesized inter-arm differences of SBP ≧5 mmHg may be related to higher pulse pressure/stroke volume index, a surrogate marker of arterial stiffness.
We extracted data on patient demographics, stroke-type (ischaemic or haemorrhagic), stroke severity, vascular risk factors, and SBP and DBP at the time of stroke presentation.
MEE was estimated as stroke work (SW = systolic blood pressure [SBP] × stroke volume [SV])/"double product" of SBP × heart rate (HR), as an estimate of O<sub>2</sub> consumption, which can be simplified as SV/HR ratio and expressed in ml/sec.
Analyses used data from the Efficacy of Nitric Oxide in Stroke trial, a multicentre randomized single-masked and outcome-masked trial of glyceryl trinitrate vs. no glyceryl trinitrate in 4011 patients recruited within 48 h of an ischaemic or haemorrhagic stroke and with raised SBP (140-220 mmHg).
Risk of total CVDs, MI, and stroke was increased with low-range prehypertension (low-range: SBP 120-129 mmHg and/or DBP 80-84 mmHg) versus normal BP - RR 1.42 (95% CI 1.29-1.55), 1.43 (1.10-1.86), and 1.52 (1.27-1.81), respectively - and risk of total CVDs, CHD, MI, and stroke was increased with high-range prehypertension (high-range: SBP 130-139 mmHg and/or DBP 85-89 mmHg) - RR 1.81 (95% CI 1.56-2.10), 1.65 (1.13-2.39), 1.99 (1.59-2.50), and 1.99 (1.68-2.36), respectively.
Despite reducing SBP, vasodilators did not significantly impair absolute CBF but improved cerebrovascular pulsatility and reactivity, suggesting therapeutic potential in preventing stroke and cerebral small vessel disease.
During the first two days after stroke onset, mean SBP for all stroke patients decreased by 14.9 mmHg (95% CI 12.3-17.4, P < 0.0001) and further 2.3 mmHg days 2-7 after onset (95% CI -0.1 to 4.7, P = 0.066).
In a prospective national study of 22 164 blacks and whites ≥45 years without baseline cognitive impairment or stroke from the REGARDS cohort study (Reasons for Geographic and Racial Differences in Stroke), enrolled 2003 to 2007 and followed through September 2015, we measured changes in cognition associated with baseline systolic and diastolic BP (SBP and DBP), as well as pulse pressure (PP) and mean arterial pressure, and we tested whether age, race, and sex modified the effects.
Factors predictive of withholding treatment with IV alteplase were: age 95 [68]; stroke onset time of 4 h 15 min [50 min]; severe dementia [no memory problems]; SBP 200 mm/Hg [140 mm/Hg].
In the lower SBP target group, moderate reducers had a higher risk of death (adjusted HR 1.6 [95% CI 1.0-2.7]), MVE (adjusted HR 2.1 [95% CI 1.4-3.2]), and stroke (adjusted HR 2.6[95% CI 1.7-4.1]) compared to mild reducers.
In the standard treatment arm, those who achieved a target SBP less than 140 mmHg displayed a substantial reduction in risk of MACE (hazard ratio = 0.65, P = 0.005), all-cause death (hazard ratio = 0.64, P = 0.02), and nonfatal stroke (hazard ratio = 0.47, P = 0.02) as compared with those whose achieved SBP was 140 mmHg or higher.
Risk of CHD and stroke increased significantly when SBP was above 125 mmHg or DBP above 72 mmHg in people without diabetes, whereas this trend was attenuated in diabetic patients.
Odds ratios for stroke severity by the National Institutes of Health Stroke Scale score, disability or death at discharge (modified Rankin Score ≥2) and 1-month mortality were calculated for patients treated vs. nontreated with beta-blockers, adjusted for admission SBP and additional risk factors.
Higher home SBP, but not office SBP, was significantly associated with increased risk of stroke among both 349 participants with normal physical function and 152 participants with impaired physical function [hazard ratio (95% confidence interval) per 14.4-mmHg increase: 1.74 (1.12-2.69) and 1.77 (1.06-2.94), respectively], with no significant interaction for physical function (P = 0.56).
In summary, among the wide heterogenetic population, modest associations between VVV of SBP and all-cause mortality, CVD incidence, CVD mortality, CHD incidence, and stroke incidence were found.
At 24 h after randomization, the differences in SBP reductions were 8.7, 9.5, and 9.6 mmHg between the antihypertensive treatment and control groups among patients receiving treatment within less than 12, 12-23, and 24-48 h after stroke onset, respectively (P < 0.001 in all subgroups).