scholarly journals Sex Differences in Blood Pressure–Lowering Therapy and Outcomes Following Intracerebral Hemorrhage

Stroke ◽  
2020 ◽  
Vol 51 (8) ◽  
pp. 2282-2286 ◽  
Author(s):  
Mayumi Fukuda-Doi ◽  
Haruko Yamamoto ◽  
Masatoshi Koga ◽  
Yuko Y. Palesch ◽  
Valerie L. Durkalski-Mauldin ◽  
...  

Background and Purpose: Evidence regarding sex differences in clinical outcomes and treatment effect following intracerebral hemorrhage is limited. Using the ATACH-2 trial (Antihypertensive Treatment in Intracerebral Hemorrhage-2) data, we explored whether sex disparities exist in outcomes and response to intensive blood pressure (BP)–lowering therapy. Methods: Eligible intracerebral hemorrhage subjects were randomly assigned to intensive (target systolic BP, 110–139 mm Hg) or standard (140–179 mm Hg) BP-lowering therapy within 4.5 hours after onset. Relative risk of death or disability corresponding to the modified Rankin Scale score of 4 to 6 was calculated, and interaction between sex and treatment was explored. Results: In total, 380 women and 620 men were included. Women were older, more prescribed antihypertensive drugs before onset, and had more lobar intracerebral hemorrhage than men. Hematoma expansion was observed less in women. After multivariable adjustment, the relative risk of death or disability in women was 1.19 (95% CI, 1.02–1.37, P =0.023). The relative risk of death or disability between intensive versus standard BP-lowering therapy was 0.91 (95% CI, 0.74–1.13) in women versus 1.13 (95% CI, 0.92–1.39) in men ( P for interaction=0.11), with inconclusive Gail-Simmon test ( P =0.16). Conclusions: Women had a higher risk of death or disability following intracerebral hemorrhage. The benefit of intensive BP-lowering therapy in women is inconclusive, consistent with the overall results of ATACH-2. Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT01176565.

2021 ◽  
pp. 174749302110446
Author(s):  
Kazunori Toyoda ◽  
Sohei Yoshimura ◽  
Mayumi Fukuda-Doi ◽  
Adnan I Qureshi ◽  
Renee’ Hebert Martin ◽  
...  

Background and aims Nicardipine has strong, rapidly acting antihypertensive activity. The effects of acute systolic blood pressure levels achieved with intravenous nicardipine after onset of intracerebral hemorrhage on clinical outcomes were determined. Methods A systematic review and individual participant data analysis of articles before 1 October 2020 identified on PubMed were performed (PROSPERO: CRD42020213857). Prospective studies involving hyperacute intracerebral hemorrhage adults treated with intravenous nicardipine whose outcome was assessed using the modified Rankin Scale were eligible. Outcomes included death or disability at 90 days, defined as the modified Rankin Scale score of 4–6, and hematoma expansion, defined as an increase ≥6 mL from baseline to 24-h computed tomography. Summary of review Three studies met the eligibility criteria. For 1265 patients enrolled (age 62.6 ± 13.0 years, 484 women), death or disability occurred in 38.2% and hematoma expansion occurred in 17.4%. Mean hourly systolic blood pressure during the initial 24 h was positively associated with death or disability (adjusted odds ratio (aOR) 1.12, 95% confidence interval (CI) 1.00–1.26 per 10 mmHg) and hematoma expansion (1.16, 1.02–1.32). Mean hourly systolic blood pressure from 1 h to any timepoint during the initial 24 h was positively associated with death or disability. Later achievement of systolic blood pressure to ≤140 mmHg increased the risk of death or disability (aOR 1.02, 95% CI 1.00–1.05 per hour). Conclusions Rapid lowering of systolic blood pressure by continuous administration of intravenous nicardipine during the initial 24 h in hyperacute intracerebral hemorrhage was associated with lower risks of hematoma expansion and 90-day death or disability without increasing serious adverse events.


Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Kanta Tanaka ◽  
Masatoshi Koga ◽  
Adnan I Qureshi ◽  
Haruko Yamamoto ◽  
Kazunori Toyoda

Background and purpose: We aimed to highlight temporal trajectories of systolic blood pressure (SBP) in patients with acute intracerebral hemorrhage (ICH) to investigate the clinical relevance of heterogeneity in responses to blood pressure lowering therapy. Methods: A post-hoc analysis of ATACH-2 trial, in which ICH patients were randomly assigned to intensive or standard SBP lowering with intravenous administration of nicardipine. Using data for all 1000 patients enrolled from 110 clinical sites, temporal changes of hourly maximum SBP up to 24 hours after randomization were analyzed with the group-based trajectory modeling (GBTM). Model selection was mainly based on the Bayesian Information Criteria. The primary outcome was death or disability (modified Rankin Scale score 4-6) at 3 months. Secondary outcomes included hematoma expansion within 24 hours and acute kidney injury (AKI). AKI was defined as an increase in serum creatinine by ≥0.3 mg/dl or to ≥1.5 times baseline within 48 hours. The outcomes were compared between the trajectory groups using multivariable logistic models with random-effects by clinical sites. Results: Of the analyzed 1000 patients, death or disability, hematoma expansion, and AKI were encountered in 367, 161, and 101 patients, respectively. GBTM revealed 4 SBP trajectory groups: early response-low SBP (38.2%), moderate SBP (16.8%), delayed response-low SBP (14.2%), and high SBP (30.8%). Nicardipine dosage was highest in the delayed response-low SBP group, 81.7% of which were from the intensive SBP lowering group. The risk of death or disability was higher only in the delayed response-low SBP group (adjusted odds ratio [aOR] 2.86; 95% confidence interval [CI] 1.66-4.93) than in the early response-low SBP group. The risk of hematoma expansion was not significantly different among the groups. The delayed response-low SBP group had higher risk of AKI (aOR 2.78; 95% CI 1.46-5.31; reference, the early response-low SBP group). Conclusions: An SBP trajectory group with delayed SBP lowering despite intensive treatment was associated with increased risk of death or disability at 3 months. Resistance to intensive SBP lowering may predict poor clinical outcomes, and intensive SBP control in these cases will increase the risk of AKI.


2005 ◽  
Vol 6 (1_suppl) ◽  
pp. S8-S11
Author(s):  
Hans-Christoph Diener

Hypertension is the most important modifiable risk factor for primary and secondary stroke prevention. All antihypertensive drugs are effective in primary prevention: the risk reduction for stroke is 30—42%. However, not all classes of drugs have the same effects: there is some indication that angiotensin receptor blockers may be superior to other classes of antihypertensive drugs in stroke prevention. Seventy-five percent of patients who present to hospital with acute stroke have elevated blood pressure within the first 24—48 hours. Extremes of systolic blood pressure (SBP) increase the risk of death or dependency. The aim of treatment should be to achieve and maintain the SBP in the range 140—160 mmHg. However, fast and drastic blood pressure lowering can have adverse consequences. The PROGRESS trial of secondary prevention with perindopril + indapamide versus placebo + placebo showed a decrease in numbers of stroke recurrences in patients given both active antihypertensive agents, more impressive for cerebral haemorrhage.There were also indications that active treatment might decrease the development of post-stroke dementia.


Author(s):  
G. B. Piccoli ◽  
G. Beltrame ◽  
F. Bonello ◽  
M. Salomone ◽  
A. Pacitti ◽  
...  

2021 ◽  
Author(s):  
Brody H Foy ◽  
Thor Sundt ◽  
Jonathan CT Carlson ◽  
Aaron D Aguirre ◽  
John M Higgins

Inflammation is the physiologic reaction to cellular and tissue damage caused by pathologic processes including trauma, infection, and ischemia. Effective inflammatory responses integrate molecular and cellular functions to prevent further tissue damage, initiate repair, and restore homeostasis, while futile or dysfunctional responses allow escalating injury, delay recovery, and may hasten death. Elevation of white blood cell count (WBC) and altered levels of other acute phase reactants are cardinal signs of inflammation, but the dynamics of these changes and their resolution are not established. Patient responses appear to vary dramatically with no clearly defined signs of good prognosis, leaving physicians reliant on qualitative interpretations of laboratory trends. We studied the human acute inflammatory response to trauma, ischemia, and infection by tracking the longitudinal dynamics of cellular and serum markers in hospitalized patients. Unexpectedly, we identified a conserved pattern of recovery defined by co-regulation of WBC and platelet (PLT) populations. Across all inflammatory conditions studied, recovering patients followed a consistent WBC-PLT trajectory shape that is well-approximated by exponential WBC decay and delayed linear PLT growth. This recovery trajectory shape may represent a fundamental archetype of human physiologic response at the cellular population scale, and provides a generic approach for identifying high-risk patients: 32x relative risk of adverse outcomes for cardiac surgery patients, 9x relative risk of death for COVID-19, and 5x relative risk of death for myocardial infarction.


2022 ◽  
Author(s):  
Philippe Bégin ◽  
Jeannie Callum ◽  
Richard Cook ◽  
Erin Jamula ◽  
Yang Liu ◽  
...  

Author(s):  
Zhe Kang Law ◽  
◽  
Rob Dineen ◽  
Timothy J England ◽  
Lesley Cala ◽  
...  

Abstract Neurological deterioration is common after intracerebral hemorrhage (ICH). We aimed to identify the predictors and effects of neurological deterioration and whether tranexamic acid reduced the risk of neurological deterioration. Data from the Tranexamic acid in IntraCerebral Hemorrhage-2 (TICH-2) randomized controlled trial were analyzed. Neurological deterioration was defined as an increase in National Institutes of Health Stroke Scale (NIHSS) of ≥ 4 or a decline in Glasgow Coma Scale of ≥ 2. Neurological deterioration was considered to be early if it started ≤ 48 h and late if commenced between 48 h and 7 days after onset. Logistic regression was used to identify predictors and effects of neurological deterioration and the effect of tranexamic acid on neurological deterioration. Of 2325 patients, 735 (31.7%) had neurological deterioration: 590 (80.3%) occurred early and 145 (19.7%) late. Predictors of early neurological deterioration included recruitment from the UK, previous ICH, higher admission systolic blood pressure, higher NIHSS, shorter onset-to-CT time, larger baseline hematoma, intraventricular hemorrhage, subarachnoid extension and antiplatelet therapy. Older age, male sex, higher NIHSS, previous ICH and larger baseline hematoma predicted late neurological deterioration. Neurological deterioration was independently associated with a modified Rankin Scale of > 3 (aOR 4.98, 3.70–6.70; p < 0.001). Tranexamic acid reduced the risk of early (aOR 0.79, 0.63–0.99; p = 0.041) but not late neurological deterioration (aOR 0.76, 0.52–1.11; p = 0.15). Larger hematoma size, intraventricular and subarachnoid extension increased the risk of neurological deterioration. Neurological deterioration increased the risk of death and dependency at day 90. Tranexamic acid reduced the risk of early neurological deterioration and warrants further investigation in ICH. URL:https://www.isrctn.com Unique identifier: ISRCTN93732214


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