[citation report] Systolic Blood Pressure Control and Mortality After Stroke in Hypertensive Patients (2024)

“…These data support the hypothesis that elevating IGF-1 expression in astrocytes significantly improves stroke outcomes after transient ischemia-reperfusion in middle-aged female SD rats. AAV5 mediatedexpression of hIGF-1 in astrocytes reduced stroke-induced motor while controls experienced a decrease in systolic blood pressure after stroke, which is associated with poorer clinical outcomes and increased mortality in stroke patients (Lin, Ovbiagele, Markovic, & Towfighi, 2015;Okin, Kjeldsen, & Devereux, 2015) especially in the acute period of stroke (Wohlfahrt et al, 2015). These novel findings are in accordance with a growing body of evidence that functional modifications of astrocytes yields major benefits for neurodegenerative diseases (Bajenaru, Zhu, Hedrick, Donahoe, Parada, & Gutmann, 2002;Furman et al, 2012Furman et al, , 2016.…”

confidence: 69%

Section: Discussionmentioning

2017

Middle aged female rats sustain larger stroke infarction and disability than younger female rats. This older group also shows age-related reduction of insulin like growth factor (IGF)-1 in serum and in astrocytes, a cell type necessary for post stroke recovery. To determine the impact of astrocytic IGF-1 for ischemic stroke, these studies tested the hypothesis that gene transfer of IGF-1 to astrocytes will improve stroke outcomes in middle aged female rats. Middle aged (10–12 month old), acyclic female rats were injected with recombinant adeno-associated virus serotype 5 (AAV5) packaged with the coding sequence of the human (h)IGF-1 gene downstream of an astrocyte-specific promoter GFAP (AAV5-GFP-hIGF-1) into the striatum and cortex. The AAV5-control consisted of an identical shuttle vector construct without the hIGF-1 gene (AAV5-GFAP-control). Six to eight weeks later, animals underwent transient (90 mins) middle cerebral artery occlusion via intraluminal suture. While infarct volume was not altered, AAV5-GFAP-hIGF-1 treatment significantly improved blood pressure and neurological score in the early acute phase of stroke (2 days) and sensory-motor performance at both the early and late (5 days) acute phase of stroke. AAV5-GFAP-hIGF-1 treatment also reduced circulating serum levels of GFAP, a biomarker for blood brain barrier permeability. Flow cytometry analysis of immune cells in the brain at 24h post stroke showed that AAV5-GFAP-hIGF-1 altered the type of immune cells trafficked to the ischemic hemisphere, promoting an anti-inflammatory profile. Collectively, these studies show that targeted enhancement of IGF-1 in astrocytes of middle-aged females improves stroke-induced behavioral impairment and neuroinflammation.

Purpose The optimal blood pressure (BP) targets in terms of mortality risk after stroke remain unclear. This study aimed to assess the relationship between BP and mortality in stroke survivors. Patients and Methods We included 1696 participants with self-reported history of stroke aged 18 years and older from the National Health and Nutrition Examination Survey (NHANES) 1999–2014 and NHANES III with public-use linked mortality files from 2015. Baseline systolic BP (SBP) and diastolic BP (DBP) levels were obtained by taking the average of 3 measures. Cox proportional hazard models and restricted cubic splines were conducted to explore the relationship between BP and all-cause mortality. Results During a median follow-up period of 5.6 years, 888 deaths occurred. After fully adjusting for confounding factors, SBP displayed a J-curve relationship (nadir 135 mm Hg), while DBP exhibited a reverse J-curve relationship (nadir 73 mm Hg) with the risk of all-cause mortality. However, the J-curve or reverse J-curve pattern between blood pressure and mortality appeared to be limited to individuals with an age >65 years, identifying a nadir of SBP/DBP of 142/73 mm Hg. The risk of mortality followed a linear relationship for SBP and DBP in stroke survivors aged ≤65 years, with risks increasing with higher SBP and lower DBP. Conclusion In this cross-sectional study that used national survey data, these data suggest a strong J-curve or reverse J-curve relationship between blood pressure and risk of all-cause mortality, whereas the pattern appears to be limited to individuals with an age >65 years, with a nadir at 142/73 mmHg. However, missing data on stroke type and stroke treatment limits the generalizability. Future prospective studies are needed to determine preferential blood pressure target in patients after stroke.

Background: It is uncertain if dexmedetomidine has more favorable pharmaco*kinetic profile than the traditional sedative drug propofol in patients who undergo endovascular therapy for acute stroke. We conducted a prospective randomized control trial to compare the safety and efficacy of dexmedetomidine with propofol for patients undergoing endovascular therapy for acute stroke. Methods: A total of 80 patients who met study inclusion criteria were received either propofol (n = 45) or dexmedetomidine (n = 35) between January 2016 and August 2018. We recorded the favorable neurologic outcome (modified Rankin score <3) both at discharge and 3 months after stroke, National Institute of Health Stroke scale (NIHSS) at 48 hours post intervention, modified thrombolysis in myocardial infarction score on digital subtraction angiography, intraprocedural hemodynamics, recovery time, relevant time intervals, satisfaction score of the surgeon, mortality, and complications. Results: There were no significant differences between the 2 groups ( P > .05) with respect to heart rate, respiratory rate, and SPO 2 during the procedure. The mean arterial pressure (MAP) was significantly low in the propofol group until 15 minutes after anesthesia was induced. No difference was recorded between the groups at the incidence of fall in MAP >20%, MAP >40% and time spent with MAP fall >20% from baseline MAP. In the propofol group, the time spent with MAP fall >40% from baseline MAP was significantly long ( P < .05). Midazolam and fentanyl were similar between the 2 groups ( P > .05) that used vasoactive drugs. The time interval from stroke onset to CT room, from stroke onset to groin puncture, and from stroke onset to recanalization/end of the procedure, was not significantly different between the 2 groups ( P > .05). The recovery time was longer in the dexmedetomidine group ( P < .05). There was no difference between the groups with respect to complications, favorable neurological outcome, and mortality both at hospital discharge and 3 months later, successful recanalization and NIHSS score after 48 hours ( P > .05). However, the satisfaction score of the surgeon was higher in the dexmedetomidine group ( P < .05). Conclusions: Dexmedetomidine was undesirable than propofol as a sedative agent during endovascular therapy in patients with acute stroke for a long-term functional outcome, though the satisfaction score of the surgeon was higher in the dexmedetomidine group.