Therapeutic effect of early intensive antihypertensive treatment on rebleeding and perihematomal edema in acute intracerebral hemorrhage

Zang, Yanjing; Zhang, Chenhao; Song, Qing; Zhang, Jing; Li, Hongxuan; Feng, Shanshan; Gu, Fang

doi:10.1111/jch.13629

Cited by 3 publications

(6 citation statements)

References 25 publications

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“…The intensive strategy resulted effective to reduce re‐bleeding and perihematomal edema in comparison to control and was associated to better short‐term functional outcome as assessed by National Institutes of Health Stroke Scale scores and Barthel Index up to 90 days . There was no significant difference in mortality between the two groups …”

Section: Targeting Blood Pressure In Cerebral Hemorrhagementioning

confidence: 92%

“…In both groups, 25 mg of urapidil injection was slowly administered intravenously in 6 hours from the onset; 100 mg of urapidil was further slowly administered via micropump in the intensive arm . The intensive strategy resulted effective to reduce re‐bleeding and perihematomal edema in comparison to control and was associated to better short‐term functional outcome as assessed by National Institutes of Health Stroke Scale scores and Barthel Index up to 90 days . There was no significant difference in mortality between the two groups …”

Section: Targeting Blood Pressure In Cerebral Hemorrhagementioning

confidence: 99%

“…In the current issue of The Journal of Clinical Hypertension , Zang et al explored the effects of aggressive BP‐lowering treatment on hematoma and PHE growth and functional outcome in patients with acute ICH. One‐hundred and twenty‐one patients with spontaneous ICH confirmed by head computed tomography and elevated systolic BP (SBP) level (150‐220 mm Hg) within 1 hour of onset were randomly assigned to early intensive or standard treatment.…”

Section: Targeting Blood Pressure In Cerebral Hemorrhagementioning

confidence: 99%

“…One‐hundred and twenty‐one patients with spontaneous ICH confirmed by head computed tomography and elevated systolic BP (SBP) level (150‐220 mm Hg) within 1 hour of onset were randomly assigned to early intensive or standard treatment. In both groups, 25 mg of urapidil injection was slowly administered intravenously in 6 hours from the onset; 100 mg of urapidil was further slowly administered via micropump in the intensive arm . The intensive strategy resulted effective to reduce re‐bleeding and perihematomal edema in comparison to control and was associated to better short‐term functional outcome as assessed by National Institutes of Health Stroke Scale scores and Barthel Index up to 90 days .…”

Section: Targeting Blood Pressure In Cerebral Hemorrhagementioning

confidence: 99%

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Managing blood pressure in acute intracerebral hemorrhage

Lattanzi

Brigo

Silvestrini

2019

J of Clinical Hypertension

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| INTRODUC TI ONIntracerebral hemorrhage (ICH) results from the rupture of cerebral vessels leading to the development of a hematoma in the brain. It comprises approximately 15%-30% of all strokes and affects more than 1 million people every year worldwide. 1 Hypertension is the most common cause of ICH, and less frequent etiologies include coagulopathies, cerebral amyloid angiopathy, vascular abnormalities, brain trauma or tumors, and infections.Cerebral hemorrhage is the stroke subtype characterized by the highest mortality and morbidity: the fatality rate is about 40% at 1 month from bleeding and most survivors retain a severe residual disability, with only 20%-40% of patients living independently at 1 year. 2 Currently, medical and surgical strategies have substantially failed to improve outcome, and the management of ICH consists mainly of supportive therapies. The understanding of the mechanisms underlying the course of hematoma and the progression of the injury in surrounding parenchyma is, hence, of paramount relevance to identify therapeutic targets and effective treatment approaches. | PRIMARY AND S ECONDARY B R AIN INJ URY FOLLOWING CEREB R AL HEMATOMASeveral mechanisms are involved in brain injury related to ICH. Primary brain injury, which occurs at the time of hemorrhage, is due to the mass effect caused by extravasation of blood, physical disruption of adjacent tissue and mechanical compression of local structures. The hematoma can also increase the intracranial pressure, impair cerebral blood flow, and lead to brain herniation. 3 Although damage occurring immediately after ICH is untreatable, it is worth noticing that around one third of patients undergo hematoma expansion (HE) within the first days after stroke. 4 Hematoma growth contributes to midline shift and early neurological deterioration, and is consistently associated with higher fatality and poorer clinical outcome. 5 Remarkably, the intensive blood pressure reduction in acute cerebral hemorrhage trial (INTERACT-1) demonstrated that each 1 mL increase in HE is associated with a raise in the risk of death and dependency by 5%. 6 Secondary brain injury is due either to the body and tissue response to the hematoma or to the toxic effects of clot components, and includes a cascade of events, as inflammation, iron-mediated oxidative stress, apoptosis, necrosis, and autophagy, which mainly result in the development of peri-hemorrhagic edema (PHE). 7Cerebral edema occurs within hours of ICH, peaks several days later and can last for weeks. 5 In the hyperacute phase, PHE involves clot retraction, trans-capillary efflux of electrolytes, water and osmotically active serum proteins, and cytotoxic edema from neuronal energy failure. In the acute phase, during the first few days, PHE is sustained by coagulation cascade, thrombin production, immune reaction, and inflammatory cells. 8,9 Finally, beginning from approximately 72 hours after ICH, PHE formation involves erythrocyte lysis and hemoglobin-induced toxicity. 10 PHE may contribute to an overall ...

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Section: Targeting Blood Pressure In Cerebral Hemorrhagementioning

confidence: 92%

Section: Targeting Blood Pressure In Cerebral Hemorrhagementioning

confidence: 99%

Section: Targeting Blood Pressure In Cerebral Hemorrhagementioning

confidence: 99%

Section: Targeting Blood Pressure In Cerebral Hemorrhagementioning

confidence: 99%

See 2 more Smart Citations

Managing blood pressure in acute intracerebral hemorrhage

Lattanzi

Brigo

Silvestrini

2019

J of Clinical Hypertension

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“…A recent study has shown that intensive BP control is associated with a decreased perihematomal edema expansion rate (PHER) at 24 hours in deep ICH, which in turn is associated with adverse outcomes in basal ganglia ICH but not in all deep ICH (e.g., thalamic ICH) [ 144 ]. Another randomized controlled trial study revealed that the volume of the hematoma at 24 hours, the volume of PHE at 72 hours, and the NIHSS scores at 30 and 90 days in patients receiving intensive antihypertensive treatment were lower than those of the placebo group, while the Barthel scores at 30 and 90 days were higher [ 225 ]. Furthermore, a study with 635 ICH patients illustrated that angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers reduced mortality, volume of perihematomal edema, and prevalence of pneumonia in patients with hypertension [ 226 ].…”

Section: Potential Therapeutic Targets For Phe After Ichmentioning

confidence: 99%

Molecular, Pathological, Clinical, and Therapeutic Aspects of Perihematomal Edema in Different Stages of Intracerebral Hemorrhage

Jiang

Guo

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Acute intracerebral hemorrhage (ICH) is a devastating type of stroke worldwide. Neuronal destruction involved in the brain damage process caused by ICH includes a primary injury formed by the mass effect of the hematoma and a secondary injury induced by the degradation products of a blood clot. Additionally, factors in the coagulation cascade and complement activation process also contribute to secondary brain injury by promoting the disruption of the blood-brain barrier and neuronal cell degeneration by enhancing the inflammatory response, oxidative stress, etc. Although treatment options for direct damage are limited, various strategies have been proposed to treat secondary injury post-ICH. Perihematomal edema (PHE) is a potential surrogate marker for secondary injury and may contribute to poor outcomes after ICH. Therefore, it is essential to investigate the underlying pathological mechanism, evolution, and potential therapeutic strategies to treat PHE. Here, we review the pathophysiology and imaging characteristics of PHE at different stages after acute ICH. As illustrated in preclinical and clinical studies, we discussed the merits and limitations of varying PHE quantification protocols, including absolute PHE volume, relative PHE volume, and extension distance calculated with images and other techniques. Importantly, this review summarizes the factors that affect PHE by focusing on traditional variables, the cerebral venous drainage system, and the brain lymphatic drainage system. Finally, to facilitate translational research, we analyze why the relationship between PHE and the functional outcome of ICH is currently controversial. We also emphasize promising therapeutic approaches that modulate multiple targets to alleviate PHE and promote neurologic recovery after acute ICH.

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