Managing blood pressure in acute intracerebral hemorrhage

Abstract

| 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 ...

J-shape relation of blood pressure reduction and outcome in acute intracerebral hemorrhage: A pooled analysis of INTERACT2 and ATACH-II individual participant data

“…19 The acute hypertensive response may be protective and preserve cerebral blood flow in the presence of increased intracranial pressure. 17 More research is warranted regarding autoregulatory indices and neuroimaging markers of ischemic risk to ensure the most appropriate control of SBP by defining the drop in SBP values that can be sustained without affecting brain metabolism, mainly in the perihematomal area. 20…”

“…19 The acute hypertensive response may be protective and preserve cerebral blood flow in the presence of increased intracranial pressure. 17 More research is warranted regarding autoregulatory indices and neuroimaging markers of ischemic risk to ensure the most appropriate control of SBP by defining the drop in SBP values that can be sustained without affecting brain metabolism, mainly in the perihematomal area. 20 Some strengths of these analyses include the relatively large dataset derived from participants recruited from a broad range of healthcare settings, with systematic evaluation and high adherence to treatment and follow-up.…”

“…Our findings that large SBP reductions over 1 h, for example, from > 200 to target < 140 mmHg, may offset any benefits that support the need to avoid overshoot and potential penumbral risk or circulatory insufficiency. 17 A singlecenter retrospective cohort of 119 patients with acute ICH reported that a severe drop in SBP was associated with an increased risk of remote cerebral ischemic lesions, neurologic deterioration during hospitalization, and longer days spent in the neuro-intensive care unit. 18 Compared with normotensive patients, a rightward shift of the cerebral autoregulatory curve may occur, and the lower limit of cerebral perfusion may be compensated at higher SBP in those International Journal of Stroke, 17 (10) with a history of hypertension.…”

Blood Pressure Model Based on Hybrid Feature Convolution Neural Network in Promoting Rehabilitation of Patients with Hypertensive Intracerebral Hemorrhage

“…Therefore, the 24 h ambulatory blood pressure monitoring curve showed a double peak and a valley. In the traditional method of administration, the drug was administered by the method of average distribution, three time per day [ 19 ]. As the drug was not given according to the time rhythm, two adverse effects can occur.…”

Relationship between miR-92b expression and hypertension, the degree of heart disease and cerebral hemorrhage

“…Under long-term hypertension, the lipids of the arteriole walls in the brain tissue will appear hyaline degeneration, broblast proliferation and macrophage aggregation will replace vascular smooth muscle cells, and the vascular lumen will be narrowed [13]. When the patient's blood pressure rises suddenly, rupture bleeding occurs [14]. Hence, it is indispensable to delve into the emergence and development of hypertension and thwart disease progression.…”