Prevention Of Reperfusion Injury Research Articles

Peptides are cardioprotective drugs of the future. Oxytocin

The widespread introduction of percutaneous coronary intervention (PCI) in the treatment of acute myocardial infarction (AMI) caused a significant reduction in the mortality rate from AMI in developed countries. However, over the past 10 years, there was no significant reduction in in-hospital mortality from AMI. It is clear that there is an urgent need to develop novel drugs that could effectively prevent reperfusion injury of the heart after successful recanalization of the infarct-related coronary artery. Enzyme-resistant peptide agonists of the oxytocin receptor could become a prototype for the creation of such drugs. It was shown oxytocin could selectively prevent cardiac reperfusion injury. The cardioprotective effect of oxytocin in coronary artery occlusion and myocardial reperfusion is distinguished by a decrease in infarct size, an improvement in cardiac contractility, and a decrease in the incidence of ventricular arrhythmias. In addition, oxytocin inhibits apoptosis and pyroptosis of cardiomyocytes in hypoxia/reoxygenation. It has been established that kinases, NO-synthase, and guanylyl cyclase are involved in an oxytocininduced increase in cardiac resistance to ischemia / reperfusion.

Cool-Shot Technique to Protect Spinal Cord during Thoracoabdominal Aortic Replacement.

Deep hypothermia helps protect the spinal cord, but is invasive. Here, we present a method to avoid reperfusion injury by selectively circulating cold blood under high pressure to the intercostal artery during reperfusion after intercostal artery reconstruction. Of the 23 patients who underwent thoracoabdominal aortic aneurysm open repair, one died. The motor evoked potential disappeared during aortic clamping in nine patients. Six patients recovered completely from aortic clamping release, two showed recovery >50% and one achieved full recovery 3 months later. Permanent motor impairment did not occur. This method could prevent reperfusion injury and paraplegia following thoracoabdominal aortic aneurysm surgery.

Abstract 050: Intraarterial cooling combined with mechanical thrombectomy in acute stroke patients: systematic review and meta‐analysis

Introduction Mechanical thrombectomy (MT) plays an important role in the treatment of intracranial large vessel occlusion (LVO) with recanalization success rate of 60%‐95%. Although the restoration of blood flow can ensue excess generation of reactive oxygen species (ROS) and inflammation which leads to cellular damage known as reperfusion injury. Recent studies have shown promising neuroprotection by reducing body temperature with the mechanism of limiting ROS and immune cells’ response. Although systemic hypothermia is associated with several adverse events and limited hypothermia affecting the specific ischemic brain tissue. Intra‐arterial cooling (IAC) combined with mechanical thrombectomy is a novel method for localized cooling. Methods Embase, and Web of Science were screened for English‐language papers including case reports/series, cohort studies and clinical trials. Studies were reviewed by 2 independent reviewers for inclusion criteria as patients with the age of >18 years old who had LVO and underwent mechanical thrombectomy combined with cold Saline infusion during mechanical thrombectomy (before or after recanalization). Statistical analyses were performed using R software version R‐4.3, P Value of <0.05 was considered significant. Results Four studies were included from initial 1177 studies, including 204 cases with MT combined with IAC (intra‐arterial 4°C saline infusion before or after recanalization) and 219 control with MT. Patients with MT+IAC had lower final infarct volume (MD=25, 95%CI [‐34.02, ‐15.98], P <0.0001), and better modified Rankin scale (mRS) after 90 days (RR=1.42, 95%CI [1.14, 1.77, P= 0.0015). There was no significant difference between MT+IAC and IAC group regarding deterioration of NIHSS in 24 hours(RR=1.09, 95%CI [0.42, 1.3, P=0.287), recanalization at 24 hours (RR=1.03, 95%CI [0.93, 1.14], P= 0.622), vascular spasm in 10 minutes (RR=2.90, , 95%CI [0.78, 10.80], P= 0.111), symptomatic intracranial hemorrhage (RR=0.78, 95%CI [0.48, 1.27], P= 0.322), coagulation abnormality (RR=0.94, , 95%CI [0.35, 2.54], P= 0.902), pneumonia (RR=1.09, 95%CI [0.79, 1.50], P= 0.585), and mortality in 90 days (RR=0.78, 95%CI [0.51, 1.20], P= 0.265). Conclusion Preliminary data is showing Intraarterial cooling combined with mechanical thrombectomy in acute stroke is a feasible and safe method for localized brain tissue cooling to prevent reperfusion injury and maximize long term outcome of MT.

Abstract 188: Rescue Left Middle Cerebral Artery Stenting With Xience Skypoint Everolimus‐Eluting Stent: Technical Report

Introduction Drug‐eluting stent (DES) use in symptomatic intracranial atherosclerosis disease (ICAD) has been described in the literature using different guiding and distal access catheters. We describe a case of deployment of a Xience Skypoint everolimus‐eluting stent (EES) (Abbott Vascular, Abbott Park, Illinois) into a symptomatic stenosed left M1 segment using Armadillo catheter (Q'Apel, Fremont, CA) with a successful result. Methods Case report and review of literature Results 67‐year‐old woman with type II diabetes mellitus, hypertension, hyperlipidemia, and recent admission for transient ischemic attack (resolving right hemiparesis and mild dysnomia in the setting of severe left M1 segment stenosis with discharge on Aspirin, Clopidogrel and Atorvastatin), presented with recurrence of symptoms, and MRI brain showing left basal ganglia acute infarction. No tPA was given low NIHSS and resolution of symptoms. Patient’s aphasia and hemiparesis worsened with segmental hypoperfusion which resolved by maintaining high blood pressures with norepinephrine drip. Decision was made to deploy a drug eluting stent into the stenosed M1 segment. Through femoral access, a 7F long destination sheath was inserted to the left common carotid origin. A 7F Armadillo catheter was then inserted into the left internal carotid artery (ICA) terminus. ASAHI Prowater coronary guidewire was inserted over which Xience Skypoint EES deployment was attempted but was unsuccessful given difficulty traversing the ICA ophthalmic segment. Ultimately, Armadillo catheter was advanced over a Phenom catheter (Medtronic) with good access into the distal M1 segment. The Phenom intermediate catheter was then removed, and the 2.25 mm x 12 mm stent was introduced through the Prowater guidewire into the segment and inflated to a pressure of 8 atm, with restoration of blood flow. Postoperatively, SBP was lowered to prevent reperfusion injury. Patient’s exam stabilized with mild dysnomia and right hemiparesis without any elevated blood pressure requirements. At 5‐months follow‐up, patient’s exam was non‐focal with NIHSS 0 and repeat DSA showed no evidence of stent occlusion and patent M1 segment. Conclusion Xience Skypoint EES can be successful in treating symptomatic MCA stenosis refractory to maximal medical therapy with good long term results.

The interplay between T lymphocytes and macrophages in myocardial ischemia/reperfusion injury.

Acute myocardial infarction is one of the most important causes of death in the world, causing a huge health and economic burden to the world. It is still a ticklish problem how to effectively prevent reperfusion injury while recovering the blood flow of ischemic myocardium. During the process of myocardial ischemia/reperfusion injury (MI/RI), the modulation of immune cells plays an important role. Monocyte/macrophage, neutrophils and endothelial cells initiate the inflammatory response and induce the release of various inflammatory cytokines, resulting in increased vascular permeability, tissue edema and damage. Meanwhile, T cells were recruited to impaired myocardium and release pro-inflammatory and anti-inflammatory cytokines. T cells and macrophages play important roles in keeping cardiac homeostasis and orchestrate tissue repair. T cells differentiation and macrophages polarization precisely regulates the tissue microenvironment in MI/RI, and shows cross action, but the mechanism is unclear. To identify potential intervention targets and propose ideas for treatment and prevention of MI/RI, this review explores the crosstalk between T lymphocytes and macrophages in MI/RI.

Cardioprotective Effects of Melatonin in Patients Undergoing PPCI

Background: One of the pitfalls of primary percutaneous coronary intervention (PPCI) is myocardial reperfusion injury caused by several pathophysiological mechanisms. Melatonin has been shown to be effective against this condition in various organs. Some of the biological effects of melatonin are associated with its capability to scavenge free radicals and reinforce the activity of antioxidant enzymes. Methods: The study population included 128 patients admitted with a diagnosis of acute ST-elevation myocardial infarction (STEMI) to the Emergency Department of Modarres Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran, who subsequently underwent PPCI. The patients were randomly assigned to two groups, each consisting of 64 cases, with those receiving 3 mg of melatonin in the emergency department before adding PPCI to the standard treatment (test group) and those receiving the standard therapy alone (control group). The myocardial blush grade (MBG) and thrombolysis in myocardial infarction frame count were assessed visually on the angiogram to evaluate microvascular integrity. Results: In the study as a whole and in subgroup analysis, the MBG showed a significant difference with melatonin prescription (2.8 ± 0.3 and 2.3 ± 0.7 in the test and control groups, respectively; P < 0.001). In patients with coronary risk factors, no difference was observed between the two groups. Nevertheless, melatonin significantly improved the MBG in patients without such risk factors. Melatonin had significant protective effects in both the right coronary and left anterior descending culprit arteries. Conclusions: This study demonstrated the effect of melatonin on preventing reperfusion injury in patients with STEMI undergoing PPCI.

Microvascular Leakage as Therapeutic Target for Ischemia and Reperfusion Injury

Reperfusion injury is a very common complication of various indicated therapies such as the re-opening of vessels in the myocardium or brain as well as reflow in hemodynamic shutdown (cardiac arrest, severe trauma, aortic cross-clamping). The treatment and prevention of reperfusion injury has therefore been a topic of immense interest in terms of mechanistic understanding, the exploration of interventions in animal models and in the clinical setting in major prospective studies. While a wealth of encouraging results has been obtained in the lab, the translation into clinical success has met with mixed outcomes at best. Considering the still very high medical need, progress continues to be urgently needed. Multi-target approaches rationally linking interference with pathophysiological pathways as well as a renewed focus on aspects of microvascular dysfunction, especially on the role of microvascular leakage, are likely to provide new insights.

Immunocytoprotection after reperfusion with Kv1.3 inhibitors has an extended treatment window for ischemic stroke.

Introduction: Mechanical thrombectomy has improved treatment options and outcomes for acute ischemic stroke with large artery occlusion. However, as the time window of endovascular thrombectomy is extended there is an increasing need to develop immunocytoprotective therapies that can reduce inflammation in the penumbra and prevent reperfusion injury. We previously demonstrated, that by reducing neuroinflammation, KV1.3 inhibitors can improve outcomes not only in young male rodents but also in female and aged animals. To further explore the therapeutic potential of KV1.3 inhibitors for stroke therapy, we here directly compared a peptidic and a small molecule KV1.3 blocker and asked whether KV1.3 inhibition would still be beneficial when started at 72 hours after reperfusion. Methods: Transient middle cerebral artery occlusion (tMCAO, 90-min) was induced in male Wistar rats and neurological deficit assessed daily. On day-8 infarction was determined by T2-weighted MRI and inflammatory marker expression in the brain by quantitative PCR. Potential interactions with tissue plasminogen activator (tPA) were evaluated in-vitro with a chromogenic assay. Results: In a direct comparison with administration started at 2 hours after reperfusion, the small molecule PAP-1 significantly improved outcomes on day-8, while the peptide ShK-223 failed to reduce infarction and neurological deficits despite reducing inflammatory marker expression. PAP-1 still provided benefits when started 72 hours after reperfusion. PAP-1 does not reduce the proteolytic activity of tPA. Discussion: Our studies suggest that KV1.3 inhibition for immunocytoprotection after ischemic stroke has a wide therapeutic window for salvaging the inflammatory penumbra and requires brain-penetrant small molecules.

Irisin Ameliorates Cerebral Vasospasm and Early Brain Injury in Rats with Experimental Subarachnoid Hemorrhage

Irisin is a cytokine mainly secreted by skeletal muscles, widely distributed in the body with functions of anti-oxidation, anti-inflammation, prevention of reperfusion injury, immune stimulation, and reduction of cerebral infarction. In this study, rats with subarachnoid hemorrhage (SAH) were used as experimental subjects, and irisin was injected intraperitoneally to investigate irisin’s effect on cerebral vasospasm and early brain injury (EBI). After establishment of the animal model of SAH, animals were administered with irisin through intraperitoneal injection. The animal tissues were taken out to assess the morphological changes, and neurons apoptosis by TUNEL staining and Nissl staining. Brain edema score was used to assess the severity of brain injury, and the relationship between related signal pathways was detected by Western blot. Administration of irisin significantly reduced cerebral vasospasm and decreased neuronal apoptosis induced by SAH. Irisin inhibited the apoptosis of prefrontal cortex mitochondrial neurons, and decreased Bax/Bcl-2 and cytochrome C in the cytoplasm. The expressions of PSD-95 and GAP-43 and BDNF in brain tissues were decreased upon SAH, but their expressions were partially restored after treatment with irisin. Irisin decreases neuronal apoptosis and mitochondrial function with up-regulation of synapse proteins, thereby exerting a protective effect on EBI and SAH.

Abstract WMP54: Hyperemia Following Endovascular Therapy For Acute Stroke Is Associated With Ischemic Lesion Growth

Introduction: A substantial proportion of acute stroke patients experience poor outcomes following successful endovascular therapy (EVT) and reperfusion injury to the brain and vasculature may be a contributor. The purpose of this pilot study was to characterize hyperemia following recanalization and test the association of hyperemia with evolution of the ischemic lesion. Methods: Acute stroke patients were included with: i) large vessel occlusion of the anterior circulation, ii) successful recanalization, and iii) evaluable MRI early after EVT. Presence of hyperemia on MRI perfusion was assessed by consensus using a modified ASPECTS. Three different approaches were used to quantify relative cerebral blood flow (rCBF) on early post-EVT, 24 hours, and 5 days. Two independent trained readers measured lesion volumes using a semi-automated validated approach. Results: Sixty-seven patients with median age of 66 [59-76], 57% female, met inclusion criteria. Hyperemia was present in 35/67 (52%) patients early post-EVT (Figure), in 32/65 (49%) patients at 24 hours, and in 19/48 (40%) patients at 5 days. In comparison to control regions, rCBF was elevated by greater than 50% in hyperemic regions. Patients with hyperemia had larger ischemic lesion volumes and early lesion growth. A strong association (R2=0.81, p<0.001) was found between early post-EVT hyperemia (p=0.027) and lesion growth based on DWI volume at 24 hours, after adjusting for DWI volume at 2 hours (p<0.001) and incomplete reperfusion at 24 hours (p=0.001). Conclusions: Hyperemia is frequently observed after successful EVT and is associated with lesion growth at 24 hours. Evidence of hyperemia may identify patients that may benefit from adjunctive therapy to prevent reperfusion injury, edema, and lesion growth.

Cardio protective effect of nicorandil in reperfusion injury among patients undergoing primary percutaneous coronary intervention.

To evaluate the effect of nicorandil in prevention of reperfusion injury during primary percutaneous coronary intervention by thrombolysis in myocardial infarction flow grade scoring. A total of 140 patients from Rawalpindi Institute of Cardiology were enrolled in this study conducted from 7th September to 10th of October 2021. These participants were allocated into two major groups. Control group received conventional acute coronary syndrome protocol regimen only whereas experimental group was given nicorandil along with conventional acute coronary syndrome protocol. During primary percutaneous coronary intervention, thrombolysis in myocardial infarction flow grade scoring was analyzed and compared. Majority of participants in nicorandil group achieved thrombolysis in myocardial infarction Grade-3 scoring which indicated reduced rate of no reflow phenomenon as compared to control group. A statistically significant difference was noted in score of both groups (p value = 0.001) signifying prophylactic use of nicorandil before primary percutaneous coronary intervention along with conventional acute coronary syndrome protocol is superior to only conventional acute coronary syndrome protocol regimen to cases in the control group. Use of nicorandil in ST elevated myocardial infarction patients before primary percutaneous coronary intervention prevents reperfusion injury thus decreasing the risk of post percutaneous coronary intervention complications and reducing mortality rate in cardiac patients suggesting its significant cardio protective role.

Join us on an amazing journey towards next-generation treatments for CNS disorders: Launch of Neuroprotection, a new high-quality journal in translational neuroscience.

Join us on an amazing journey towards next-generation treatments for CNS disorders: Launch of Neuroprotection, a new high-quality journal in translational neuroscience.

Peroxiredoxin 6 Prevents Reperfusion Injury to Isolated Rat Kidney

Peroxiredoxin 6 Prevents Reperfusion Injury to Isolated Rat Kidney

CYANOTIC HEART DISEASE: AN OVERVIEW OF TETRALOGY OF FALLOT

Tetralogy of Fallot (TOF) is the most common cyanotic heart disease with anomalies consist of: ventricular septal defect (VSD), overriding aorta, pulmonary stenosis and hypertrophic of the right ventricular. It also has various anomalies type such as TOF with absent pulmonary valve, TOF with pulmonary atresia, TOF with atrioventricular septal defect, TOF with coronary artery anomalies, etc which will be discussed in detail. Proper diagnosis is required when dealing with the TOF continue with radiological examination. Adequate history taking and correct physical examination are necessary in dealing with congenital heart defects, especially TOF case. In this overview, we also discuss about the comprehensive management, from tet spell management, palliative management of TOF that required shunt with various technique, and surgical total corrective of TOF with many approach such as transannular accompany with right ventriculotomy or transatrial with transpulmonary or beating heart surgery technique to prevent reperfusion injury complication.

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury.

Myocardial ischemia and reperfusion injury (MIRI), induced by coronary heart disease (CHD), causes damage to the cardiomyocytes. Furthermore, evidence suggests that thrombolytic therapy or primary percutaneous coronary intervention (PPCI) does not prevent reperfusion injury. There is still no ideal animal model for MIRI. This study aims to improve the MIRI model in rats to make surgery easier and more feasible. A unique method for establishing MIRI is developed by using a soft tube during a key step of the ischemic period. To explore this method, thirty rats were randomly divided into three groups: sham group (n = 10); experimental model group (n = 10); and existing model group (n = 10). Findings of triphenyltetrazolium chloride staining, electrocardiography, and percent survival are compared to determine the accuracies and survival rates of the operations. Based on the study results, it has been concluded that the improved surgery method is associated with a higher survival rate, elevated ST-T segment, and larger infarct size, which is expected to mimic the pathology of MIRI better.

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Myocardial ischemia and reperfusion injury (MIRI), induced by coronary heart disease (CHD), causes damage to the cardiomyocytes. Furthermore, evidence suggests that thrombolytic therapy or primary percutaneous coronary intervention (PPCI) does not prevent reperfusion injury. There is still no ideal animal model for MIRI. This study aims to improve the MIRI model in rats to make surgery easier and more feasible. A unique method for establishing MIRI is developed by using a soft tube during a key step of the ischemic period. To explore this method, thirty rats were randomly divided into three groups: sham group (n = 10); experimental model group (n = 10); and existing model group (n = 10). Findings of triphenyltetrazolium chloride staining, electrocardiography, and percent survival are compared to determine the accuracies and survival rates of the operations. Based on the study results, it has been concluded that the improved surgery method is associated with a higher survival rate, elevated ST-T segment, and larger infarct size, which is expected to mimic the pathology of MIRI better.

The effect of Tianjiang Xueshuantong Wan pills on ischemia-reperfusion injury after thrombolysis in acute cerebral infarction

ObjectiveThe aim of this study is to investigate the effect of Tianjiang Xueshuantong Wan pills on reperfusion injury after venous thrombolysis in acute cerebral infarction. MethodsThe strategy used in this study is a randomised controlled clinical trial. In total, 72 cases were included, with 36 in the trial group and 36 in the control group, with a 1:1 ratio. Both groups were given standardised treatment for acute cerebral infarction. Based on the rt-PA intravenous thrombolysis, the test group took Tianjiang Xueshuantong Wan pills orally, whereas the control group solely utilised rt-PA for intravenous thrombolysis and did not take the test medicine orally.The patients’ intracranial hemorrhage was clarified by head CT scan, and the occurrence of reperfusion injury was recorded during the entire trial. ResultsThere were no significant differences in serum IL-6, MDA, SOD and TNF concentrations and NIHSS scores between the two groups before therapy (P > 0.05). After treatment, the serum concentrations of IL-6, MDA and TNF in the experimental group were significantly decreased compared with the control group, while the serum concentrations of SOD were significantly increased compared with the control group, with statistical significance (P > 0.05). After seven days of treatment, the total effective rate in the experimental group was 88.89%, while the data in the control group was 75%. There was a statistically significant difference between the experimental and control groups. ConclusionTianjiang Xueshuantong Wan pills can effectively prevent reperfusion injury following intravenous thrombolysis in individuals with cerebral infarction while improving patients’ neurological deficits.

A Potent Inhibitor of Aminopeptidase P2 Reduces Reperfusion Injury in Models of Myocardial Infarction and Stroke.

During a myocardial infarction or ischemic stroke, blood flow to the heart or brain is partially blocked. This results in reduced delivery of oxygen and nutrients and, ultimately, tissue damage. Initial treatment involves removing the clot and restoring blood flow (reperfusion). However, this treatment is not as effective as one would hope because the reperfusion process itself can cause a different type of damage (reperfusion injury) that contributes up to 50% of the total damage. Bradykinin is an autocoid that is released from blood vessel endothelial cells during ischemia and reperfusion and has the potential to prevent reperfusion injury. However, bradykinin is rapidly inactivated by enzymes on endothelial cells, limiting its beneficial effects. One of these enzymes is aminopeptidase P2. We designed a potent and specific inhibitor of aminopeptidase P2 called ST-115, [(S)-2-mercapto-4-methylpentanoyl]-4(S)-fluoro-Pro-Pro-3(R)-beta-Pro. When ST-115 is administered intravenously at the start of reperfusion, it reduces bradykinin degradation. This increases bradykinin's concentration in the capillaries and enhances its protective effects. We tested ST-115 in a mouse model of myocardial infarction and found that the damaged area of the heart was reduced by 58% compared with mice given saline. In a rat model of ischemic stroke, ST-115 reduced functional deficits in a skilled walking test by 60% and reduced brain edema by 51%. It reduced brain infarct size by 48% in a major subset of rats with small strokes. The results indicate that ST-115 can ameliorate reperfusion injury and can ultimately serve as a therapeutic for acute myocardial infarction and ischemic stroke. SIGNIFICANCE STATEMENT: We have shown that our aminopeptidase P2 inhibitor, ST-115, can reduce tissue injury caused by episodes of ischemia followed by reperfusion. It was successful in rodent models of myocardial infarction and stroke. The clinical use would involve the intravenous administration of ST-115 at the induction of reperfusion. In the case of stroke, the successful technique of thrombectomy could be combined with ST-115 administration to simultaneously reduce both ischemic and reperfusion injury.

COMPLETE REPAIR OF TETRALOGY OF FALLOT (TOF) ON BEATING HEART SURGERY WITHOUT AORTIC CROSS CLAMPING : REPORT OF A CASE

Introduction: Reperfusion injury is a well-known phenomenon that occurred in cardioplegic techniques with cardiopulmonary bypass. Therefore great effort is made to prevent reperfusion injury. Beating Heart Continuous Coronary Perfusion (BHCCP) surgery is one of the alternative techniques to improve an ischemic reperfusion injury in open-heart surgery, either in pediatric or in adult. This technique can be done in complete repair of tetralogy of Fallot (TOF). Purpose: To report our first experience in doing complete repair of TOF using beating heart technique without aortic cross-clamping Case Report: A five-year-old boy came on to ER on January 6th, 2012, with a history of cyanotic since birth. His echocardiography and catheterization concluded a tetralogy of Fallot with a McGoon ratio of 1.95 (the diameter of RPA and LPA were 9.14 mm and 8.79 mm, respectively). A complete repair of TOF was done using beating heart surgery without aortic cross-clamping technique. One month post-surgery evaluation, there weren't any neurological or motor disorders. Echocardiography results showed no residual pulmonary stenosis, but 0.2 mm residual VSD was found. Conclusion: This heart rate technique is an alternative method of myocardial protection in cardiac surgery. In several cardiac centres globally, this technique is relatively safe and can be used during surgery, especially in the total correction of TOF.

Blood Pressure Management After Endovascular Thrombectomy.

Endovascular thrombectomy (EVT) has changed the landscape of acute stroke therapy and has become the standard of care for selected patients presenting with anterior circulation large-vessel occlusion (LVO) stroke. Despite successful reperfusion, many patients with LVO stroke do not regain functional independence. Particularly, patients presenting with extremes of blood pressure (BP) or hemodynamic variability are found to have a worse clinical recovery, suggesting blood pressure optimization as a potential neuroprotective strategy. Current guidelines acknowledge the lack of randomized trials to evaluate the optimal hemodynamic management during the immediate post-stroke period. Following reperfusion, lower blood pressure targets may be warranted to prevent reperfusion injury and promote penumbral recovery, but adequate BP targets adjusted to individual patient factors such as degree of reperfusion, infarct size, and overall hemodynamic status remain undefined. This narrative review outlines the physiological mechanisms of BP control after EVT and summarizes key observational studies and clinical trials evaluating post-EVT BP targets. It also discusses novel treatment strategies and areas of future research that could aid in the determination of the optimal post-EVT blood pressure.