OBJECTIVE: Cerebral malperfusion (CM) is a common comorbidity in acute type A aortic dissection (ATAAD), which is associated with high mortality and poor neurological prognosis. This meta-analysis investigated the surgical strategy of ATAAD patients with CM, aiming to compare the difference in therapeutic effectiveness between the central repair-first and the early reperfusion-first according to clinical outcomes.
METHODS: The meta-analysis and systematic review was conducted based on studies sourced from the PubMed, Embase, and Cochrane literature database, in which cases of ATAAD with CM underwent surgical repair were included. Data for baseline characteristics, mortality, survival were extracted, and risk ratio (RR) values and the pooled mortality were calculated.
RESULTS: A total of 17 retrospective studies were analyzed, including 1010 cases of ATAAD with CM underwent surgical repair. The pooled early mortality in early reperfusion group was lower (8.1%; CI, 0.02 to 0.168) than that in the central repair group (16.2%; CI, 0.115 to 0.216). The pooled long-term mortality was 7.9% in the early reperfusion cohort and 17.4% the central repair-first cohort, without a statistically significant heterogeneity (I [2] = 51.271%; p = 0.056). The mean time of symptom-onset-to-the-operation-room in all the reports was 8.87 ± 12.3 h.
CONCLUSIONS: This meta-analysis suggested that early reperfusion-first may achieved better outcomes compared to central repair-first in ATAAD patients complicated with CM to some extent. Early operation and early restoration of cerebral perfusion may reduce the occurrence of some neurological complications.
BACKGROUND: The meta-analysis was registered in the International Prospective Register of Systematic Reviews database (No. CRD CRD42023475629) on Nov. 8th, 2023.

Early metoprolol administration protects against myocardial ischemia-reperfusion injury, but its effect on infarct size progression (ischemic injury) is unknown. Eight groups of pigs (total n = 122) underwent coronary artery occlusion of varying duration (20, 25, 30, 35, 40, 45, 50, or 60 min) followed by reperfusion. In each group, pigs were randomized to i.v. metoprolol (0.75 mg/kg) or vehicle (saline) 20 min after ischemia onset. The primary outcome measure was infarct size (IS) on day7 cardiac magnetic resonance (CMR) normalized to area at risk (AAR, measured by perfusion computed tomography [CT] during ischemia). Metoprolol treatment reduced overall mortality (10% vs 26%, p = 0.03) and the incidence and number of primary ventricular fibrillations during infarct induction. In controls, IS after 20-min ischemia was ≈ 5% of the area AAR. Thereafter, IS progressed exponentially, occupying almost all the AAR after 35 min of ischemia. Metoprolol injection significantly reduced the slope of IS progression (p = 0.004 for final IS). Head-to-head comparison (metoprolol treated vs vehicle treated) showed statistically significant reductions in IS at 30, 35, 40, and 50-min reperfusion. At 60-min reperfusion, IS was 100% of AAR in both groups. Despite more prolonged ischemia, metoprolol-treated pigs reperfused at 50 min had smaller infarcts than control pigs undergoing ischemia for 40 or 45 min and similar-sized infarcts to those undergoing 35-min ischemia. Day-45 LVEF was higher in metoprolol-treated vs vehicle-treated pigs (41.6% vs 36.5%, p = 0.008). In summary, metoprolol administration early during ischemia attenuates IS progression and reduces the incidence of primary ventricular fibrillation. These data identify metoprolol as an intervention ideally suited to the treatment of STEMI patients identified early in the course of infarction and requiring long transport times before primary angioplasty.

Ischemic stroke is a critical disease caused by cerebral artery occlusion in the central nervous system (CNS). Recent therapeutic advances, such as neuroendovascular intervention and thrombolytic therapy, have allowed recanalization of occluded brain arteries in an increasing number of stroke patients. Although previous studies have focused on rescuing neural cells that still survive despite decreased blood flow, expanding the therapeutic time window may allow more patients to undergo reperfusion in the near future, even after lethal ischemia, which is characterized by death of mature neural cells, such as neurons and glia. However, it remains unclear whether early reperfusion following lethal ischemia results in positive outcomes. The present study used two ischemic mouse models-90-min transient middle cerebral artery occlusion (t-MCAO) paired with reperfusion to induce lethal ischemia and permanent middle cerebral artery occlusion (p-MCAO)-to investigate the effect of early reperfusion up to 8 w following MCAO. Although early reperfusion following 90-min t-MCAO did not rescue mature neural cells, it preserved the vascular cells within the ischemic areas at 1 d following 90-min t-MCAO compared to that following p-MCAO. In addition, early reperfusion facilitated the healing processes, including not only vascular but also neural repair, during acute and chronic periods and improved recovery. Furthermore, compared with p-MCAO, early reperfusion after t-MCAO prevented behavioral symptoms of neurological deficits without increasing negative complications, including hemorrhagic transformation and mortality. These results indicate that early reperfusion provides beneficial effects presumably via cytoprotective and regenerative mechanisms in the CNS, suggesting that it may be useful for stroke patients that experienced lethal ischemia.

Timely restoration of tissue-level cerebral blood flow is the goal of thrombolytic therapy in patients presenting with an acute ischemic stroke. We aimed to identify the incidence and predictors of reperfusion immediately following treatment with intravenous recombinant tissue plasminogen activator (IV rt-PA).
This study included patients with acute ischemic stroke triaged using magnetic resonance imaging (MRI) with perfusion-weighted imaging (PWI) and treated with IV rt-PA who were subsequently enrolled in our natural history study and underwent repeat MRI with PWI approximately 2 hours posttreatment. Early reperfusion was defined as >80% decrease in the size of initial perfusion deficit on the 2 hours follow-up MRI. Demographics, stroke risk factors, presenting National Institutes of Health Stroke Scale score, and location of the thrombosis were compared between patients with and without early reperfusion.
Of the 49 patients included in this study, 21 (43%) had early reperfusion. The mean age for patients with early reperfusion was significantly lower in comparison to the patients without early reperfusion (64 vs. 76, P = .01). The prevalence of hyperlipidemia was significantly lower among patients with early reperfusion (24% vs. 54%, P = .036). Patients with early reperfusion were less likely to have large-vessel occlusion (LVO) (internal carotid artery terminus or proximal middle cerebral artery) (24% vs. 50%, P = .06). In a multivariate analysis, the presence of an LVO was an independent predictor of lack of early reperfusion (OR [95%Cl]: .13 [.019-.89], P = .038).
Early reperfusion was found in a substantial percentage of the patients treated with IV rt-PA. It was more common in patients without LVO.

Coronary malperfusion is one of the most dreadful complications of acute aortic dissection because it causes catastrophic acute myocardial infarction in patients who are already severely ill. Our strategy was as follows. After the administration of heparin, emergency percutaneous coronary intervention (PCI) was urgently performed at the same time as starting to prepare the operating room. A stent was then placed to cover the full length of dissected coronary artery. Patients whose cardiac function improved after successful coronary artery reperfusion were transferred to the operating room to undergo central repair surgery. If the cardiac function did not recover even after coronary reperfusion, and the patient required extracorporeal membrane oxygenation, we considered the best supportive care without performing central repair surgery. In patients with left coronary malperfusion, we believe that preoperative PCI must be performed immediately. Preoperative PCI might delay central repair surgery and potentially increase the risk of catastrophic cardiac tamponade. However, the benefit of PCI in preserving cardiac function exceeds the risk of cardiac tamponade. The indications of PCI before central repair in patients with right coronary malperfusion should be considered after assessing each patient\'s condition, including the presence or absence of cardiac tamponade and right ventricular infarction, left ventricular function, the immediate availability of cardiologists or cardiac surgeons, and the speed of preparing the operating room.

The control of malperfusion is the key to improving the outcomes of surgery for type A acute aortic dissection. We revised our treatment strategy to reperfuse each ischemic organ before central repair.
Our current early reperfusion strategy consists of percutaneous coronary artery intervention for coronary malperfusion, direct surgical fenestration for carotid artery occlusion, active perfusion of the superior mesenteric artery for visceral malperfusion, and external shunting from the brachial artery to the femoral artery for lower limb ischemia. Central repair is performed without delay after reperfusion therapy, but if irreversible organ damage is recognized, further aggressive treatment is discontinued.
Among 438 patients who underwent initial treatment for type A acute aortic dissection, malperfusion in one or more organs was diagnosed in 108 patients (24%). We applied an early reperfusion strategy in 33 patients, (coronary, 14 patients; carotid, 4; visceral, 7; lower extremity, 8). Central repair was then performed in 28 patients. One patient (3.6%) died of pneumonia; 27 patients overcame the ischemic organ damage and survived. Among the 108 patients with malperfusion, 10 patients (9.3%) were treated medically without early reperfusion and central repair. During the same period, mortality from central repair procedures in patients with malperfusion who had not received early reperfusion therapy was 12 of 65 (18%), and the mortality of patients without malperfusion was 9 of 262 (3.4%). Malperfusion was a serious risk factor for hospital death, but the mortality rate of the patients with an early reperfusion strategy was significantly (P < .01) lower than the patients without early reperfusion.
Our strategy might improve the outcomes of surgery for type A acute aortic dissection with malperfusion. This strategy enables us to avoid unproductive central repair procedures in irreversibly damaged patients.

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In this brief report, computed tomography perfusion (CTP) thresholds predicting follow-up infarction in patients presenting 20 to 23 seconds and cerebral blood flow <5 to 7 ml/min-1/(100 g)-1 or relative cerebral blood flow <0.14 to 0.20 optimally predicted the final infarct. These thresholds are stricter than published thresholds.