Acute type A aortic dissection is a severe cardiovascular disease characterized by rapid onset and high mortality. Traditionally, urgent open aortic repair is performed after admission to prevent aortic rupture and death. However, when combined with malperfusion syndrome, the low perfusion of the superior mesenteric artery can further lead to intestinal necrosis, significantly impacting the surgery\'s prognosis and potentially resulting in adverse consequences, bringing. This presents great significant challenges in treatment. Based on recent domestic and international research literature, this paper reviews the mechanism, current treatment approaches, and selection of surgical methods for poor organ perfusion caused by acute type A aortic dissection. The literature review findings suggest that central aortic repair can be employed for the treatment of acute type A aortic dissection with inadequate perfusion of the superior mesenteric artery. The superior mesenteric artery can be windowed and (/or) stented, followed by delayed aortic repair. Priority should be given to revascularization of the superior mesenteric artery, followed by central aortic repair. During central aortic repair, direct blood perfusion should be performed on the distal true lumen of the superior mesenteric artery, leading to resulting in favorable therapeutic outcomes. The research results indicate that even after surgical aortic repair, intestinal ischemic necrosis may still occur. In such cases, prompt laparotomy and necessary necrotic bowel resection are crucial for saving the patient\'s life.

OBJECTIVE: The mortality of acute type A aortic dissection (ATAAD) with malperfusion syndrome (MPS) is high. However, the management strategy remains controversial. We aimed to evaluate the strategy for MPS at our institution.
METHODS: Among 724 patients with ATAAD, 167 patients with MPS were treated with immediate central repair (1st stage) or an optimized strategy (2nd stage). In 2nd stage, the optimized strategy used was based on 6-hour threshold from symptom onset. For MPS with symptom onset within 6 hours, immediate central repair was performed followed by endovascular reperfusion if malperfusion persisted. With symptom onset beyond 6 hours, individualized delayed central repair was performed. We compared outcomes between the 1st and 2nd stage.
RESULTS: The in-hospital mortality of ATAAD was significantly decreased when the optimized strategy was used (4.3% in 2nd stage vs. 12.5% in 1st stage, P<0.01). In 2nd stage, the in-hospital mortality for MPS was decreased (10.2% vs. 33.9%, P<0.01). Moreover, the in-hospital mortality for MPS with symptom onset within or beyond 6 hours decreased from 24% to 7.5% and from 41.2% to 11.8%, respectively. The operative mortality of MPS in 2nd stage was comparable with patients without MPS (4.0% vs. 2.4%, P>0.05).
CONCLUSIONS: The optimized strategy significantly improved the outcomes of MPS. The 6-hour threshold from symptom onset could be very useful in determining the timing of central repair. For MPS with symptom onset within 6 hours, immediate central repair is reasonable. For those with symptom onset beyond 6 hours, individualized delayed central repair should be considered.

BACKGROUND: Preoperative malperfusion of acute type A aortic dissection (ATAAD) remains a catastrophic complication that is associated with high postoperative morbidity and mortality. The relationship between malperfusion and long-term survival in the Chinese population is unknown.
METHODS: A total of 771 patients who underwent ATAAD surgery between January 2009 and December 2018 at our center were included. In-hospital mortality, complications, morbidity, and long-term survival were analyzed.
RESULTS: Preoperative malperfusion was identified in 292 of 771 patients (37.9%), the in-hospital mortality rate was 20.9% in patients with preoperative malperfusion and 9.2% in those without. Independent predictors of in-hospital mortality included any malperfusion (odds ratio [OR], 5.132; p = .001), pericardial tamponade (OR, 1.808; p = .046), advanced age (OR, 1.028; p = .003), and cardiopulmonary bypass time (OR, 1.008; p = .001). Immediate emergency surgery (OR, 0.492; p = .007) and antegrade cerebral perfusion perioperatively (OR, 0.477; p = .020) were protective against postoperative mortality. The postoperative survival rates at 1, 3, and 5 years were 94.4% ± 1.5%, 91.9% ± 1.8%, and 83.0% ± 3.2% in patients with malperfusion and 94.7% ± 1.1%, 90.2% ± 1.7%, and 84.4% ± 2.7%, respectively, in those without. Preoperative malperfusion did not significantly affect the long-term outcomes of operative survivors (log-rank p = .601).
CONCLUSIONS: Malperfusion resulted in an unfavorable prognosis in the short term, but showed almost equal long-term survival in patients without malperfusion of ATAAD. Emergency central repair might be considered to further improve the outcomes of ATAAD with malperfusion.

Blunt traumatic aortic injury (BTAI) is a rare but life-threatening emergency that is usually caused by sudden acceleration/deceleration injuries in vehicular accidents. We describe our initial experience of a retrograde two-stage hybrid treatment approach for the emergent management of a 63-year-old motorcyclist who presented with a complicated BTAI with malperfusion syndrome. To our best knowledge, this uncommon BTAI case with fatal distal malperfusion saved by an urgent retrograde two-stage hybrid procedure has been reported rarely. This early reperfusion strategy with two-stage retrograde endovascular technique could be an effective and life-saving treatment option for polytrauma patients with suitable aortic anatomy.

To describe endovascular treatment of mesenteric malperfusion in a multichannel aortic dissection (MCAD) with full true lumen (TL) collapse following thoracic endovascular aortic repair (TEVAR).
A 54-year-old man presented with chronic mesenteric ischemia and a previous TEVAR for MCAD complicated by superior mesenteric artery (SMA) malperfusion. Computed tomography angiography (CTA) demonstrated a 3-channel aortic dissection with a \"false-true-false\" configuration. The SMA was malperfused through the collapsed TL. CTA also showed a secondary entry tear, measuring 18 mm in diameter, at the end of the previous endograft. Direct open surgery or endovascular revascularization of the SMA was not feasible. A plan was devised to improve SMA perfusion by increasing the TL inflow. With the assistance of intravascular ultrasound (IVUS), an endograft was placed through one false lumen in the abdominal aorta and through the TL in the descending thoracic aorta to seal the secondary entry tear. Symptoms of mesenteric ischemia resolved 2 days after the procedure. At 1 year, he is asymptomatic, has gained weight, and has improved SMA perfusion and remodeling of the 3-channel dissection on CTA.
IVUS imaging can help evaluate the complex hemodynamics of MCAD. Patient-specific endovascular treatment of MCAD with mesenteric malperfusion seems to be a feasible bailout alternative treatment for urgent, complex cases without reconstruction options.