Endovascular Fenestration/Stenting First Followed by Delayed Open Aortic Repair for Acute Type A Aortic Dissection With Malperfusion Syndrome

Abstract

Background: Immediate open repair of acute type A aortic dissection is traditionally recommended to prevent death from aortic rupture. However, organ failure because of malperfusion syndrome (MPS) might be the most imminent life-threatening problem for a subset of patients.

Methods: From 1996 to 2017, among 597 patients with acute type A aortic dissection, 135 patients with MPS were treated with upfront endovascular reperfusion (fenestration/stenting) followed by delayed open repair (OR). We compared outcomes between the first and second decades and observed mortalities with those expected with an "upfront OR for every patient" approach, determined using prognostic models from the literature (Verona, Leipzig-Halifax, Stockholm, Penn, and GERAADA [German Registry for Acute Aortic Dissection Type A] models).

Results: Overall, in-hospital mortality improved between the 2 decades (21.0% versus 10.7%, P<0.001). In the second decade, for patients with MPS initially treated with fenestration/stenting, mortality from aortic rupture decreased from 16% to 4% ( P=0.05), the risk of dying from organ failure was 6.6 times higher than dying from aortic rupture (hazard ratio=6.63; 95% CI, 1.5-29; P=0.01), and 30-day mortality after OR for MPS patients was 3.7%. Compared to the expected mortalities with the upfront OR for every patient models, our observed 30-day and in-hospital mortalities (9% and 11%, respectively) of all patients with acute type A aortic dissection were significantly lower ( P≤0.03).

Conclusions: Immediate OR is the strategy to prevent death from aortic rupture for the majority of patients with acute type A aortic dissection. However, relatively stable (no rupture, no tamponade) patients with MPS benefit from a staged approach: upfront endovascular reperfusion followed by aortic OR at resolution of organ failure.

Keywords: acute aortic syndrome; acute cardiac care; aortic disease; aortic dissection; aortic surgery; endovascular fenestration/stenting; malperfusion; malperfusion syndrome.

Figure 1.. Algorithm for clinical decision making.

All patients with acute type A aortic dissection were managed through this algorithm, and only patients with MPS (tissue/organ necrosis and dysfunction) but no aortic rupture or cardiac tamponade were treated with upfront endovascular revascularization by interventional radiology followed by delayed open aortic repair. ICU = intensive care unit. MPS = malperfusion syndrome.

Figure 2.. Comparison of in-hospital outcomes of all patients with acute type A aortic dissection between the first decade (1996–2007) and second decade (2008–2017).

The overall in-hospital mortality decreased by 50% from first decade to second decade (p < 0.001). IR = endovascular treatment of malperfusion syndrome by interventional radiology.

Figure 3:. Perioperative outcomes of patients with acute type A aortic dissection and malperfusion syndrome (MPS) after upfront endovascular treatment by interventional radiology (IR) for visceral and/or extremity MPS.

There is a trend of decreased overall in-hospital mortality (black) between the two decades, but not significantly different (p=0.46). The in-hospital mortality due to aortic rupture (dark gray) was significantly lower in the second decade (4% vs 16%, p=0.05). The in-hospital mortality due to organ failure between IR and open aortic repair was not significantly different between the two decades.

Figure 4:. Thirty-day outcomes after endovascular treatment by interventional radiology (IR).

The risk of death between IR and open aortic repair from organ failure vs. from aortic rupture was similar in the first decade with proportional hazard ratio (HR) of 1.15; however, significantly increased in the second decade with proportional HR of 6.63, p = 0.013. Proportional hazard assumption satisfied in both decades (Schoenfeld residuals test: p = 0.52 in the first and p = 0.12 in the second decade, respectively). Data expressed as (number, percentage). HR = cause-specific hazard ratio of death from organ failure/death from aortic rupture.

Figure 5.. Comparison of observed “in-hospital mortality” at the University of Michigan with that expected following an “upfront open repair for every patient” approach, according to Verona, Leipzig-Halifax, and Stockholm prognostic models, during the second decade (2008–2017).

All patients (n=354) includes patients without any MPS (n=269), with MPS but unstable (tamponade or rupture) (n=7), with non-IR-amenable MPS (ie, isolated cerebral, coronary, or spinal MPS) (n=29), and with IR-amenable MPS (ie, visceral or extremity) (n=49). IR indicates endovascular treatment (interventional radiology); OR, open repair; and MPS, malperfusion syndrome.

Figure 6.. Comparison of observed “30-day mortality after first intervention” at the University of Michigan with that expected following an “upfront open repair for every patient” approach, according to Penn and GERAADA prognostic models, during the second decade (2008–2017).

First intervention is defined as either endovascular treatment of malperfusion syndrome or open repair of acute type A aortic dissection, whichever occurred first. All patients (n=354) include patients without any MPS (n=269), with MPS but unstable (tamponade or rupture) (n=7), with non-IR-amenable MPS (ie, isolated cerebral, coronary, or spinal MPS) (n=29), and with IR-amenable MPS (ie, visceral or extremity) (n=49). GERAADA indicates German Registry for Acute Aortic Dissection type A; IR, endovascular treatment (interventional radiology); MPS, malperfusion syndrome; and OR, open repair.

Figure 7.. Long-term Kaplan-Meier survival analysis.

A, Comparison of overall survival since hospital admission in the first versus second decade for all patients. B, Comparison of overall survival after hospital discharge (landmark survival analysis) in the first decade versus the second decade only for patients who underwent open repair. C, Overall survival since hospital admission for patients of ATAAD without any MPS who underwent upfront OR versus those with MPS treated with upfront endovascular reperfusion followed by OR of ATAAD, including 9 patients who had delayed OR >30 days after IR. ATAAD indicates acute type A aortic dissection; IR, interventional radiology; and MPS, malperfusion syndrome.

Figure 7.. Long-term Kaplan-Meier survival analysis.

A, Comparison of overall survival since hospital admission in the first versus second decade for all patients. B, Comparison of overall survival after hospital discharge (landmark survival analysis) in the first decade versus the second decade only for patients who underwent open repair. C, Overall survival since hospital admission for patients of ATAAD without any MPS who underwent upfront OR versus those with MPS treated with upfront endovascular reperfusion followed by OR of ATAAD, including 9 patients who had delayed OR >30 days after IR. ATAAD indicates acute type A aortic dissection; IR, interventional radiology; and MPS, malperfusion syndrome.

Figure 7.. Long-term Kaplan-Meier survival analysis.

A, Comparison of overall survival since hospital admission in the first versus second decade for all patients. B, Comparison of overall survival after hospital discharge (landmark survival analysis) in the first decade versus the second decade only for patients who underwent open repair. C, Overall survival since hospital admission for patients of ATAAD without any MPS who underwent upfront OR versus those with MPS treated with upfront endovascular reperfusion followed by OR of ATAAD, including 9 patients who had delayed OR >30 days after IR. ATAAD indicates acute type A aortic dissection; IR, interventional radiology; and MPS, malperfusion syndrome.