Predictors and outcomes in patients undergoing surgery for acute type A aortic dissection requiring concomitant venoarterial extracorporeal membrane oxygenation support—a retrospective multicentre cohort study
Preoperative malperfusion, advanced age and stroke are well studied risk factors for patients’ outcome following surgery for acute type A aortic dissection (ATAAD) . Lesser is known about ventricular failure and consecutive low cardiac output syndrome (LCOS) requiring the use of venoarterial extracorporeal membrane oxygenation (ECMO), which may be one of the worst-case scenarios in perioperative treatment of ATAAD . In the setting of ATAAD, multiple reasons lead to ventricular failure, especially in case of preoperative tamponade leading to resuscitation or obstruction of the coronary arteries by the haematoma up to involvement of coronary dissection leading to malperfusion and potentially leading to additional coronary artery bypass grafting during aortic repair . So far, only limited data are available evaluating the outcome of patients receiving perioperative venoarterial ECMO support, indicating mortality rates far above 70% . Additionally, it is unclear if there is a realistic chance of weaning from venoarterial ECMO for these patients or if it can even act as a bridging therapy to more advanced surgical treatments like left ventricular assist devices or heart transplantation in very selected cases. This highlights the importance of the identification of independent risk factors and predictors for mortality in this subgroup. We report a multicentre experience of patients undergoing surgery for ATAAD and receiving perioperative support with venoarterial ECMO. We focus on the chance of successful weaning and evaluate the pre-ECMO lactate peak as a potential candidate for survival assessment.   Ethics approval The local ethics committees of participating centres officially approved this study (Berlin EA2/096/20, Innsbruck UN 5106, Freiburg 24-1247-S1, Köln 201212_1, Bern 2020–01149). It complies with the Declaration of Helsinki. Patient population Study design followed the STROBE (STrengthening the Reporting of OBservational studies in Epidemiology.) statement. Out of 3719 patients undergoing surgery for ATAAD between 2004 and 2023 at 5 different European aortic centres, 117 (3.1%) patients needed perioperative ECMO support. These 117 patients constitute the retrospective multicentre study cohort. Patients who received preoperative ECMO implantation before aortic repair were not included in this study ( n = 10) given the high mortality reported in literature. Additionally, iatrogenic ATAAD and patients with subacute/chronic aortic dissection (onset ≥ 14 days) were excluded. Quantification of preoperative organ malperfusion in ATAAD was described recently and followed the structure of the German Registry for Acute Aortic Dissection Type A . Surgical procedure Median sternotomy was the standard operative access. After establishing cardiopulmonary bypass, systemic cooling was initiated. The level of hypothermia mainly included moderate hypothermia ranging from 20°C to 28°C in combination with antegrade cerebral perfusion during caudal circulatory arrest. The main arterial cannulation sites were the right axillary artery, the right femoral artery or direct central cannulation of the ascending aorta or the aortic arch. After induction of cardioplegic arrest and inspection of the entry site, the ascending aorta was resected with or without the aortic arch. Total arch replacement, with or without the use of the frozen elephant trunk technique, was performed in case of an aneurysm or located entry tear. This also accounted for the aortic root. Concomitant coronary artery bypass grafting (CABG) using vein grafts was carried out primarily in case of severe aortic root destruction with involvement of the dissection into the coronary artery (Neri B lesion) or circumferential detachment of the coronary artery (Neri C lesion) or presence of severe calcification in combination with preoperative or intraoperative coronary malperfusion. CABG was performed in the setting of acute aortic repair. The decision for ECMO support and measurement of lactate The decision for venoarterial ECMO support was either made at the end of the operation or during the postoperative course on the intensive care unit (ICU). If weaning from cardiopulmonary bypass after reperfusion was not possible despite inotropic and vasoactive support, intraoperative ECMO implantation was performed. It was distinguished whether it was a primary left ventricular, right ventricular or biventricular pump failure based on transoesophageal echocardiographic findings. Whenever possible, the inserted cannulas were used for continuing ECMO support. In selected cases of peripheral malperfusion, the cannulation site was switched from femoral artery to the side branch of the surgical prosthesis in order to establish antegrade flow. Details on arterial cannulation site of ECMO are displayed in Table . The pre-ECMO lactate peak (mg/dl) was defined as the highest available lactate peak in an arterial blood gas analysis right before venoarterial ECMO implantation. This was also the case for the pre-ECMO creatine kinase-MB (CK-MB) peak (U/l), which was measured via blood sample analysis to assess the extent of myocardial injury. Definition of outcomes and follow-up Primary endpoints were 30-day mortality and successful weaning of venoarterial ECMO support after haemodynamic stabilization. Open chest therapy was defined as non-sternal closure at the end of the operation due to pronounced bleeding and/or cardiopulmonary oedema. The reasons for death were divided into cardiac and non-cardiac reasons. Cardiac was defined by the underlying ventricular failure and consecutive LCOS. Non-cardiac was divided into 4 different entities, whereas the presence of more than one reason was also possible: multiorgan failure despite ECMO support; cerebral ischaemic and/or haemorrhagic stroke and/or cerebral oedema; sepsis and consecutive septic shock; and aortic rupture and/or extensive bleeding and consecutive haemorrhagic shock. A postoperative cerebral computed tomography scan was mandatory for the diagnosis of stroke and cerebral oedema. The follow-up was 97.5% complete for 30-day mortality. Only 3 patients (2.5%) were lost to follow-up after discharge before 30 days. The median survival time was 6 (1–27) days. Follow-up was closed in March 2024. Statistical analysis Continuous variables were tested for normal distribution by using the Shapiro–Wilk test and additional visualization using histograms. All continuous variables were not normally distributed. Therefore, they were presented as median with corresponding interquartile range (IQR; 25th–75th percentile). Categorical data were represented as absolute numbers with corresponding percentages. Multivariable binary logistic regression analysis was performed to identify independent risk factors for 30-day mortality. All variables included in Table (preoperative variables), Table (intraoperative variables) and Table (variables for venoarterial ECMO support) were considered for the initial logistic regression model. To include pre-ECMO CK-MB peak as a variable in the regression model, single imputation by using predictive mean matching considering all preoperative variables was performed. Variables for the regression model were chosen using the backward selection technique based on the Akaike information criterion. All selected variables were then used for the multivariable binary logistic regression and are shown in Table . Univariable binary logistic regression was performed complementary. A receiver operating curve was designed to measure the prediction accuracy of pre-ECMO lactate peak for 30-day mortality. The corresponding area under the curve (AUC) was defined as acceptable with a value >0.70. Restricted cubic splines were used to investigate the association between pre-ECMO lactate peak and survival. Kaplan–Meier curves including a log-rank test were prepared to illustrate and compare survival between groups according to the indication for ECMO implantation. All P -values are 2-sided. The α -level was defined at 0.05. Statistical analysis was performed using R (The R Foundation for Statistical Computing) version 4.3.2.   The local ethics committees of participating centres officially approved this study (Berlin EA2/096/20, Innsbruck UN 5106, Freiburg 24-1247-S1, Köln 201212_1, Bern 2020–01149). It complies with the Declaration of Helsinki.   Study design followed the STROBE (STrengthening the Reporting of OBservational studies in Epidemiology.) statement. Out of 3719 patients undergoing surgery for ATAAD between 2004 and 2023 at 5 different European aortic centres, 117 (3.1%) patients needed perioperative ECMO support. These 117 patients constitute the retrospective multicentre study cohort. Patients who received preoperative ECMO implantation before aortic repair were not included in this study ( n = 10) given the high mortality reported in literature. Additionally, iatrogenic ATAAD and patients with subacute/chronic aortic dissection (onset ≥ 14 days) were excluded. Quantification of preoperative organ malperfusion in ATAAD was described recently and followed the structure of the German Registry for Acute Aortic Dissection Type A .   Median sternotomy was the standard operative access. After establishing cardiopulmonary bypass, systemic cooling was initiated. The level of hypothermia mainly included moderate hypothermia ranging from 20°C to 28°C in combination with antegrade cerebral perfusion during caudal circulatory arrest. The main arterial cannulation sites were the right axillary artery, the right femoral artery or direct central cannulation of the ascending aorta or the aortic arch. After induction of cardioplegic arrest and inspection of the entry site, the ascending aorta was resected with or without the aortic arch. Total arch replacement, with or without the use of the frozen elephant trunk technique, was performed in case of an aneurysm or located entry tear. This also accounted for the aortic root. Concomitant coronary artery bypass grafting (CABG) using vein grafts was carried out primarily in case of severe aortic root destruction with involvement of the dissection into the coronary artery (Neri B lesion) or circumferential detachment of the coronary artery (Neri C lesion) or presence of severe calcification in combination with preoperative or intraoperative coronary malperfusion. CABG was performed in the setting of acute aortic repair.   The decision for venoarterial ECMO support was either made at the end of the operation or during the postoperative course on the intensive care unit (ICU). If weaning from cardiopulmonary bypass after reperfusion was not possible despite inotropic and vasoactive support, intraoperative ECMO implantation was performed. It was distinguished whether it was a primary left ventricular, right ventricular or biventricular pump failure based on transoesophageal echocardiographic findings. Whenever possible, the inserted cannulas were used for continuing ECMO support. In selected cases of peripheral malperfusion, the cannulation site was switched from femoral artery to the side branch of the surgical prosthesis in order to establish antegrade flow. Details on arterial cannulation site of ECMO are displayed in Table . The pre-ECMO lactate peak (mg/dl) was defined as the highest available lactate peak in an arterial blood gas analysis right before venoarterial ECMO implantation. This was also the case for the pre-ECMO creatine kinase-MB (CK-MB) peak (U/l), which was measured via blood sample analysis to assess the extent of myocardial injury.   Primary endpoints were 30-day mortality and successful weaning of venoarterial ECMO support after haemodynamic stabilization. Open chest therapy was defined as non-sternal closure at the end of the operation due to pronounced bleeding and/or cardiopulmonary oedema. The reasons for death were divided into cardiac and non-cardiac reasons. Cardiac was defined by the underlying ventricular failure and consecutive LCOS. Non-cardiac was divided into 4 different entities, whereas the presence of more than one reason was also possible: multiorgan failure despite ECMO support; cerebral ischaemic and/or haemorrhagic stroke and/or cerebral oedema; sepsis and consecutive septic shock; and aortic rupture and/or extensive bleeding and consecutive haemorrhagic shock. A postoperative cerebral computed tomography scan was mandatory for the diagnosis of stroke and cerebral oedema. The follow-up was 97.5% complete for 30-day mortality. Only 3 patients (2.5%) were lost to follow-up after discharge before 30 days. The median survival time was 6 (1–27) days. Follow-up was closed in March 2024.   Continuous variables were tested for normal distribution by using the Shapiro–Wilk test and additional visualization using histograms. All continuous variables were not normally distributed. Therefore, they were presented as median with corresponding interquartile range (IQR; 25th–75th percentile). Categorical data were represented as absolute numbers with corresponding percentages. Multivariable binary logistic regression analysis was performed to identify independent risk factors for 30-day mortality. All variables included in Table (preoperative variables), Table (intraoperative variables) and Table (variables for venoarterial ECMO support) were considered for the initial logistic regression model. To include pre-ECMO CK-MB peak as a variable in the regression model, single imputation by using predictive mean matching considering all preoperative variables was performed. Variables for the regression model were chosen using the backward selection technique based on the Akaike information criterion. All selected variables were then used for the multivariable binary logistic regression and are shown in Table . Univariable binary logistic regression was performed complementary. A receiver operating curve was designed to measure the prediction accuracy of pre-ECMO lactate peak for 30-day mortality. The corresponding area under the curve (AUC) was defined as acceptable with a value >0.70. Restricted cubic splines were used to investigate the association between pre-ECMO lactate peak and survival. Kaplan–Meier curves including a log-rank test were prepared to illustrate and compare survival between groups according to the indication for ECMO implantation. All P -values are 2-sided. The α -level was defined at 0.05. Statistical analysis was performed using R (The R Foundation for Statistical Computing) version 4.3.2.   Pre- and intraoperative variables The study cohort consisted of 117 patients. Preoperative variables are shown in Table . The median age was 61 (IQR 55–69) years and almost half of the patients (46%) were female. Preoperative shock was present in 47 (40%) patients and 27 (23%) of them underwent preoperative resuscitation. Coronary malperfusion was the most present type of preoperative organ malperfusion in 55 (47%) patients. The intraoperative variables are depicted in Table . Median cardiopulmonary bypass time was 291 (IQR 238–387) and aortic cross-clamp time 136 (IQR 97–173) min. The main arterial cannulation technique was the axillary artery in 52 (44%) patients. Additional replacement of the aortic root was performed in 55 (47%) patients and 32 (27%) underwent total arch replacement. Concomitant CABG was performed in 49 (42%) patients. Variables for ECMO support The results for ECMO support are shown in Table . The majority of 87 (74%) patients received intraoperative implantation of ECMO due to weaning failure from cardiopulmonary bypass, whereas 30 (26%) patients underwent ECMO implantation during the early postoperative course in the ICU due to the development of ventricular failure and consecutive LCOS. The main indication was a biventricular failure in 51 (44%) patients, followed by isolated right in 39 (33%) and isolated left ventricular failure and 27 (23%) patients. The median pre-ECMO lactate peak was 85 (IQR 57–131) mg/dl and the median pre-ECMO CK-MB peak was 63 (IQR 23–232) U/l. Outcomes and survival The postoperative variables are shown in Table . Six patients (5%) died intraoperatively despite ECMO implantation, 3 of them experienced aortic rupture in downstream segments and in the other 3 maintaining sufficient circulation was not possible. Median time in the ICU was 7 (IQR 2–18) days and time on ECMO 3 (IQR 1–7) days. Successful weaning of venoarterial ECMO was achieved in 36 (31%) patients. Thirty-day mortality was 72% (84 patients) and in-hospital mortality 80% (94 patients). The leading cause of death was non-cardiac in the majority of patients (55%, 65 patients). Multiorgan failure despite ECMO support was the main reason in 45 (39%) of patients, fatal neurologic injury and sepsis accounted for almost 30% of early deaths. Those 3 early postoperative complications limited the duration of ECMO support and were the driving reasons for a withdrawal of life support. Cardiac causes of death—continuous and/or recurring ventricular failure and consequent LCOS—accounted for death in 29 patients (25%). The 90-day survival probability according to type of ventricular failure including patients at risk is shown in Fig. . No significant difference in terms of right-, left- or biventricular failure was observed ( P = 0.390). However, there was a trend towards a higher chance of successful weaning from ECMO in the case of isolated right ventricular failure when compared to the left- and biventricular failure ( P = 0.050). Independent risk factors for mortality and validation of pre-ECMO lactate as predictor for survival The results of uni- and multivariable binary logistic regression for 30-day mortality are shown in Table . The pre-ECMO lactate peak [odds ratio (OR) 1.02, 95% confidence interval (CI) 1.005–1.032], the presence of preoperative shock (OR 9.49, 95% CI 1.785–96.504) and the need for total arch replacement (OR 6.67, 95% CI 1.639–34.695) were independent associates for 30-day mortality. The corresponding receiver operating curve for the pre-ECMO lactate peak is illustrated in Fig. A. Pre-ECMO lactate peak was identified as a valid predictor for 30-day mortality (AUC 0.73). Furthermore, restricted cubic splines indicated a relevant association between the pre-ECMO lactate peak and overall survival ( P = 0.004) (Fig. B). The median lactate of 85 mg/dl represented the threshold with an increased risk.   The study cohort consisted of 117 patients. Preoperative variables are shown in Table . The median age was 61 (IQR 55–69) years and almost half of the patients (46%) were female. Preoperative shock was present in 47 (40%) patients and 27 (23%) of them underwent preoperative resuscitation. Coronary malperfusion was the most present type of preoperative organ malperfusion in 55 (47%) patients. The intraoperative variables are depicted in Table . Median cardiopulmonary bypass time was 291 (IQR 238–387) and aortic cross-clamp time 136 (IQR 97–173) min. The main arterial cannulation technique was the axillary artery in 52 (44%) patients. Additional replacement of the aortic root was performed in 55 (47%) patients and 32 (27%) underwent total arch replacement. Concomitant CABG was performed in 49 (42%) patients.   The results for ECMO support are shown in Table . The majority of 87 (74%) patients received intraoperative implantation of ECMO due to weaning failure from cardiopulmonary bypass, whereas 30 (26%) patients underwent ECMO implantation during the early postoperative course in the ICU due to the development of ventricular failure and consecutive LCOS. The main indication was a biventricular failure in 51 (44%) patients, followed by isolated right in 39 (33%) and isolated left ventricular failure and 27 (23%) patients. The median pre-ECMO lactate peak was 85 (IQR 57–131) mg/dl and the median pre-ECMO CK-MB peak was 63 (IQR 23–232) U/l.   The postoperative variables are shown in Table . Six patients (5%) died intraoperatively despite ECMO implantation, 3 of them experienced aortic rupture in downstream segments and in the other 3 maintaining sufficient circulation was not possible. Median time in the ICU was 7 (IQR 2–18) days and time on ECMO 3 (IQR 1–7) days. Successful weaning of venoarterial ECMO was achieved in 36 (31%) patients. Thirty-day mortality was 72% (84 patients) and in-hospital mortality 80% (94 patients). The leading cause of death was non-cardiac in the majority of patients (55%, 65 patients). Multiorgan failure despite ECMO support was the main reason in 45 (39%) of patients, fatal neurologic injury and sepsis accounted for almost 30% of early deaths. Those 3 early postoperative complications limited the duration of ECMO support and were the driving reasons for a withdrawal of life support. Cardiac causes of death—continuous and/or recurring ventricular failure and consequent LCOS—accounted for death in 29 patients (25%). The 90-day survival probability according to type of ventricular failure including patients at risk is shown in Fig. . No significant difference in terms of right-, left- or biventricular failure was observed ( P = 0.390). However, there was a trend towards a higher chance of successful weaning from ECMO in the case of isolated right ventricular failure when compared to the left- and biventricular failure ( P = 0.050).   The results of uni- and multivariable binary logistic regression for 30-day mortality are shown in Table . The pre-ECMO lactate peak [odds ratio (OR) 1.02, 95% confidence interval (CI) 1.005–1.032], the presence of preoperative shock (OR 9.49, 95% CI 1.785–96.504) and the need for total arch replacement (OR 6.67, 95% CI 1.639–34.695) were independent associates for 30-day mortality. The corresponding receiver operating curve for the pre-ECMO lactate peak is illustrated in Fig. A. Pre-ECMO lactate peak was identified as a valid predictor for 30-day mortality (AUC 0.73). Furthermore, restricted cubic splines indicated a relevant association between the pre-ECMO lactate peak and overall survival ( P = 0.004) (Fig. B). The median lactate of 85 mg/dl represented the threshold with an increased risk.   In this retrospective multicentre cohort study, we report—to the best of our knowledge—the largest current experience of patients undergoing surgery for ATAAD receiving perioperative venoarterial ECMO support due to LCOS. This patient cohort represents a subgroup at high risk in surgical treatment of ATAAD with tremendously high mortality. Based on this, considerable arguments arise questioning the realistic chance of weaning from venoarterial ECMO and even considering ECMO as potential futile indication given the patient’s overall prognosis. Given the high rate of preoperative tamponade and coronary malperfusion, surgeons were confronted with complex and haemodynamically unstable patients at admission. This might explain the rather high rate of emergent femoral cannulation of 36% causing retrograde arterial flow for CPB. In general, all institutions involved in this study follow a clear preference of antegrade flow via axillary or central cannulation. Once decision for ECMO need was made, patients with preoperative distal malperfusion underwent a switch of cannulation sites to establish antegrade flow via the sidebranch of the prosthesis. This guarantees perfusion of the true lumen and avoids retrograde perfusion of the false lumen via distal re-entries, a clear benefit in ATAAD patients when addressing distal malperfusion. Additionally antegrade flow via the sidebranch or axillary artery should be the preferred cannulation strategy in this setting of LCOS in order to reduce afterload for the left ventricle. In this study, a successful weaning rate of 31% was achieved. Given the comparably young age of 61 (IQR 55–69) years of our patient cohort, perioperative ECMO enabled survival of 20% of these patients who otherwise would not have survived ATAAD. The duration of ECMO was comparatively short with a median of 3 (IQR 1–7) days for the total cohort and 5 (IQR 5–7) days for the patients who were successfully weaned. This might be driven by the fact that primarily non-cardiac causes were the main reasons of death in this cohort, mainly progressive multiorgan failure despite venoarterial ECMO support. In a recent study with data from the observational, multicentre ‘PC-ECMO’ registry investigating the outcomes of patients with postcardiotomy cardiogenic shock after surgery for ATAAD requiring venoarterial ECMO support, a total of 62 patients were analysed and compared to non-dissection patients . In-hospital mortality accounted for 74.2%, while 37.1% of patients were successfully weaned from venoarterial ECMO. These results are comparable to the findings of this study and further reveal that in this patient cohort, venoarterial ECMO emerged as an effective rescue option, demonstrating comparable in-hospital mortality and postoperative outcomes to the general patient cohort with postcardiotomy cardiogenic shock. A Chinese single-centre observation on 27 patients who underwent surgery for ATAAD and received venoarterial ECMO support, 9 (33.3%) patients were successfully weaned . The overall in-hospital mortality was 81.5%. The main causes of death were multiorgan failure, neurological complications and bleeding. Similar outcome results on early morbidity are presented in this study, which furthermore accounts for the rather short duration of ECMO support in our patient cohort. Lethal early complications during ECMO after surgical repair for ATAAD have also been reported by other groups. Sultan et al.  provided data from the Pennsylvania Health Care Cost Containment Council with median time from ECMO implantation to death of 1 day. The rate of coronary malperfusion (47%) was high in our study cohort when compared to reported incidences of coronary involvement in ATAAD of 9% in single-centre reports . This observation has also been pointed out on a recently published systematic review and meta-analysis by Sá et al.  on the use of ECMO after surgical repair for ATAAD. This clearly highlights the complexity of patients suffering from lethal aortic event with coronary complications. Furthermore, it also underlines the importance of rapid diagnosis and initiation of surgery due to not only the well-known hourly death rate of aortic dissection but also the ongoing coronary ischaemia and potential irreversible myocardial damage in these patients. Markers for myocardial injury have been assessed by Hou et al.  comparing preoperative CK-MB levels between successful and failed weaning candidates. CK-MB levels were lower in patients who were successfully weaned from venoarterial ECMO compared to those who failed to wean and died [14 (6–30) vs 55 (28–138) U/l, P < 0.01]. This could indicate that the extent of myocardial injury measured by CK-MB before ECMO implantation might be a relevant indicator for non-successful weaning and mortality. However, the pre-ECMO CK-MB peak was not associated with 30-day mortality in this study, whereas different timepoints of CK-MB measurement may cause relevant bias and make conclusions difficult. Instead, the pre-ECMO lactate peak emerged as a valid predictor for 30-day mortality. A rising lactate before ECMO implantation may originate from many different sources both from systemic malperfusion in as well as local organ malperfusion (coronary, peripheral and visceral) caused by ATAAD. A previous study on pre-ECMO lactate peak in case of extracorporeal cardiopulmonary resuscitation discovered that the pre-ECMO lactate levels in patients with refractory cardiac arrest were associated with 1-year survival . The authors concluded that the pre-ECMO lactate may be an easily accessible and quickly available point-of-care measurement which might act as an early prognostic marker when considering initiation or continuation of extracorporeal cardiopulmonary resuscitation treatment. In our study, preoperative lactate peak emerged as strong predictor for 30-day mortality. Furthermore, a threshold of 85 mg/dl was identified and associated with impaired survival. Lactate levels should be considered in perioperative decision-making in the heart team but should not be the single basis for or against the decision for perioperative ECMO support. Limitations This study is limited by its retrospective nature. Furthermore, it lacks information about the quality of life of the survivors, which would be of great interest in context of a severe course of ICU treatment after ECMO support and surgery for ATAAD. In terms of validation of the pre-ECMO lactate peak, lactate sources driven by local malperfusion should be evaluated based on specific radiographic assessment in every single patient, which was not possible in this study. A corresponding lactate clearance after ECMO implantation could give more detailed insights in addition to the lactate peak for further identification of patients at high risk during the immediate course after ECMO implantation.   This study is limited by its retrospective nature. Furthermore, it lacks information about the quality of life of the survivors, which would be of great interest in context of a severe course of ICU treatment after ECMO support and surgery for ATAAD. In terms of validation of the pre-ECMO lactate peak, lactate sources driven by local malperfusion should be evaluated based on specific radiographic assessment in every single patient, which was not possible in this study. A corresponding lactate clearance after ECMO implantation could give more detailed insights in addition to the lactate peak for further identification of patients at high risk during the immediate course after ECMO implantation.   Patients requiring perioperative venoarterial ECMO support due to LCOS after surgery for ATAAD show tremendously high morbidity and mortality. Nevertheless, ECMO as salvage treatment was successfully weaned in almost one-third of patients and generated 20% of hospital survivors. The pre-ECMO lactate peak is a valid predictor for mortality and shows a strong correlation with survival. Decision-making for venoarterial ECMO support can be crucial under the circumstances of ATAAD and should be well balanced against the high-risk profile in this patient cohort. Lactate levels in conjunction with clinical parameters should be considered as an additive measure when considering this treatment option.   