Showing papers by "Gilbert R. Upchurch published in 2014"

Predicting In-Hospital Mortality in Acute Type B Aortic Dissection Evidence From International Registry of Acute Aortic Dissection

Abstract: Background— The outcome of patients with acute type B aortic dissection (ABAD) is strongly related to their clinical presentation. The purpose of this study was to investigate predictors for mortality among patients presenting with ABAD and to create a predictive model to estimate individual risk of in-hospital mortality using the International Registry of Acute Aortic Dissection (IRAD). Methods and Results— All patients with ABAD enrolled in IRAD between 1996 and 2013 were included for analysis. Multivariable logistic regression analysis was used to investigate predictors of in-hospital mortality. Significant risk factors for in-hospital death were used to develop a prediction model. A total of 1034 patients with ABAD were included for analysis (673 men; mean age, 63.5±14.0 years), with an overall in-hospital mortality of 10.6%. In multivariable analysis, the following variables at admission were independently associated with increased in-hospital mortality: increasing age (odds ratio [OR], 1.03; 95% confidence interval [CI], 1.00–1.06; P =0.044), hypotension/shock (OR, 6.43; 95% CI, 2.88–18.98; P =0.001), periaortic hematoma (OR, 3.06; 95% CI, 1.38–6.78; P =0.006), descending diameter ≥5.5 cm (OR, 6.04; 95% CI, 2.87–12.73; P P P =0.001), and limb ischemia (OR, 3.02; 95% CI, 1.05–8.68; P =0.040). Based on these multivariable results, a reliable and simple bedside risk prediction tool was developed. Conclusions— We present a simple prediction model using variables that are independently associated with in-hospital mortality in patients with ABAD. Although it needs to be validated in an independent population, this model could be used to assist physicians in their choice of management and for informing patients and their families.

Inhibition of Interleukin-1β Decreases Aneurysm Formation and Progression in a Novel Model of Thoracic Aortic Aneurysms

Abstract: Background—Thoracic aortic aneurysms (TAAs) are common, but experimental TAA models are limited and the role of interleukin-1β (IL-1β) is undetermined. Methods and Results—IL-1β protein was measured in human TAAs and control aortas, and IL-1β protein was increased ≈20-fold in human TAAs. To develop an experimental model of TAAs, 8- to10-week-old male C57Bl/6 mice (wild type [WT]) underwent thoracotomy with application of periadventitial elastase (WT TAA) or saline (WT control; n=30 per group). Elastase treatment to thoracic aortas resulted in progressive dilation until day 14 with maximal dilation of 99.6±24.7% compared with 14.4±8.2% for WT saline control (P<0.0001). WT TAAs demonstrated elastin fragmentation, smooth muscle cell loss, macrophage infiltration, and increased IL-1β expression. Next, TAAs were induced in mice deficient of IL-1β (IL-1β knockout) or IL-1 receptor (IL-1R knockout; n=10 each). Genetic deletion of IL-1β and IL-1R significantly decreased thoracic aortic dilation (IL-1β knockout=54...

Predictors of false lumen thrombosis in type B aortic dissection treated with TEVAR

Abstract: Background: Thoracic endovascular aortic repair (TEVAR) offers a less invasive treatment option in type B aortic dissection (TBAD) patients and its value has been demonstrated in acute and chronic dissection patients. Total false lumen thrombosis (FLT) is associated with better long-term outcome in these patients, however, this is not obtained in all patients. The purpose of this study was to investigate predictors of FLT. Methods: We retrospectively investigated patients who underwent TEVAR for a type B dissection in a large referral center between 2005 and 2012. All patients with a CT angiogram (CTA) obtained preoperatively, postoperatively and after one year of follow-up were selected for analysis. Volume measurements and several morphologic characteristics were analyzed for all scans using Aquarius iNtuition software (TeraRecon, San Mateo, Calif, USA). Multivariate logistic regression analyses were used to study the influence of these characteristics on FLT. Results: Of 132 patients that received TEVAR for an aortic dissection, 43 patients (mean age, 60.3±14.2; 30 male) met our inclusion criteria, of whom 16 (37%) developed full FLT after 1 yr of follow-up. Multivariate logistic regression showed that side branch involvement [odds ratio (OR), 0.03; 95% confidence interval (CI), 0.00-0.92; P=0.045] and a total patent false lumen (FL) at presentation (OR, 0.01; 95% CI, 0.00-0.58; P=0.027) were associated with decreased complete FLT. Volumetric data showed significantly more reduction of the thoracic false lumen in FLT patients compared with non-FLT (–52.3% vs. –32.4%; P=0.043) and also a tendency of less volume increase in the abdominal segment (–5.0±37.5 vs. 21.8±44.3; P=0.052). Conclusions: Patients admitted with type B dissection and branch vessel involvement or a patent entry tear after TEVAR are less likely to develop FLT and aortic remodeling during follow-up. These findings suggest that these patients may require a more extensive procedure and more intensive follow-up to prevent longterm complications.

Phosphorylation of AKT and Abdominal Aortic Aneurysm Formation

Abstract: It is hypothesized that differential AKT phosphorylation between sexes is important in abdominal aortic aneurysm (AAA) formation. Male C57BL/6 mice undergoing elastase treatment showed a typical AAA phenotype (80% over baseline, P < 0.001) and significantly increased phosphorylated AKT-308 (p308) and total-AKT (T-AKT) at day 14 compared with female mice. Elastase-treated Raw cells produced increased p308 and significant amounts of matrix metalloproteinase 9 (MMP-9), and these effects were suppressed by LY294002 treatment, a known AKT inhibitor. Male and female rat aortic smooth muscle cells treated with elastase for 1, 6, or 24 hours demonstrated that the p308/T-AKT and AKT-Ser-473/T-AKT ratios peaked at 6 hours and were significantly higher in the elastase-treated cells compared with controls. Similarly, male cells had higher phosphorylated AKT/T-AKT levels than female cells. LY294002 also inhibited elastase-induced p308 formation more in female smooth muscle cells than in males, and the corresponding cell media had less pro-MMP-9. AKT siRNA significantly decreased secretion of pro-MMP-9, as well as pro-MMP-2 and active MMP-2 from elastase-treated male rat aortic smooth muscle cells. IHC of male mice AAA aortas showed increased p308, AKT-Ser-473, and T-AKT compared with female mice. Aortas from male AAA patients had a significantly higher p308/T-AKT ratio than female AAA tissues. These data suggest that AKT phosphorylation is important in the upstream regulation of MMP activity, and that differential phosphorylation may be important in sex differences in AAA.

B2 Cells Suppress Experimental Abdominal Aortic Aneurysms

Abstract: Recent reports of rupture in patients with abdominal aortic aneurysm (AAA) receiving B-cell depletion therapy highlight the importance of understanding the role of B cells (B1 and B2 subsets) in the development of AAA. We hypothesized that B2 cells aggravate experimental aneurysm formation. The IHC staining revealed infiltration of B cells in the aorta of wild-type (C57BL/6) mice at day 7 after elastase perfusion and persisted through day 21. Quantification of immune cell types using flow cytometry at day 14 showed significantly greater infiltration of mononuclear cells, including B cells (B2: 93% of total B cells) and T cells in elastase-perfused aortas compared with saline-perfused or normal aortas. muMT (mature B-cell deficient) mice were prone to AAA formation similar to wild-type mice in two different experimental AAA models. Contradicting our hypothesis, adoptive transfer of B2 cells suppressed AAA formation (102.0% ± 7.3% versus 75.2% ± 5.5%; P P

5-Lipoxygenase Pathway in Experimental Abdominal Aortic Aneurysms

Abstract: Objective—The impact of leukotriene production by the 5-lipoxygenase (5-LO) pathway in the pathophysiology of abdominal aortic aneurysms (AAAs) has been debated. Moreover, a clear mechanism through which 5-LO influences AAA remains unclear. Approach and Results—Aneurysm formation was attenuated in 5-LO–/– mice, and in lethally irradiated wild-type mice reconstituted with 5-LO–/– bone marrow in an elastase perfusion model. Pharmacological inhibition of 5-LO–attenuated aneurysm formation in both aortic elastase perfused wild-type and angiotensin II–treated LDLr–/– (low-density lipoprotein receptor) mice, with resultant preservation of elastin and fewer 5-LO and MMP9 (matrix metalloproteinase)-producing cells. Separately, analysis of wild-type mice 7 days after elastase perfusion showed that 5-LO inhibition was associated with reduced polymorphonuclear leukocyte infiltration to the aortic wall. Importantly, 5-LO inhibition initiated 3 days after elastase perfusion in wild-type mice arrested progression of sm...

Utility of 18 F-FDG and 11C-PBR28 microPET for the assessment of rat aortic aneurysm inflammation

Abstract: The utility of 18 F-FDG and 11C-PBR28 to identify aortic wall inflammation associated with abdominal aortic aneurysm (AAA) development was assessed. Utilizing the porcine pancreatic elastase (PPE) perfusion model, abdominal aortas of male Sprague-Dawley rats were infused with active PPE (APPE, AAA; N = 24) or heat-inactivated PPE (IPPE, controls; N = 16). Aortic diameter increases were monitored by ultrasound (US). Three, 7, and 14 days after induction, APPE and IPPE rats were imaged using 18 F-FDG microPET (approximately 37 MBq IV) and compared with 18 F-FDG autoradiography (approximately 185 MBq IV) performed at day 14. A subset of APPE (N = 5) and IPPE (N = 6) animals were imaged with both 11C-PBR28 (approximately 19 MBq IV) and subsequent 18 F-FDG (approximately 37 MBq IV) microPET on the same day 14 days post PPE exposure. In addition, autoradiography of the retroperitoneal torso was performed after 11C-PBR28 (approximately 1,480 MBq IV) or 18 F-FDG (approximately 185 MBq IV) administration at 14 days post PPE exposure. Aortic wall-to-muscle ratios (AMRs) were determined for microPET and autoradiography. CD68 and translocator protein (TSPO) immunohistochemistry (IHC), as well as TSPO gene expression assays, were performed for validation. Mean 3 (p = 0.009), 7 (p < 0.0001) and 14 (p < 0.0001) days aortic diameter increases were significantly greater for APPE AAAs compared to IPPE controls. No significant differences in 18 F-FDG AMR were determined at days 3 and 7 post PPE exposure; however, at day 14, the mean 18 F-FDG AMR was significantly elevated in APPE AAAs compared to IPPE controls on both microPET (p = 0.0002) and autoradiography (p = 0.02). Similarly, mean 11C-PBR28 AMR was significantly increased at day 14 in APPE AAAs compared to IPPE controls on both microPET (p = 0.04) and autoradiography (p = 0.02). For APPE AAAs, inhomogeneously increased 18 F-FDG and 11C-PBR28 uptake was noted preferentially at the anterolateral aspect of the AAA. Compared to controls, APPE AAAs demonstrated significantly increased macrophage cell counts by CD68 IHC (p = 0.001) as well as increased TSPO staining (p = 0.004). Mean TSPO gene expression for APPE AAAs was also significantly elevated compared to IPPE controls (p = 0.0002). Rat AAA wall inflammation can be visualized using 18 F-FDG and 11C-PBR28 microPET revealing regional differences of radiotracer uptake on microPET and autoradiography. These results support further investigation of 18 F-FDG and 11C-PBR28 in the noninvasive assessment of human AAA development.

for the assessment of rat aortic aneurysm inflammation

Abstract: Background: The utility of 18 F-FDG and 11 C-PBR28 to identify aortic wall inflammation associated with abdominal aortic aneurysm (AAA) development was assessed. Methods: Utilizing the porcine pancreatic elastase (PPE) perfusion model, abdominal aortas of male Sprague-Dawley rats were infused with active PPE (APPE, AAA; N = 24) or heat-inactivated PPE (IPPE, controls; N = 16). Aortic diameter increases were monitored by ultrasound (US). Three, 7, and 14 days after induction, APPE and IPPE rats were imaged using 18 F-FDG microPET (approximately 37 MBq IV) and compared with 18 F-FDG autoradiography (approximately 185 MBq IV) performed at day 14. A subset of APPE (N = 5) and IPPE (N = 6) animals were imaged with both 11 C-PBR28 (approximately 19 MBq IV) and subsequent 18 F-FDG (approximately 37 MBq IV) microPET on the same day 14 days post PPE exposure. In addition, autoradiography of the retroperitoneal torso was performed after 11 C-PBR28 (approximately 1,480 MBq IV) or 18 F-FDG (approximately 185 MBq IV) administration at 14 days post PPE exposure. Aortic wall-to-muscle ratios (AMRs) were determined for microPET and autoradiography. CD68 and translocator protein (TSPO) immunohistochemistry (IHC), as well as TSPO gene expression assays, were performed for validation. Results: Mean 3 (p = 0.009), 7 (p < 0.0001) and 14 (p < 0.0001) days aortic diameter increases were significantly greater for APPE AAAs compared to IPPE controls. No significant differences in 18 F-FDG AMR were determined at days 3 and 7 post PPE exposure; however, at day 14, the mean 18 F-FDG AMR was significantly elevated in APPE AAAs compared to IPPE controls on both microPET (p=0.0002) and autoradiography (p=0.02). Similarly, mean 11 C-PBR28 AMR was significantly increased at day 14 in APPE AAAs compared to IPPE controls on both microPET (p = 0.04) and autoradiography (p = 0.02). For APPE AAAs, inhomogeneously increased 18 F-FDG and 11 C-PBR28 uptake was noted preferentially at the anterolateral aspect of the AAA. Compared to controls, APPE AAAs demonstrated significantly increased macrophage cell counts by CD68 IHC (p = 0.001) as well as increased TSPO staining (p = 0.004). Mean TSPO gene expression for APPE AAAs was also significantly elevated compared to IPPE controls (p = 0.0002). Conclusion: Rat AAA wall inflammation can be visualized using 18 F-FDG and 11 C-PBR28 microPET revealing regional differences of radiotracer uptake on microPET and autoradiography. These results support further investigation of 18 F-FDG and 11 C-PBR28 in the noninvasive assessment of human AAA development.

Chest pain from excluded inferior vena cava filter after stent placement.

Abstract: A 52-year-old patient presented with chronic substernal chest pain 18 months following exclusion of an inferior vena cava (IVC) filter with a self-expanding IVC stent. After a thorough work-up revealed no other possible cause of chest pain, the filter and stent were removed with subsequent resolution of chest pain. Intraoperatively, filter struts were found to have penetrated the posteromedial wall of the IVC and were abutting the periaortic neural plexus. Referred chest pain due to strut penetration of the caval wall is a novel complication of both IVC filters and IVC stents, demonstrating a need for continued surveillance.

Abstract 103: Cross-Talk Between Macrophages, Smooth Muscle Cells and Endothelial Cells in Response to Cigarette Smoke: The Effects on MMP2 and -9

Abstract: Introduction: Abdominal Aortic Aneurysm (AAA) development is linked to smoking and is characterized by extracellular matrix remodeling by MMP2 and -9. We hypothesized that MMP2 and -9 secretions and regulation in response to cigarette smoke is modulated by interactions between resident cells within the aorta, namely, aortic smooth muscles, endothelial cells, and infiltrating macrophages and could influence AAA formation and/or progression. Methods: Aqueous extract of cigarette smoke (AEC) was applied to male rat aortic smooth muscle (RASMC), endothelial (RAEC) or RAW cells in serum free medium (SFM). After 24h the cells were washed, fresh SFM was added and collected after 24h. This conditioned media (CM) was applied to the cells for 24h, again washed, fresh SFM added, and then incubated for 72h, at which point the media was saved for MMP2 and -9 analysis by zymography while the cellular protein was used to determine the ratio (pS/pJ) of phospho-Stat3 (pStat3) and phospho-Jak2 (pJak2) by western blot. Results: Unstimulated CM from RAW cells increased MMP2 by 24% (p=0.0357), MMP9 by 282.1% (p=0.0004) and pS/pJ by 136.5% in RASMC. AEC-CM from RAW and RAEC cells increased MMP9 by 200.5% (p=0.0004) and 17.1% (p=0.0301) respectively in RASMC and corresponding increases in pS/pJ (305.7% and 227.6%, respectively). AEC-CM derived from RAW cells induced RAEC to produce moderate amounts of MMP2 (16.5%, p=0.0140) and MMP9 (29.5%, p=0.0207) and a 137.0% increase in pS/pJ. RAW cells receiving unstimulated CM from RASMC and RAEC cells produced significant amounts of MMP9 (127.7%, p=0.0026 and 236.8%, p=0.0020, respectively) and increased levels of pS/pJ ratios (45.2% and 1282.8%, respectively). Moreover, AEC-CM from RASMC and RAEC induced significant production of MMP9 from RAW cells (154.8%, p=0.0001 and 162.4%, p=0.0022, respectively) and increase in pS/pJ ratios (1348.2%, and 1493.9%, respectively) over baseline. Conclusion: This is the first in vitro study demonstrating that cigarette smoke results in differential interactions between aortic smooth muscle cells, endothelial cells, and macrophage lineage cells resulting in enhanced levels of MMP2, MMP9, pStat3 and pJak2. These interactions may play an important role in AAA formation under in vivo conditions.

Cardiovascular Surgery Importance of Refractory Pain and Hypertension in Acute Type B Aortic Dissection Insights From the International Registry of Acute Aortic Dissection (IRAD)

Abstract: Background—In patients with acute type B aortic dissection, presence of recurrent or refractory pain and/or refractory hypertension on medical therapy is sometimes used as an indication for invasive treatment. The International Registry of Acute Aortic Dissection (IRAD) was used to investigate the impact of refractory pain and/or refractory hypertension on the outcomes of acute type B aortic dissection. Methods and Results—Three hundred sixty-five patients affected by uncomplicated acute type B aortic dissection, enrolled in IRAD from 1996 to 2004, were categorized according to risk profile into 2 groups. Patients with recurrent and/or refractory pain or refractory hypertension (group I; n69) and patients without clinical complications at presentation (group II; n296) were compared. “High-risk” patients with classic complications were excluded from this analysis. The overall in-hospital mortality was 6.5% and was increased in group I compared with group II (17.4% versus 4.0%; P0.0003). The in-hospital mortality after medical management was significantly increased in group I compared with group II (35.6% versus 1.5%; P0.0003). Mortality rates after surgical (20% versus 28%; P0.74) or endovascular management (3.7% versus 9.1%; P0.50) did not differ significantly between group I and group II, respectively. A multivariable logistic regression model confirmed that recurrent and/or refractory pain or refractory hypertension was a predictor of in-hospital mortality (odds ratio, 3.31; 95% confidence interval, 1.04 to 10.45; P0.041). Conclusions—Recurrent pain and refractory hypertension appeared as clinical signs associated with increased in-hospital mortality, particularly when managed medically. These observations suggest that aortic intervention, such as via an endovascular approach, may be indicated in this intermediate-risk group. (Circulation. 2010;122: 1283-1289.)

Abstract 492: Resolvin D2 Inhibits Murine Abdominal Aortic Aneurysm and Increases M2 Macrophage Differentiation

Abstract: Objectives: Macrophages are critical to abdominal aortic aneurysm (AAA) formation; however, the role of anti-inflammatory M2 macrophages is not known. Resolvins have been shown to play a protective role in neointimal hyperplasia; however, their role in AAA has not been established. We hypothesized that treatment with Resolvin D2 (RvD2) attenuates murine AAA formation through alterations in macrophage polarization and cytokine expression. Methods: Male C57/B6 mice (n=9/group) of 8-12 weeks of age received RvD2 (100 ng/kg/treatment) or vehicle only every third day beginning three days prior to abdominal aortic perfusion with elastase. Aortas were harvested 14 days following elastase perfusion. Cytokine analysis (n=5/group) or confocal microscopy (n=4/group) was performed. Cytokine profiles were analyzed using a murine antibody array. To determine the effect of RvD2 on macrophage polarization, confocal staining for macrophages (Mac2), M1 (MCP-1) and M2 (Arg-1) macrophage subtypes, α-actin and 4',6-diamidino-...

Iliac Artery Injuries

Abstract: Injury to the iliac arteries remains a devastating injury with significant morbidity and mortality that continues to challenge trauma surgeons. Patients typically present in significant metabolic disarray as a result of massive hemorrhage. Damage control techniques should be employed for patients who are coagulopathic, hypothermic, or acidotic. Definitive arterial repair can be accomplished by various techniques, selection of which should depend upon the extent and location of injury. Penetrating injury typically requires open repair, whereas most blunt injuries are amenable to endovascular therapies. Early communication between the trauma surgeon, vascular surgeon, and interventional radiologist is necessary. Fasciotomies should be strongly considered in patients with injury to the common or external iliac arteries or in patients with crush injury in order to avoid development of compartment syndrome.

Iliac Vein Injuries

Abstract: Iliac vein injuries are highly lethal and present a substantial challenge to manage. They account for ~5% of cardiovascular injuries following trauma and are difficult to diagnose and repair due to their location deep in the pelvis. A high index of suspicion must be maintained to make a rapid diagnosis and have a chance at repair. Injury most frequently follows penetrating trauma, but iliac vein damage can also result from blunt force. Injuries are frequently associated with concomitant injury to the bowel and bladder with mortality following repair ranging between 20% and 50%. Iliac vein injuries may either be repaired surgically with lateral venorrhaphy or ligation. Additionally, endovascular repair techniques are a promising adjunct to open repair. The following text will review the causes, diagnosis, and management of iliac vein injuries.

Abstract 19899: TEVAR in Acute Type B Aortic Dissection: Insights from the International Registry of Acute Aortic Dissection (IRAD), Interventional Cohort (IVC)

Abstract: OBJECTIVE: Thoracic endovascular aortic repair (TEVAR) has evolved in to a common therapy for complicated acute type B aortic dissection (ABAD). Recently, the International Registry of Acute Aortic Dissection (IRAD) database was expanded with an interventional cohort (IVC) to further examine details of interventional and surgical treatments. METHODS: ABAD patients treated with TEVAR enrolled in IRAD IVC were studied (n=157). Mean age at intervention was 62±13y. Intra-procedural details were analysed and related to in-hospital outcomes. Indications for TEVAR were identified in 63%, including malperfusion (41%), periaortic hematoma (18%), hypotension/shock (2%), refractory/recurrent pain and hypertension (38%), and aortic diameter > 5.0 cm (4%). RESULTS: addition to TEVAR, visceral artery stenting (including celiac, SMA and renal artery) was required in 22%. This cohort was more likely to manifest malperfusion (50 vs 14%, p=.001) and acute renal failure (46 vs 8%, p CONCLUSIONS: The extent of disease and complexity of the procedure, indicated by several patient- and TEVAR specific details, dictates adverse early outcomes in ABAD after TEVAR. Knowledge of those interventional details may be of importance in the perioperative assessment of patients presenting with ABAD.

Commentary on "Medical and Surgical Management of a Descending Aorta Penetrating Atherosclerotic Ulcer and Associated Ascending Intramural Hematoma" by Henn, M.C. et al.

Abstract: Dear Editor: Henn et al. [1] have nicely described a case scenario whereby a penetrating atherosclerotic ulcer (PAU) of the descending aorta extends with intramural hematoma (IMH) into the ascending aorta. For those of us who manage a lot of acute aortic pathology, this clinical scenario occurs not that infrequently. Based on the dictum that all type A pathology is treated first, the question is whether these patients should be managed by replacement of their ascending aorta first with subsequent repair of their PAU at a later date. Should the ascending be repaired and then insert an endograft distally in an open technique in the same setting? Or should we do as the authors have suggested: just treat the PAU with a covered stent endograft in the descending thoracic aorta? Surprisingly, there is little literature or data to help us manage this clinical scenario. In the present case report, the authors describe a case in which a stent graft was placed in the descending thoracic aorta with subsequent resolution of the ascending aortic IMH. I personally have done this before, as well, with mixed results. There are multiple questions that remain unresolved about this scenario (and others I am sure our readers have asked). For example, does one balloon the endovascular prosthesis that was used to treat the PAU? Is it safe to carry a wire over into the arch and ascending aorta? What is the risk of creating a true type A dissection in these patients? Finally, what are the criteria for a spinal drain in these cases? One might also ask the authors what was their plan, had the IMH in the ascending aorta progressed to a full blown dissection both acutely and chronically; a reverse elephant trunk with repair of the arch, or just repair of the ascending aorta? Does having a stent graft in place change the management of these complex patients and almost ensure that circulatory arrest is required to remove the stent graft placed for a PAU? I am reminded of two things in particular associated with this case, as the technical performance of an endograft in this position is not difficult. However, as a vascular surgeon, it would be imperative that I have a thorough discussion of this case with my cardiac surgery partners before taking a case like this one on (no matter how technically easy it is!). Second, I remember when Drs. Mike Deeb and Dave Williams at the University of Michigan started treating all of the type A dissection patients with malperfusion by fenestration and stenting first, prior to taking the patients to the operating room for their type A repair. At the time, this approach was believed to be heresy by some. Yet, they persevered and many patients were saved with renal, mesenteric, and spinal arteries perfused (i.e., few patients with dead gut, on dialysis, or paralyzed) with nearly identical improved mortality rates compared to those patients who were just taken straight to the operating room with malperfusion. It should give us all pause to think that maybe just treating the PAU in the present scenario was the right thing to do. Congratulations to the authors.