Regionalization of Emergent Vascular Surgery for Patients With Ruptured AAA Improves Outcomes.

OBJECTIVE: Safe and efficient endovascular aneurysm repair (EVAR) for ruptured abdominal aortic aneurysm (r-AAA) requires advanced infrastructure and surgical expertise not available at all US hospitals. The objective was to assess the impact of regionalizing r-AAA care to centers equipped for both open surgical repair (r-OSR) and EVAR (r-EVAR) by vascular surgeons. METHODS: A retrospective review of all patients with r-AAA undergoing open or endovascular repair in a 12-hospital region. Patient demographics, transfer status, type of repair, and intraoperative variables were recorded. Outcomes included perioperative morbidity and mortality. RESULTS: Four hundred fifty-one patients with r-AAA were treated from 2002 to 2015. Three hundred twenty-one patients (71%) presented initially to community hospitals (CHs) and 130 (29%) presented to the tertiary medical center (MC). Of the 321 patients presenting to CH, 133 (41%) were treated locally (131 OSR; 2 EVAR) and 188 (59%) were transferred to the MC. In total, 318 patients were treated at the MC (122 OSR; 196 EVAR). At the MC, r-EVAR was associated with a lower mortality rate than r-OSR (20% vs 37%, P = 0.001). Transfer did not influence r-EVAR mortality (20% in r-EVAR presenting to MC vs 20% in r-EVAR transferred, P > 0.2). Overall, r-AAA mortality at the MC was 20% lower than CH (27% vs 46%, P < 0.001). CONCLUSIONS: Regionalization of r-AAA repair to centers equipped for both r-EVAR and r-OSR decreased mortality by approximately 20%. Transfer did not impact the mortality of r-EVAR at the tertiary center. Care of r-AAA in the US should be centralized to centers equipped with available technology and vascular surgeons.

Anatomic characteristics of abdominal aortic aneurysms presenting with delayed rupture after endovascular aneurysm repair.

OBJECTIVE: Endovascular aneurysm repair (EVAR) has become the mainstay of treatment for abdominal aortic aneurysms (AAAs) requiring repair. Delayed rupture after EVAR represents a rare but potentially fatal complication. The purpose of this study was to review the frequency and characteristics of patients presenting with secondary rupture and to define the relationship between rupture after EVAR and initial compliance with instructions for use (IFU). METHODS: This is a retrospective study of a prospectively maintained database. Patients presenting with delayed rupture after EVAR were identified from January 2002 to December 2014. Medical records and imaging were reviewed to define anatomic characteristics and compliance with IFU criteria. Demographics, comorbidities, preoperative imaging, and long-term outcomes were analyzed. Patients were divided into two groups according to compliance with IFU criteria. Outcomes included type of repair (open vs secondary endovascular) as well as perioperative morbidity and mortality. RESULTS: A total of 3081 patients underwent EVAR for AAA from 2002 to 2014. Of the 3081 patients, 45 experienced delayed rupture after EVAR. The mean time interval between initial repair and rupture was 38 months. All patients with delayed ruptures had a type Ia endoleak. Mean follow-up after secondary repair was 44.1 months, and overall mortality was 6.7% (n = 3). Patients were divided in two groups according to compliance with IFU criteria: within the IFU and outside the IFU. There was no significant difference in comorbidities between the two groups except smoking, which was more frequent in the outside the IFU group (25% vs 21%; P = .03). Patients repaired outside the IFU had a higher incidence of type Ia endoleak before presenting with a rupture (44% vs 6%; P = .001), more frequently required open repair (44% vs 12%; P = .002), and had higher perioperative mortality (10.3% vs 0%; P = .01). On review of preoperative computed tomography scans, the outside the IFU group had larger aneurysm sac diameters (7.2 vs 5.6 cm; P = .04), larger proximal neck diameters (28 vs 24 mm; P = .01), shorter proximal necks (12 vs 21 mm; P = .007), and a higher degree of neck angulation >40 degrees (56 vs 11%; P < .001). CONCLUSIONS: Delayed rupture after EVAR is a rare but potentially fatal complication. In patients presenting with secondary rupture, EVAR performed outside the IFU was associated with higher perioperative mortality and need for open repair. Careful selection of patients based on AAA anatomy and adherence to the IFU criteria may reduce the incidence of delayed rupture.

Chronic mesenteric ischemia outcome analysis and predictors of endovascular failure.

OBJECTIVE: Outcomes of open revascularization (OR) and endovascular revascularization (ER) for chronic mesenteric ischemia (CMI) were analyzed to identify predictors of endovascular failure. METHODS: A retrospective study was performed of all consecutive patients with CMI (161 patients, 215 vessels) treated from 2008 to 2012. Demographics, comorbidities, clinical presentation, etiology, and treatment modalities were compared. Outcomes included technical success, restenosis requiring reintervention, complications, mortality, and hospital length of stay. RESULTS: There were 116 patients who were first treated with ER (72%) and 45 patients with OR (28%). Overall mortality was 6.8% (11/161). Among the ER patients, 27 developed restenosis and required OR (23%). Patients treated with ER were older (73 vs 66 years; P = .014), had similar comorbidities, and had higher rate of short lesions (≤2 cm) on preoperative angiograms (23% vs 47%; P = .004). Primary patency at 3 years was higher in the OR group compared with the ER group (91% vs 74%; P = .018). Long-term survival rates were higher in the ER group (95% vs 78%; P = .003). Hospital length of stay and intensive care unit length of stay were shorter in the ER group (<.001). Perioperative mortality (30-day) was not statistically significant between the groups (5.2% vs 11%; P = .165). A subgroup analysis was performed between the patients with successful ER and failure of ER requiring OR. Patients with failure of ER had significantly higher rates of aortic occlusive disease (86% vs 49%; P = .005) and long lesions ≥2 cm on angiography (57% vs 12%; P < .001) that were close to the mesenteric takeoff. Perioperative mortality was higher in the ER failure group (15% vs 2%; P = .009). CONCLUSIONS: ER has similar perioperative mortality and shorter hospitalization but higher rate of restenosis requiring reintervention compared with OR. Patients with ER who required reintervention appear to have longer lesions as well as higher rates of aortic occlusive disease on preoperative angiography. Patients who crossed over from ER to OR had higher perioperative mortality than either primary open or endovascular patients. These findings may guide treatment selection in patients with CMI undergoing ER or OR.

Novel lipid droplet-associated serine hydrolase regulates macrophage cholesterol mobilization.

OBJECTIVE: Lipid-laden macrophages or foam cells are characterized by massive cytosolic lipid droplet (LD) deposition containing mostly cholesterol ester (CE) derived from the lipoproteins cleared from the arterial wall. Cholesterol efflux from foam cells is considered to be atheroprotective. Because cholesterol is effluxed as free cholesterol, CE accumulation in LDs may limit free cholesterol efflux. Our objective was to identify proteins that regulate cholesterol trafficking through LDs. APPROACH AND RESULTS: In a proteomic analysis of the LD fraction of RAW 264.7 macrophages, we identified an evolutionarily conserved protein with a canonical GXSXG lipase catalytic motif and a predicted α/ß-hydrolase fold, the RIKEN cDNA 1110057K04 gene, which we named LD-associated hydrolase (LDAH). LDAH association with LDs was confirmed by immunoblotting and immunocytochemistry. LDAH was labeled with a probe specific for active serine hydrolases. LDAH showed relatively weak in vitro CE hydrolase activity. However, cholesterol measurements in intact cells supported a significant role of LDAH in CE homeostasis because LDAH upregulation and downregulation decreased and increased, respectively, intracellular cholesterol and CE in human embryonic kidney-293 cells and RAW 264.7 macrophages. Mutation of the putative nucleophilic serine impaired active hydrolase probe binding, in vitro CE hydrolase activity, and cholesterol-lowering effect in cells, whereas this mutant still localized to the LD. LDAH upregulation increased CE hydrolysis and cholesterol efflux from macrophages, and, interestingly, LDAH is highly expressed in macrophage-rich areas within mouse and human atherosclerotic lesions. CONCLUSIONS: The data identify a candidate target to promote reverse cholesterol transport from atherosclerotic lesions.

Endovascular repair of ruptured infrarenal abdominal aortic aneurysm is associated with lower 30-day mortality and better 5-year survival rates than open surgical repair.

OBJECTIVE: Endovascular aneurysm repair (EVAR) decreases 30-day mortality for patients with ruptured abdominal aortic aneurysms (r-AAAs) compared with open surgical repair (OSR). However, which patients benefit or whether there is any long-term survival advantage is uncertain. METHODS: From 2002 to 2011, 283 patients with r-AAA underwent EVAR (n = 120 [42.4%]) or OSR (n = 163 [57.6%]) at Albany Medical Center. All data were collected prospectively. Patients were analyzed on an intention-to-treat basis, and outcomes were evaluated by a logistic regression multivariable model. Kaplan-Meier analysis was used to compare long-term survival. RESULTS: The EVAR patients had a significantly lower 30-day mortality than did the OSR patients (29/120 [24.2%] vs 72/163 [44.2%]; P < .005) and better cumulative 5-year survival (37% vs 26%; P < .005). Men benefited more from EVAR (mortality: 20.9% for EVAR vs 44.3% for OSR; P < .001) than did women (mortality: 32.4% vs 43.9%; P = .39). Age ≥80 years was a significant predictor of death for EVAR (odds ratio [OR], 1.07; P = .003) but not for OSR (OR, 1.04; P = .056). Preexisting hypertension was a significant predictor of survival for both EVAR (OR, 0.17; P < .001) and OSR (OR, 0.48; P = .021). Almost one fourth of EVAR patients (21/91 [23.1%]) required secondary interventions. Survival advantage was maintained for EVAR patients to 5 years. CONCLUSIONS: For r-AAA, EVAR reduces the 30-day mortality and improves long-term survival up to 5 years. However, whereas open survivors require few graft-related interventions, up to 23% of EVAR patients will require reintervention for endoleaks or graft migration. Close follow-up of all EVAR survivors is mandatory.

Women derive less benefit from elective endovascular aneurysm repair than men.

BACKGROUND: Women have a lower chance of surviving elective open abdominal aortic repair. The reasons for this are not clear. Endovascular repair has clearly reduced early and midterm morbidity and mortality for patients with large abdominal aortic aneurysms (AAAs). However, most patients are male. It is unclear whether there has been any reduction in elective morbidity for females or what the extent of that reduction has been. We prospectively analyzed outcomes for elective endovascular aneurysm repair (EVAR) in women at our center and compared results with those for elective open surgery and emergent open and endovascular repair. METHODS: All patients undergoing elective and emergency AAA from 2002 to 2009 were prospectively entered into a database. Demographic details, including gender, were tabulated. Outcome measures were operative blood loss, incidence of type 1 endoleaks, length of in-hospital stay, postoperative complications, 30-day all-cause mortality, and secondary interventions during the follow-up period. Statistical analysis was performed using Fischer exact test and Student t test. A multivariate analysis was also performed. RESULTS: From 2002 to 2009, there were 2631 abdominal aortic aneurysms (AAA) open and endovascular repairs performed in our center (1698 endovascular aneurysm repairs [EVARs], 933 "open"). Males comprised 1995 (76%) of patients; females 636 (24%). There were 1592 elective EVARs (1248 male, 344 female) and 106 emergency EVARs (73 male, 33 female). Elective open repair was performed in 788 patients (579 male, 209 female) and emergency open repair in 149 (73 male, 76 female). For women, elective EVAR resulted in significantly greater mortality rates than men (3.2% vs 0.96%, P < .005). There was a greater incidence of intraoperative aortic neck or iliac artery rupture (4.1% vs 1.2% P = .002) and use of Palmaz stents for type 1 endoleaks (16.1% vs 8%, P = .0009). Mean blood loss was greater in females (327 mL vs 275 mL, P = .038). Perioperative complications were also more frequent in women: leg ischemia (3.5% vs 0.6%, P = .003) and colon ischemia requiring colectomy (0.9% vs 0.2%, P = .009). Mean hospital stay was also longer (3.7 days vs 2.2 days, P = .0001). In contrast, there were no gender differences for any of these outcome measures for elective open repair or emergency open surgery or EVAR. There was no significant difference in death rates between EVAR and open repair in women (3.2% vs 5.7%). In males, the 30-day mortality was 0.96% for elective EVAR and 4.7% for elective open surgery. Following logistic regression, female gender remains a significant risk even when the effects of aneurysm size and age are considered (odds ratio 3.4, P < .01). CONCLUSIONS: Mortality for females undergoing elective EVAR is significantly greater than for males. It is also more hazardous. Colon ischemia, native arterial rupture, and type 1 endoleaks are more frequent. Elective endovascular aneurysm repair benefits men more than women.

Ligation of macrophage Fcγ receptors recapitulates the gene expression pattern of vulnerable human carotid plaques.

Stroke is a leading cause of death in the United States. As ∼60% of strokes result from carotid plaque rupture, elucidating the mechanisms that underlie vulnerability is critical for therapeutic intervention. We tested the hypothesis that stable and vulnerable human plaques differentially express genes associated with matrix degradation. Examination established that femoral, and the distal region of carotid, plaques were histologically stable while the proximal carotid plaque regions were vulnerable. Quantitative RT-PCR was used to compare expression of 22 genes among these tissues. Distal carotid and femoral gene expression was not significantly different, permitting the distal carotid segments to be used as a paired control for their corresponding proximal regions. Analysis of the paired plaques revealed differences in 16 genes that impact plaque stability: matrix metalloproteinases (MMP, higher in vulnerable), MMP modulators (inhibitors: lower, activators: higher in vulnerable), activating Fc receptors (FcγR, higher in vulnerable) and FcγR signaling molecules (higher in vulnerable). Surprisingly, the relative expression of smooth muscle cell and macrophage markers in the three plaque types was not significantly different, suggesting that macrophage distribution and/or activation state correlates with (in)stability. Immunohistochemistry revealed that macrophages and smooth muscle cells localize to distinct and non-overlapping regions in all plaques. MMP protein localized to macrophage-rich regions. In vitro, treatment of macrophages with immune complexes, but not oxidized low density lipoprotein, C-reactive protein, or TNF-α, induced a gene expression profile similar to that of the vulnerable plaques. That ligation of FcγR recapitulates the pattern of gene expression in vulnerable plaques suggests that the FcγR → macrophage activation pathway may play a greater role in human plaque vulnerability than previously appreciated.

Treatment options for delayed AAA rupture following endovascular repair.

PURPOSE: Delayed abdominal aortic aneurysm (AAA) rupture is a well recognized complication of endovascular aneurysm repair (EVAR). We wanted to evaluate the frequency, etiology, and outcomes of delayed AAA rupture following EVAR, and identify treatment options that facilitate improved survival. METHODS: From 2002 to 2009, 1768 patients underwent elective and emergent EVAR. At a mean follow-up of 29 months, 27 (1.5%) patients presented with delayed AAA rupture and required repair by either open surgical conversion or endovascular means. All data were prospectively collected in a vascular registry, and outcomes analyzed. RESULTS: Over a mean follow-up of 29 months, the incidence of delayed AAA rupture after elective EVAR was 1.4% (24 of 1615 patients), and after emergent EVAR for ruptured AAA was 2.8% (3 of 106 patients). Of the 27 delayed AAA rupture patients, 20 (74%) were considered "lost to follow-up," and, at presentation, 17 (63%) patients had Type 1 endoleak with stent graft migration, three (11%) had Type 1 endoleak without stent graft migration, five (19%) had Type 2 endoleak, and two (7%) had undetermined etiology for aneurysm rupture. Fifteen (55%) patients underwent open surgical repair via retroperitoneal approach with partial (n = 8; 53%) or complete (n = 7; 47%) stent graft explants and aortoiliac reconstruction, 11 (41%) patients underwent a second EVAR, and one (4%) patient refused treatment and died. Supraceliac aortic clamp was required in three (20%) patients with open surgical conversion, and supraceliac occlusion balloon was required in two (18%) patients with EVAR. There were three (11%) postoperative deaths; two following open surgical conversion and one following EVAR. One additional redo-EVAR patient has undergone successful elective conversion to open surgical repair for persistent type II endoleak and increase in AAA size. CONCLUSIONS: Delayed AAA rupture following EVAR can be successfully managed in most patients by open surgical conversion or secondary EVAR. The approach to each patient should be individualized; complete stent graft explant is not necessary in most patients; a secondary EVAR for delayed AAA rupture with or without an elective conversion to open surgical repair remains a viable option. Vigilant routine follow-up is needed for all patients after EVAR.

Long-term outcomes of secondary procedures after endovascular aneurysm repair.

PURPOSE: This study evaluated the outcomes of secondary procedures after endovascular aneurysm repair (EVAR). METHODS: From 2002 to 2009, 1768 patients underwent EVAR for treatment of 1662 elective (94%) and 106 emergent (6%) infrarenal abdominal aortic aneurysm (AAA) with a variety of Food and Drug Administration-approved and commercially available stent grafts. Postoperative follow-up included clinical examination, pulse volume recording, duplex ultrasound imaging, and computed tomography and magnetic resonance angiography at 1, 6, and 12 months, and yearly thereafter. Patients with type I and III endoleaks, unexplained endotension, limb occlusion, stent graft migration, with and without type I endoleak, and aneurysm rupture underwent secondary interventions. Type II endoleak at >6 months without a decrease in the aneurysm sac underwent translumbar embolization. Data were prospectively collected. RESULTS: EVAR was performed in 1768 patients. During a mean follow-up of 34 (SD, 30.03) months, 339 patients (19.2%) required additional secondary procedures for aneurysm-related complications, including type I (n = 51, 15.0%), type II (n = 136, 40.1%), and type III (n = 5, 1.5%) endoleaks; endotension (n = 8, 2.4%), stent graft migration proximal fixation site (n = 46, 13.6%), stent graft iliac limb thrombosis or stenosis (n = 25, 7.4%), subsequent iliac aneurysm formation (n = 39, 11.5%), or aneurysm rupture after EVAR (n = 29, 8.6%). The mean age was 74 (SD, 9.15) years. Mean AAA size was 5.7 (SD 3.24) cm. Compared with secondary procedures for AAA rupture, the nonrupture patients had a significantly lower mortality (1.6% vs 17.2%, P < .05) and a higher likelihood of being managed by endovascular means (98.8% vs 44.8%, P < .05). When nonruptured EVAR patients required urgent secondary procedures for type I endoleaks and stent graft migration or limb thrombosis, the mortality was 6.0% vs 0.5% for elective procedures (P < .05). CONCLUSIONS: Our long-term EVAR experience indicates that 18% of patients require additional secondary procedures, and most of these patients can be managed by endovascular means with an acceptable overall mortality of 2.9%. Most type I and II endoleaks can be successfully treated by transluminal embolization, and most patients with delayed aneurysm rupture after EVAR can be successfully managed by endovascular or open surgical repair.

Outcomes of planned celiac artery coverage during TEVAR.

OBJECTIVE: Successful thoracic endovascular aneurysm repair (TEVAR) requires adequate proximal and distal fixation and seal. We report our experience of planned celiac artery coverage during endovascular repair of complex thoracic aortic aneurysms (TAA). METHODS: Since 2004, 228 patients underwent TEVAR under elective (n=162, 71%) and emergent circumstances (66, 29%). Patients with inadequate distal stent grafts landing zones during TEVAR underwent detailed evaluation of the gastroduodenal arcade with communicating collaterals between the celiac and superior mesenteric artery (SMA) by computed tomography angiography and intraoperative arteriogram. If needed, in presence of a patent SMA and demonstration of collaterals to the celiac artery, the stent grafts were extended to the SMA with celiac artery coverage. Furthermore, instances when further lengthening of distal thoracic stent graft landing zone was needed to obtain an adequate seal, the SMA was partially covered with the endograft, and a balloon expandable stent was routinely deployed in proximal SMA to maintain patency. Outcome data were prospectively collected and analyzed retrospectively. RESULTS: Thirty-one of 228 (14%) patients with TEVAR required celiac artery interruption; 24 (77%) had demonstrable collaterals to the SMA. Twelve (39%) of 31 patients underwent additional partial SMA coverage by stent graft, and proximal SMA stent. The majority of patients were females (n=20, 65%), the mean age was 74 years (range 55-87 years), and the mean TAA size was 6.5 cm. Postoperative complications included visceral ischemia in 2 (6%) patients, paraplegia in 2 (6%) patients, and death in 2 (6%) patients. All type 1b endoleaks (n=2, 6%) and type 2 endoleaks vial retrograde flow from the celiac artery (n=3, 10%) were successfully treated by transfemoral coil embolization. Over a mean follow-up of 15 months, there have been no other complications of mesenteric ischemia, spinal cord ischemia, SMA in-stent stenosis, or conversion to open surgical repair. CONCLUSIONS: Our findings suggest that celiac artery coverage to facilitate adequate distal sealing during TEVAR with complex TAA is relatively safe in the presence of SMA-celiac collaterals. Pre-existing SMA stenosis can be successfully treated by balloon expandable stents during TEVAR, and endoleaks arising from distal stent grafts attachment site or via retrograde flow from the celiac artery can be successfully managed by transfemoral coil embolization. Although early results are encouraging, long-term efficacy of these procedures remains to be determined and vigilant follow-up is needed.

Ruptured abdominal aortic aneurysm: endovascular program development and results.

Improvements in endovascular technology and techniques have allowed us to treat patients in ways we never thought possible. Today endovascular treatment of ruptured abdominal aortic aneurysms is associated with markedly decreased morbidity and mortality when compared to the open surgical approach, yet there are several fundamental obstacles in our ability to offer these endovascular techniques to most patients with ruptured aneurysms. This article will focus on the technical aspects of endovascular aneurysm repair for rupture, with particular attention to developing a standardized multidisciplinary approach that will help ones ability to deal with not just the technical aspects of these procedures, but also address some of the challenges including: the availability of preoperative CT, the choice of anesthesia, percutaneous vs. femoral cut-down approach, use of aortic occlusion balloons, need for bifurcated vs. aorto-uniiliac stentgrafts, need for adjunctive procedures, diagnosis and treatment of abdominal compartment syndrome, and conversion to open surgical repair.

Strategies to improve spinal cord ischemia in endovascular thoracic aortic repair: Outcomes of a prospective cerebrospinal fluid drainage protocol.

PURPOSE: Although endovascular repair of thoracic aortic aneurysm has been shown to reduce the morbidity and mortality rates, spinal cord ischemia remains a persistent problem. We evaluated our experience with spinal cord protective measures using a standardized cerebrospinal fluid (CSF) drainage protocol in patients undergoing endovascular thoracic aortic repair. METHODS: From 2004 to 2006, 121 patients underwent elective (n = 52, 43%) and emergent (n = 69, 57%) endovascular thoracic aortic stent graft placement for thoracic aortic aneurysm (TAA) (n = 94, 78%), symptomatic penetrating ulceration (n = 11, 9%), pseudoaneurysms (n = 5, 4%) and traumatic aortic transactions (n = 11, 9%). In 2005, routine use of a CSF drainage protocol was established to minimize the risks of spinal cord ischemia. The CSF was actively drained to maintain pressures <15 mm Hg and the mean arterial blood pressures were maintained at >/=90 mm Hg. Data was prospectively collected in our vascular registry for elective and emergent endovascular thoracic aortic repair and the patients were divided into 2 groups (+CSF drainage protocol, -CSF drainage protocol). A chi(2) statistical analysis was performed and significance was assumed for P < .05. RESULTS: Of the 121 patients with thoracic stent graft placement, the mean age was 72 years, 62 (51%) were male, and 56 (46%) underwent preoperative placement of a CSF drain, while 65 (54%) did not. Both groups had similar comorbidities of coronary artery disease (24 [43%] vs 27 [41%]), hypertension (44 [79%] vs 50 [77%]), chronic obstructive pulmonary disease (18 [32%] vs 22 [34%]), and chronic renal insufficiency (10 [17%] vs 12 [18%]). None of the patients with CSF drainage developed spinal cord ischemia (SCI), and 5 (8%) of the patients without CSF drainage developed SCI within 24 hours of endovascular repair (P< .05). All patients with clinical symptoms of SCI had CSF drain placement and augmentation of systemic blood pressures to >/=90 mm Hg, and 60% (3 of 5 patients) demonstrated marked clinical improvement. CONCLUSION: Perioperative CSF drainage with augmentation of systemic blood pressures may have a beneficial role in reducing the risk of paraplegia in patients undergoing endovascular thoracic aortic stent graft placement. However, selective CSF drainage may offer the same benefit as mandatory drainage.

Establishing a protocol for endovascular treatment of ruptured abdominal aortic aneurysms: outcomes of a prospective analysis.

PURPOSE: In our transition from elective abdominal aortic aneurysm (AAA) to emergent ruptured AAA (r-AAA) repair with endovascular techniques, we recognized that the availability of endovascularly trained staff in the operating rooms and emergency departments, and adequate equipment were the limiting factors. To this end, we established a multidisciplinary protocol that facilitates endovascular repair (EVAR) of r-AAA. METHODS: In January 2002, we instituted a multidisciplinary approach that included the vascular surgeons, emergency department physicians, anesthesiologists, operating room staff, radiology technicians, and availability of a variety of stent-grafts to expedite EVAR of r-AAAs. Five patients with symptomatic, not ruptured AAAs suitable for EVAR underwent simulation of patients presenting to the emergency department with r-AAAs. Emergency department physicians alerted the on-call vascular surgery team (vascular surgeon, vascular resident or fellow) and the operating room staff, emergently performed an abdominal computed tomography (CT) scan in only hemodynamically stable patients with systolic blood pressures > or =80 mm Hg, and transported the patient to the operating room. The vascular surgeon informed the operating room staff to set up for EVAR and open surgical repair in an operating room equipped with interventional capabilities. The operating room setup was rehearsed with the anesthesiologists, operating room staff, and radiology technicians who were knowledgeable of the sequence of steps involved. Since then, 40 patients have undergone emergent EVAR for r-AAAs with general anesthesia. RESULTS: No complications developed in any of the symptomatic (simulation) patients, and 40 (95%) of 42 patients with r-AAAs had a successful EVAR with Excluder (n = 27, 68%), AneuRx (n = 9, 23%), or the Zenith (n = 4, 10%) stent-grafts. The mean age was 73 years (range, 54 to 88 years), and pre-existing comorbidities included coronary artery disease in 26 (65%), hypertension in 23 (58%), chronic obstructive pulmonary disease in 7 (18%), renal insufficiency not on dialysis in two (5%), and diabetes in nine (23%). Fourteen (38%) patients were diagnosed with r-AAAs at another hospital and subsequently were transferred to us, and 26 (62%) presented directly to the emergency department at our institution. At the initial presentation, 30 patients (75%) were hemodynamically stable and either had a CT scan at an outside hospital or in the emergency department, and 10 (25%) hemodynamically unstable patients with systolic blood pressures <80 mm Hg were rushed to the operating room for EVAR without a preoperative CT scan. The mean time from the presumptive diagnosis of a r-AAA in the emergency department to the operating room for EVAR was 20 minutes (range, 10 to 35 minutes), and the mean operative time from skin incision to closure was 80 minutes (range, 35 to 125 minutes). Seven patients (18%) needed supraceliac aortic occlusion balloon, and six (15%) needed aortouniiliac stent-grafts. The mean blood loss was 455 mL (range, 115 to 1100 mL). Two patients each (5%) developed myocardial infarction, renal failure, and ischemic colitis, seven (18%) developed abdominal compartment syndrome, and seven (18%) died. Over a mean follow-up of 17 months, three patients with endovascular r-AAA repair required four secondary procedures. CONCLUSIONS: The early results show that emergent endovascular treatment of hemodynamically stable and unstable patients is associated with a limited mortality of 18% once a standardized protocol is established. There is an increased recognition of emerging complications with an endovascular approach, and a synchrony of disciplines must be developed to initiate a successful program for endovascular treatment of r-AAAs.

Combined carotid endarterectomy and coronary artery bypass grafting in patients with asymptomatic high-grade stenoses: an analysis of 758 procedures.

PURPOSE: Surgical treatment of hemodynamically significant carotid artery stenoses has been well documented, especially in the asymptomatic patient. However, in those patients presenting with hemodynamically significant asymptomatic carotid artery disease who are to undergo cardiac surgery, optimal treatment remains controversial. In this study, we analyze our experience with patients who underwent synchronous carotid endarterectomy (CEA) and coronary artery bypass graft procedures (CABG) for hemodynamically significant (>70%) asymptomatic carotid artery stenosis and coronary artery disease (CAD). METHODS: Demographics and outcomes of all patients undergoing synchronous CEA/CABG for asymptomatic carotid stenosis between April 1980 and January 2005 were reviewed from our vascular registry and patient charts. We included patients who underwent standard patching of their carotid artery and those undergoing eversion CEA. All neurologic events within the first 30 days that persisted >24 hours were considered a stroke. For purposes of comparison, we also reviewed outcomes for patients undergoing synchronous CEA/CABG for symptomatic carotid stenosis. RESULTS: Asymptomatic carotid artery stenosis (>70%) was the indication in 702 patients (276 women and 426 men) undergoing 758 CEAs. In the asymptomatic group, 22 patients, of which 21 succumbed to cardiac dysfunction, and one died from a hemorrhagic stroke. The overall mortality rate was 3.1%. Seven permanent nonfatal neurologic deficits occurred in this series (1 woman, 6 men). The combined stroke mortality was 4.3%. This compares to a 30-day stroke mortality of 6.1% in 132 symptomatic combined CEA/CABG patients. The difference in stroke mortality in women compared with men was not significant. CONCLUSION: In this experience, patients presenting with hemodynamically significant (>70%) asymptomatic carotid artery stenosis can undergo synchronous CEA/CABG with low morbidity and mortality.

Factors associated with abdominal compartment syndrome complicating endovascular repair of ruptured abdominal aortic aneurysms.

BACKGROUND: Endovascular treatment of ruptured abdominal aortic aneurysms (r-AAAs) has the potential to offer improved outcomes. As our experience with endovascular repair of r-AAA evolved, we recognized that the development of abdominal compartment syndrome (ACS) led to an increase in morbidity and mortality. We therefore reviewed our experience to identify risk factors associated with the development of ACS. METHODS: From January 2002 to December 2004, 30 patients underwent emergent endovascular repair of r-AAA by using commercially available stent grafts. All patients who developed ACS underwent emergent laparotomy. Physiological and clinical parameters were analyzed between patients with and without ACS after endovascular r-AAA repair. RESULTS: Over the past 3 years, 30 patients underwent endovascular r-AAA repair, and 6 (20%) patients developed ACS. Patients with ACS had a higher incidence of the need for aortic occlusion balloon (67% vs 12%; P = .01), a markedly longer activated partial thromboplastin time (128 +/- 84 seconds vs 49 +/- 31 seconds; P = .01), a greater need for blood transfusion (8 +/- 2.5 units vs 1.8 +/- 1.7 units; P = .08), and a higher incidence of conversion to aortouni-iliac devices because of ongoing hemodynamic instability and an inability to expeditiously cannulate the contralateral gate (67% vs 8%) when compared with patients without ACS. The mortality was significantly higher in the patients with ACS (67%; 4 of 6) compared with patients without ACS (13%; 3 of 24; P = .01). CONCLUSIONS: ACS is a potential complication of endovascular repair of r-AAA and negatively affects survival. Factors associated with the development of ACS include (1) use of an aortic occlusion balloon, (2) coagulopathy, (3) massive transfusion requirements, and (4) conversion of bifurcated stent grafts into aortouni-iliac devices. We recommend that, after endovascular repair of r-AAA, these patients undergo vigilant monitoring for the development of ACS.

Safety and efficacy of eversion carotid endarterectomy for the treatment of recurrent stenosis: 20-year experience.

Current options for treating recurrent carotid stenosis (RCS) include standard longitudinal arteriotomy and patch angioplasty with or without carotid endarterectomy (s-PCEA), carotid-carotid bypass, or carotid angioplasty and stent (CAS). Eversion carotid endarterectomy (e-CEA) is an effective procedure for treating primary carotid stenosis, yet it has not been reported for treating RCS. We evaluated the feasibility and outcome of e-CEA for treating of RCS in comparison to s-PCEA. The records of all patients undergoing elective CEA for symptomatic and asymptomatic high-grade RCS from January 1981 to July 2002 were reviewed. Although during the earlier period s-PCEA was performed preferentially, this paradigm changed to e-CEA being the preferred technique for treatment of RCS. During the course of postoperative follow-up when duplex sonography suggested high-grade RCS, the diagnosis was confirmed via arteriography. Data on cranial nerve injury, recurrent stenosis, stroke, and death were prospectively collected into a vascular registry database and analyzed retrospectively, Students' t-test and chi-square analysis were used to compare the group's baseline characteristics and outcomes. Over a 21-year period, 7001 patients underwent primary CEA for symptomatic (n = 2405, 34%) or asymptomatic (n = 4596, 66%) high-grade stenosis via standard (n = 1501, 21%) or eversion (n = 5500, 79%) techniques. Fifteen (25%) patients had 70 to 80% stenosis, 30 (51%) had 81 to 90% stenosis, and 14 (24%) had 91 to 99% stenosis. During this time period, 59 patients presented with symptomatic (n = 18, 31%) or asymptomatic (n = 41, 69%) high-grade RCS and underwent operative repair via s-PCEA (n = 22, 37%) or eversion (n = 37, 63%) techniques. The mean time interval for repeat carotid surgery for RCS was 49 months in the s-PCEA group and 48 months in the e-CEA group. Permanent cranial nerve injuries, stroke, and recurrent restenosis occurred in one (4.5%), one (4.5%), and one (4.5%) of the patients undergoing s-PCEA, respectively. In the e-CEA group, these events occurred in one (27%), none (0%), and one (2.7%) patients, respectively, There were no deaths during the 30-day postoperative period. Eversion CEA is a feasible option for the treatment of many RCSs and can be performed safely with a low rate of cranial nerve injury, recurrent stenosis, stroke, and death.

Does sac size matter? Findings based on surgical exploration of excluded abdominal aortic aneurysms.

PURPOSE: To prospectively examine the outcomes of excluded abdominal aortic aneurysms (AAA) that continue to expand without evidence of endoleak. METHODS: From 1984 to 1998, 1218 patients underwent operative retroperitoneal exclusion of AAA and aortoiliac reconstructions. During the procedure, the aneurysm sac was ligated proximally, as well as distally, which created an ideal in-vivo model of excluded AAA sacs with or without endoleaks. From January 2002 to June 2003, 15 of these patients were identified as having an increase in AAA sac size with or without an endoleak on duplex ultrasonography. These patients were prospectively evaluated by computed tomography and diagnostic arteriography. Patients with a demonstrable endoleak underwent embolization, and the remainder underwent open surgical exploration. RESULTS: Eight patients had arteriographically demonstrated endoleaks that were treated with coil embolization. The remaining 7 patients (6 men; mean age 76 years, range 68-81) without a demonstrable endoleak underwent elective surgical exploration and sac endoaneurysmorrhaphy. The mean time interval between the original surgery and aneurysm sac exploration was 76 months (range 52-92); during this time, the mean aneurysm sac size increased by 2.7 cm (range 1.3-5.2). The mean sac pressure was 53 mmHg, and the sac walls were noticeably thickened, with markedly dilated vasa vasorum. The sac contained yellow, fibrinous material with clear serous fluid (5 patients without any evidence of retrograde flow) or liquefied thrombus with serosanguinous fluid (2 patients with retrograde flow from lumbar arteries). No AAA sacs were pulsatile. CONCLUSIONS: Continued expansion of excluded AAA sacs can occur from causes other than a missed endoleak. Exudation of fluid from thickened sac wall and vasa vasorum, as well as local enzymatic activity, might lead to the formation of a sac hygroma. Furthermore, these findings raise questions as to the need for surgical exploration of all patients with an enlarging AAA sac in the setting of low sac pressures and no definable endoleak.

Infrarenal abdominal aortic aneurysm repair via endovascular versus open retroperitoneal approach.

The beneficial effects of open surgical abdominal aortic aneurysm (AAA) repair via a left retroperitoneal approach have been established. We compared the short-term outcome of infrarenal AAA repair via an endovascular approach with that of an open retroperitoneal approach. From October 2001 to April 2003, patients with infrarenal AAA >5 cm were offered repair via an endovascular approach (group I) with a variety of industry-made stent grafts or with an open retroperitoneal surgical approach (group II). Data were prospectively collected in the vascular registry and complications were analyzed. Data comparison between the two groups was done by using chi-squared analysis and two-tailed Students t-test. Statistical significance was identified at p < 0.05. Over an 18-month period, 492 patients underwent evaluation for AAA. Of these, 446 patients had infrarenal AAA and underwent either endovascular (group I: n = 175, male 85%, female 15%) or open surgical repair (group II: n = 232, male 74%, female 26%) via a left retroperitoneal approach. Group I patients had a higher incidence of coronary artery disease (66% vs. 35%, p < 0.05), hypertension (74% vs. 43%, p < 0.05), chronic obstructed pulmonary disease (29% vs. 12%, p < 0.05), and diabetes mellitus (20% vs. 7%, p < 0.05), a lower mean amount of intraoperative blood loss (277 cc vs. 1452 cc, p < 0.05), and shorter length of stay in the hospital (1.7 days vs., 7.3 days, p < 0.05). Group I also had fewer complications of myocardial infarction (1.7% vs. 5.2%, p = NS), renal failure (0% vs. 2.6%, p < 0.05), pulmonary failure (1.7% vs. 2.6%, p = NS), ischemic colitis requiring colectomy (0.6% vs. 2.6%, p < 0.05), multisystem organ failure (0% vs. 1.3%, p = NS), and death (0.6% vs. 1.3%, p < 0.05). Despite increased preexisting comorbidities, patients undergoing endovascular aneurysm repair had less morbidity, mortality, and blood loss and a shorter in-hospital length of stay than patients undergoing open surgical aneurysm repair via a left retroperitoneal approach.

Outcome of popliteal artery aneurysms after exclusion and bypass: significance of residual patent branches mimicking type II endoleaks.

PURPOSE: Popliteal aneurysms (PAs) often are treated with exclusion and bypass. However, excluded aneurysms can transmit systemic pressure from persistent flow through collateral arteries (endoleak), resulting in aneurysm growth and rupture. We used duplex ultrasound scanning for postoperative surveillance more than 2 years after PA repair with exclusion and bypass, to determine the presence of flow and aneurysm growth. METHODS: From 1995 to 2001, 23 patients with 26 PAs (mean diameter, 3.2 cm; range, 1.6-5.6 cm) underwent surgical repair and were available for more than 2 years of follow-up. The popliteal artery was ligated proximal and distal to the aneurysm, and autogenous revascularization was performed. All patients who underwent PA endoaneurysmorrhaphy through a posterior approach were excluded from the study. During long-term follow-up, aneurysm sac flow and size were evaluated with duplex ultrasound scanning, computed tomography, or magnetic resonance angiography, and standard angiography. Patients with increased PA size and persistent flow were offered repair through a posterior approach. RESULTS: Over 7 years, 26 PAs (symptomatic, 11; asymptomatic, 15) treated with aneurysm exclusion and bypass were available for more than 2 years of follow-up (mean, 38 months; range, 24-78 months). In the postoperative period 16 PAs (62%) became thrombosed, 10 (38%) had persistent collateral flow through geniculate vessels, 6 (23%) increased in size, and 3 (12%) ruptured; 1 (4%) resulted in limb loss. Operative findings for all ruptured PAs and 3 of 6 PAs with increased sac size that underwent aneurysm sac exploration and endoaneurysmorrhaphy revealed retrograde flow through geniculate vessels, mimicking type II endoleak. CONCLUSIONS: These findings question the effectiveness of PA exclusion through proximal or distal ligation and bypass. In addition, retrograde flow into the aneurysm sac (ie, type II endoleak after endovascular abdominal aortic aneurysm repair) may transmit systemic pressure that can result in aneurysm rupture. We recommend PA treatment with aneurysm sac decompression and ligation of geniculate vessels whenever possible and routine postoperative surveillance of the excluded aneurysm sac.

Effects of bilateral hypogastric artery interruption during endovascular and open aortoiliac aneurysm repair.

PURPOSE: Hypogastric artery interruption is sometimes required during aortoiliac aneurysm repair. We have not experienced some of the life-threatening complications of pelvic ischemia reported by others. Therefore we analyzed our experience to identify factors that help minimize pelvic ischemia with unilateral and bilateral hypogastric artery interruption. METHODS: From 1995 to 2003, 48 patients with aortoiliac aneurysm required interruption of both hypogastric arteries as part of endovascular (n = 32) or open surgical (n = 16) repair. During endovascular aneurysm repair coils were placed at the origin of the hypogastric arteries, and bilateral hypogastric artery interruptions were staged at 1 to 2 weeks when possible. Open surgery necessitated oversewing or excluding the origins of the hypogastric arteries and extending the prosthetic graft to the external iliac or femoral artery. Collateral branches from the external iliac and femoral arteries were preserved, and patients received systemic heparinization (50 units/kg). RESULTS: There was no buttock necrosis, ischemic colitis requiring colon resection, or death with the bilateral hypogastric artery interruption. Initially buttock claudication developed in 20 patients (42%), but persisted in only 7 patients (15%) at 1 year. New onset of impotence occurred in 4 of 28 patients (14%), and there were no neurologic deficits. CONCLUSIONS: Bilateral hypogastric artery interruptions can be accomplished with limited morbidity. When hypogastric artery interruption is needed during endovascular aneurysm repair, certain principles help minimize pelvic ischemia. These include hypogastric artery interruption at its origin to preserve the pelvic collateral vessels, staging bilateral hypogastric artery interruptions when possible, preserving collateral branches from the femoral and external iliac arteries, and providing adequate heparinization of the patient during these procedures.