Prior Abdominal Aortic Aneurysm Repair Research Articles

Intervention for Aortic Rupture After Prior Abdominal Aortic Aneurysm Repair: Is EVAR the Best Approach?

Intervention for Aortic Rupture After Prior Abdominal Aortic Aneurysm Repair: Is EVAR the Best Approach?

Predicting Outcomes Following Endovascular Abdominal Aortic Aneurysm Repair Using Machine Learning.

To develop machine learning (ML) models that predict outcomes following endovascular aneurysm repair (EVAR) for abdominal aortic aneurysm (AAA). EVAR carries non-negligible perioperative risks; however, there are no widely used outcome prediction tools. The National Surgical Quality Improvement Program targeted database was used to identify patients who underwent EVAR for infrarenal AAA between 2011 and 2021. Input features included 36 preoperative variables. The primary outcome was 30-day major adverse cardiovascular event (composite of myocardial infarction, stroke, or death). Data were split into training (70%) and test (30%) sets. Using 10-fold cross-validation, 6 ML models were trained using preoperative features. The primary model evaluation metric was area under the receiver operating characteristic curve. Model robustness was evaluated with calibration plot and Brier score. Subgroup analysis was performed to assess model performance based on age, sex, race, ethnicity, and prior AAA repair. Overall, 16,282 patients were included. The primary outcome of 30-day major adverse cardiovascular event occurred in 390 (2.4%) patients. Our best-performing prediction model was XGBoost, achieving an area under the receiver operating characteristic curve (95% CI) of 0.95 (0.94-0.96) compared with logistic regression [0.72 [0.70-0.74)]. The calibration plot showed good agreement between predicted and observed event probabilities with a Brier score of 0.06. Model performance remained robust on all subgroup analyses. Our newer ML models accurately predict 30-day outcomes following EVAR using preoperative data and perform better than logistic regression. Our automated algorithms can guide risk mitigation strategies for patients being considered for EVAR.

Thoracic Endovascular Aortic Repair for Metachronous Thoracic Aortic Aneurysms Following Prior Infrarenal Abdominal Aortic Aneurysm Repair

Thoracic endovascular aortic repair (TEVAR) for metachronous thoracic aortic aneurysms (M-TAA) after prior abdominal aortic aneurysm repair has been shown to be associated with higher risk of spinal cord ischemia compared with primary TEVAR. However, data regarding the impact of the type of prior repair on outcomes are scarce. In this study, we examined perioperative outcomes and long-term mortality after TEVAR for M-TAA compared with primary TEVAR for TAA. We identified all patients who underwent TEVAR for TAA of the descending thoracic aorta in the Vascular Quality Initiative from 2013 to 2022. Only patients undergoing primary TEVAR or TEVAR after infrarenal open (iOAR) or endovascular (EVAR) repair were included. We performed univariate analyses to identify differences in baseline and procedural characteristics, and multivariable analyses for perioperative outcomes and 5-year mortality using logistic and Cox regression models. We included 1493 patients who underwent primary TEVAR (n = 1213; 81%) or TEVAR after prior iOAR (n = 135; 9%) or prior EVAR (n = 145; 10%). Compared with primary TEVAR, patients undergoing TEVAR for metachronous aneurysms were older, more commonly male, White, and more frequently had a history of genetic disorders and other comorbidities. Patients with M-TAA were more often asymptomatic at repair, presented with larger diameters, and required higher contrast volume and longer procedural time, relative to patients undergoing primary TEVAR. After risk adjustment, compared with primary TEVAR, prior EVAR was associated with higher perioperative mortality (10% vs 3.9%; odds ratio [OR]: 4.5, 95% confidence interval [CI]: 2.0-9.9; P < .001) (Table) and 5-year mortality (40% vs 24%; hazard ratio: 1.9, 95% CI: 1.3-2; P = .001) (Fig), along with higher odds of acute kidney injury (10% vs 6.2%; OR: 2.0, 95% CI: 1.0-3.8; P = .04). However, other in-hospital complications including spinal cord ischemia were not notably different. On the other hand, TEVAR after prior iOAR was associated with similar perioperative mortality (4% vs 4%; OR: 0.8, 95% CI: 0.3-2.0; P = .75), 5-year mortality (28% vs 24%; hazard ratio: 1.2, 95% CI: 0.72-1.9; P = .54), and in-hospital complication and reintervention rates, relative to primary TEVAR. Type of prior repair has a significant impact on outcomes in patients undergoing intervention for M-TAA. Further efforts should aim to identify the reasons behind these differences in outcomes to help improve care of patients with M-TAA.TablePerioperative outcomes and 5-year mortality after primary TEVAR and TEVAR after prior iOAR or EVARPrimary TEVARPrior iOARPrior EVARPrimary TEVAR vs prior iOARPrimary TEVAR vs prior EVARUnadjusted event rates, %Odds ratio (95% CI)P valueOdds ratio (95% CI)P valuePerioperative mortality3.94.49.71.2 (0.32-3.7).754.5 (2.0-9.9)<.001Any complication1814230.92 (0.50-1.6).771.5 (0.89-2.3).13 AKI6.26.7101.3 (0.56-2.9).492.0 (1.0-3.8).04 Postoperative dialysis1.01.51.42.1 (0.24-1.2).461.4 (0.07-9.1).78 Spinal cord ischemia2.60.72.80.22 (0.01-1.2).161.3 (0.35-3.5).69 Leg ischemia1.90.72.11.2 (0.06-7.2).862.0 (0.42-7.0).33 Bowel ischemia0.501.4NANA3.0 (0.40-15).22 Stroke3.11.54.10.63 (0.10-2.3).541.3 (0.40-3.3).58 Pulmonary complication5.06.76.91.8 (0.72-4.0).181.9 (0.83-3.8).11 Cardiac complication2.53.02.81.7 (0.45-5.2).971.02 (0.23-3.2).97Reintervention4.93.76.21.2 (0.38-3.0).761.5 (0.64-3.3).30Unadjusted estimatesHazard ratio (95% CI)P valueHazard ratio (95% CI)P value5-year mortality2325401.2 (0.72-1.9).541.9 (1.3-2.8).001AKI, Acute kidney injury; CI, confidence interval; iOAR, infrarenal open aortic repair; TEVAR, thoracic endovascular aortic repair.Boldface P values represent significance P < .05.*Adjusted for age, gender, diameter, race, saccular, presentation, prior myocardial infarction, prior congestive heart failure, hypertension, diabetes, chronic obstructive pulmonary disease, smoking, renal dysfunction, prior medication use (aspirin, statin, and β-blocker), and genetic history. Open table in a new tab

The role of intraluminal thrombus formation for expansion of abdominal aortic aneurysms.

Though the pathophysiology of initiation, formation, and expansion of abdominal aortic aneurysm (AAA) has been intensely researched, the distinct mechanisms driving these processes still remain unclear. In particular, human studies on predictors of AAA progression as a major determinant of rupture risk are scarce. All consecutive abdominal aortic ultrasound sonographic examinations performed at the duplex laboratory of the Division of Angiology of the Medical University of Vienna between 1999 and 2012 were reviewed. Patients with repeated measurements of the infrarenal aortic diameter, who had no prior AAA repair were included. Detailed informations on AAA, including length, anterior-posterior and transversal measurements of diameter, and intraluminal thrombus formation/size were obtained from ultrasound examination; patients' comorbidities, cardiovascular risk factors, and medications were obtained from outpatient charts. The expansion rate of AAA in relation to intraluminal thrombus size, gender, age, comorbidities, cardiovascular risk factors, and pharmacotherapy was evaluated. Independent predictors of AAA growth were identified through mixed effects models. In total, 166 patients (123 men and 43 women, mean age 68 ± 9 years) were included. Patients were followed over a mean period of 1.4 ± 1.2 years with a mean number of follow-up investigations of 4.4 ± 2.7. Overall, mean maximum AAA diameter at baseline was 37.4 ± 8.2 mm. The average expansion rate of AAA diameter throughout the follow-up period was 2.0 mm per year (95 % confidence interval: 1.6-2.4). At initial investigation, intraluminal thrombus formation was present in 56.6 % of all patients. AAA diameter at baseline, time of follow-up as well as presence and size of intraluminal thrombus formation were identified as independent predictors of AAA expansion rate. Importantly, gender and presence of cardiovascular risk factors were not associated with AAA progression rate. Intraluminal thrombus formation seems to be a key determinant for progression of AAA diameter. Further prospective longitudinal studies are warranted to confirm the potential impact of thrombus formation on AAA development and its implication on monitoring and treatment decisions in patients with AAA.

Endovascular Treatment of Delayed Rupture Following Prior Abdominal Aortic Aneurysm Repair Achieves Better Survival Rates

To test the hypothesis that endovascular treatment of delayed aneurysm rupture achieves significantly better survival rates compared to surgical conversion. All patients sustaining delayed rupture following prior exclusion of an abdominal aortic aneurysm (AAA) either by endovascular aneurysm repair (EVAR) or open graft replacement from March 1995 through December 2011 were retrieved from a prospectively maintained database at a tertiary care university hospital. During the study period, 35 patients (32 men; mean age 72.9 years) presented with delayed rupture at a median 2.4 years (interquartile range 1.3-4.3) after initial AAA repair by EVAR (n=22) or open surgery (n=13). Causes of post-EVAR rupture were graft-related endoleaks, while ruptures after open repair occurred at anastomotic suture sites. Patients were divided into groups regarding type of treatment for delayed rupture: 20/35 (57%) underwent successful EVAR (10 redo procedures), 13/35 (37%) had surgery (3 redo procedures), and 2/35 (6%) patients received comfort care only. The primary endpoint was 30-day mortality. The 30-day mortality after curative treatment was 25% (5/20) for endovascular treatment compared to 54% (7/13) for surgery (p=0.14). Including additional deaths beyond 30 days, the overall in-hospital mortality was 52% (17/33). The Kaplan-Meier survival estimate for patients undergoing endovascular treatment was significantly higher (p=0.011). Endovascular treatment of delayed rupture is feasible and helps to reduce mortality. Our data suggest that endovascular procedures are a superior treatment option for EVAR-suitable patients with delayed rupture compared with surgical conversion.

Acute Aortic Dissection Presenting as Painless Paraplegia

A 60-year-old man with hypertension, hyperlipidemia, and a prior abdominal aortic aneurysm repair in 1995 presented with sudden weakness of both legs. His blood pressure was 91/56 mmHg, his pulse was 107 beats/min, and he had flaccid paraplegia with a spinal sensory level at T6. Magnetic resonance imaging (MRI) of the thoracic spinal cord showed no lesion. Chest and abdominal computed tomography (CT) with contrast showed a large Type B dissecting aortic aneurysm (Figs. 1 and ​and2).2). The following day, he developed acute renal failure requiring hemodialysis, as the dissection extended into his right renal artery. The patient was medically managed and died one week later. Figure 1. Axial thoraco-abdominal CT showing a large dissecting aneurysm (with true [asterisk] and false [white arrows] lumens). Figure 2. Coronal chest CT demonstrating a large dissecting aneurysm (with true [asterisk] and false [white arrows] lumens). Acute aortic dissection (AD) usually presents in hypertensive males over the age of 60 years, as a sudden tearing chest pain radiating to the back.1 Paraplegia due to spinal cord ischemia and infarction as a presenting manifestation of AD has been found in 1.9 % cases.2 However, painless paraplegia, as in this case, is exceedingly rare and limited to six case reports.3–8 Paralysis in AD is due to anterior spinal artery syndrome, which usually includes loss of pain and temperature sensation, with preservation of vibration and proprioception sensation. This pattern typically manifests after spinal shock resolves over weeks.

Propensity-matched cohort validates findings of the VALOR trial

The Evaluation of the Medtronic Vascular Talent Thoracic Stent Graft System for the Treatment of Thoracic Aortic Aneurysms (VALOR) trial findings noted superior 30-day and 1-year outcomes of the Talent thoracic endograft (Medtronic Vascular, Santa Rosa, Calif) compared with surgical repair of descending thoracic aneurysms (DTAs). Data from 195 prospective thoracic endovascular aneurysm repair (TEVAR) patients treated with the Talent device and 189 retrospective controls undergoing open surgical repair (OSR) from three centers of excellence were included in the trial after completion of TEVAR enrollment and compared. Such comparisons are biased by baseline differences among TEVAR vs OSR, however, propensity score (PS) analysis can reduce bias and validate such comparisons. Logistic regression was used to generate a PS (range, 0-1) to identify baseline characteristics more likely in TEVAR. The PS estimated the probability that any patient would undergo TEVAR (eg, a PS of 0.99 represents a 99% chance a patient belongs to TEVAR). PSs were then generated for all patients, and TEVAR and OSR patients were divided into tertiles based on the PS to reduce up to 80% of inherent bias. Outcomes from the middle tertile (T2), patients equally likely (midrange PS) to be in TEVAR or OSR and therefore best matched, were compared using regression analysis and were also compared with the outcomes in the overall trial group. Correlates of membership in TEVAR were smaller aneurysm (P < .001), anticoagulants (P < .01), no previous abdominal aortic aneurysm (AAA) repair (P < .01), no peripheral vascular disease (P = .001), statin use (P = .002), aspirin use (P = .002), older age (P = .028), race (P = .007), male gender (P = .02), and heart failure (P = .035). T2 included 68 TEVAR (PS, 0.58 ± 0.2) and 67 OSR patients (PS, 0.46 ± 0.2). VALOR overall reported differences in aneurysm size (56 mm TEVAR vs 69 mm open) and prior AAA repair (19% TEVAR vs 37% open), and this adjusted to no differences in T2 patients. In the well-matched T2 cohort, TEVAR patients had similar 30-day mortality (0% vs 3% OSR; P = .2) and improved 1-year aneurysm-related mortality rates (0% TEVAR vs 8% OSR; P = .05) compared with the OSR patients. This finding was in concurrence with the VALOR trial reporting similar benefit in TEVAR patients. The all-cause 1-year mortality showed a favorable trend for TEVAR in the VALOR trial; however, in T2 patients, 1-year all-cause mortality was similar in both groups of patients (17% TEVAR vs 15% OSR; P = .8). Age (P = .01), history of cerebrovascular accident (P < .05), antiarrhythmia medication (P = .04), and renal disease (P < .03) independently predicted all-cause and aneurysm-related mortality by regression analysis. PS analysis is an important tool for elimination of bias inherent when retrospective controls are used. Its application to VALOR validates the long-term benefit in aneurysm-related mortality conferred by TEVAR in patients undergoing endovascular DTA repair.

Spinal Cord Protection with a Cerebrospinal Fluid Drain in a Patient Undergoing Thoracic Endovascular Aortic Repair

Paralysis and paraparesis are dreaded complications of thoracic endovascular aortic repair (TEVAR) that occur with an incidence of 2%-6%. Risks factors include the type of thoracic aortic pathology treated, coverage of the left subclavian artery origin without revascularization, concomitant infrarenal abdominal aortic aneurysm repair, extent of stent graft coverage of the thoracic aorta, and renal failure. Cerebral spinal fluid (CSF) drains have been advocated as one of several protective strategies to prevent spinal cord ischemia. This case discussion briefly addresses the evidence supporting the use of CSF drains in patients undergoing TEVAR and offers an algorithm for managing CSF drains.

PP76. Thoracic Stent Implantation and Conventional Surgical Repair after Previous Abdominal Ortic Aneurysm Surgery

Patients with descending thoracic aneurysm (DTA) repair after previous abdominal aortic aneurysm (AAA) surgery have a high risk for spinal cord ischemia and renal dysfunction. This study evaluates the outcome after thoracic endograft implantation and conventional descending aneurysm surgery in patients with prior AAA repair.

Open vs. endovascular repair of isolated iliac artery aneurysms: A 12-year experience

To examine contemporary operative techniques and outcomes for repair of isolated iliac artery aneurysms. We retrospectively reviewed the charts of all patients who underwent repair of an isolated iliac artery aneurysm from February 1995 to June 2007. Mycotic aneurysms and patients with concurrent infrarenal abdominal aortic aneurysms greater than 3.5 cm in diameter were excluded from analysis. Patients with prior abdominal aortic aneurysm repair were not excluded. Fifty-six patients (96% male; mean age, 72 +/- 10 years) had either open (n = 24) or endovascular (n = 32) repair with median follow-up of 36 months. Seven patients were treated for rupture, six with open repair, and one with an endograft. Average aneurysm size for patients in the open and endovascular repair cohorts was 4.5 +/- 2.4 cm and 4.0 +/- 1.1 cm, respectively (P = .35). One episode of endograft limb thrombosis at five months was treated with catheter-directed thrombolytic therapy and stent placement. Thirty-day mortality for patients undergoing elective and emergent open repair was 1/18 (6%) and 1/6 (17%), respectively. There was no 30-day mortality for the endovascular group. Median length of stay was 10.5 days in the open group and one day in the endovascular elective group (P < .01). There was no mid-term aneurysm-related mortality in either group. Primary patency rates were similar between the open and endovascular groups at five years (100% vs. 96%, P = .07). Aneurysm sac diameter decreased in 67% (21/28) of patients that underwent endovascular repair. One patient with a Type III endoleak required relining of the endograft with a second endograft at 72 months. These data demonstrate that in appropriately selected patients, endovascular repair of isolated iliac artery aneurysms is a safe, effective alternative to open repair with mid-term follow-up. Endovascular repair is associated with a significantly reduced hospital length of stay and may be associated with decreased need for transfusion and mortality when compared with open repair.

Thoracic stent implantation after previous abdominal aortic aneurysm surgery

Objectives: Patients required a thoracic or thoracoabdominal aortic aneurysm (TAAA) repair after previous abdominal aortic aneurysm (AAA) surgery have a high risk for spinal cord ischemia (up to 20%) and renal dysfunction (up to 15%), reported in the literature. The purpose of this study was to evaluate the technical possibility of the thoracic stent implantation and the morbidity after this procedure in patients with prior AAA repair.

TEVAR following prior abdominal aortic aneurysm surgery: Increased risk of neurological deficit

Evidence regarding the impact of prior abdominal aortic aneurysm (AAA) repair on the risk of neurological deficit after thoracic endovascular aortic aneurysm repair (TEVAR) is lacking. The purpose of this study was to characterize the risk of TEVAR-related neurological deficit in patients who previously underwent infrarenal AAA surgery. Prospective maintained databases of patients undergoing TEVAR in the participating institutions were searched for patients with a history of prior AAA surgery before TEVAR. Patient and procedural characteristics and postoperative mortality and morbidity were subsequently centrally collected and systematically entered in a database. Univariate and multivariate logistic regression were performed associating variables with postoperative spinal cord ischemia (SCI). Seventy-two patients were identified that underwent TEVAR after prior AAA repair. The risk of SCI was 12.5% (n = 9) and significantly higher than the 1.7% risk of SCI in patients without prior AAA repair (relative risk [RR] 7.2, 95% confidence interval [CI] 2.6 to 19.6, P < .0001). Symptoms of SCI completely resolved in 4 patients with prior AAA repair. Univariate analysis demonstrated that the following variables were significant predictors of SCI in patients with prior AAA repair: preoperative renal insufficiency (odds ratio [OR] 29.5; 95% CI 5.3-164, P < .001), increased length of aorta coverage by TEVAR (OR 1.1; 95% CI 1.0-1.2, P .039) and a lengthened time interval between prior AAA repair and TEVAR (OR 1.2; 95% CI 1.0-1.4, P .026). Preoperative renal insufficiency was also significantly associated with the risk of SCI in multivariate analysis (P .011). Prior infrarenal AAA repair is associated with dramatic increased risk of SCI after TEVAR compared to patients without prior AAA surgery. Preoperative renal insufficiency appears to be an important predictor of SCI after TEVAR in patients with prior AAA repair. A thorough understanding of the risk profile in patients requiring TEVAR following prior AAA surgery is essential when determining appropriate surgical recommendations. If the diameter and rupture risk are large and TEVAR is indicated, the best available care should be offered for maximal protection of the spinal cord in these patients.

Strategies to Manage Paraplegia Risk After Endovascular Stent Repair of Descending Thoracic Aortic Aneurysms

Paraplegia is a recognized complication after endovascular stent repair of descending thoracic aortic aneurysms. A management algorithm employing neurologic assessment, somatosensory evoked potential monitoring, arterial pressure augmentation, and cerebrospinal fluid drainage evolved to decrease the risk of postoperative paraplegia. Patients in thoracic aortic aneurysm stent trials from 1999 to 2004 were analyzed for paraplegic complications. Lower extremity strength was assessed after anesthesia and in the intensive care unit. A loss of lower extremity somatosensory evoked potential or lower extremity strength was treated emergently to maintain a mean arterial pressure 90 mmHg or greater and a cerebrospinal fluid pressure 10 mm Hg or less. Seventy-five patients (male = 49, female = 26, age = 75 +/- 7.4 years) had descending thoracic aortic aneurysms repaired with endovascular stenting. Lumbar cerebrospinal fluid drainage (n = 23) and somatosensory evoked potential monitoring (n = 15) were performed selectively in patients with significant aneurysm extent or with prior abdominal aortic aneurysm repair (n = 17). Spinal cord ischemia occurred in 5 patients (6.6%); two had lower extremity somatosensory evoked potential loss after stent deployment and 4 developed delayed-onset paraplegia. Two had full recovery in response to arterial pressure augmentation alone. Two had full recovery and one had near-complete recovery in response to arterial pressure augmentation and cerebrospinal fluid drainage. Spinal cord ischemia was associated with retroperitoneal bleed (n = 1), prior abdominal aortic aneurysm repair (n = 2), iliac artery injury (n = 1), and atheroembolism (n = 1). Early detection and intervention to augment spinal cord perfusion pressure was effective for decreasing the magnitude of injury or preventing permanent paraplegia from spinal cord ischemia after endovascular stent repair of descending thoracic aortic aneurysm. Routine somatosensory evoked potential monitoring, serial neurologic assessment, arterial pressure augmentation, and cerebrospinal fluid drainage may benefit patients at risk for paraplegia.

Endovascular Treatment of Failed Prior Abdominal Aortic Aneurysm Repair

Failure of endovascular or conventional abdominal aortic aneurysm (AAA) repair may occur as a result of attachment site endoleak (type I) or paraanastomotic aneurysm and pseudoaneurysm formation. This study examined the results of the use of secondary endovascular grafts for the treatment of failed prior infrarenal AAA repair procedures. Forty-seven patients were treated with endovascular grafts. These included 14 patients with type I endoleaks (5 proximal, 8 distal, 1 proximal and distal) and 33 patients with paraanastomotic aneurysms after standard open surgical AAA repair (3 proximal aorta, 5 distal aorta, 21 iliac, 4 proximal and distal). The interval between the primary aortic procedure and the endovascular repair was significantly shorter for failed endovascular procedures (mean, 18.2 months; range, 1-42 months) than for failed conventional procedures (mean, 108.9 months; range, 12-216 months) (p <0.01). The endovascular devices used for correction of the failed AAA repairs were Talent (23), physician-made (19), AneuRx (2), Vanguard (2), and Excluder (1). Transrenal fixation was used for repair of all proximal anastomotic failures. Mean follow-up after reintervention was 12.2 months in patients with failed endovascular grafts and 10.6 months in patients with failed conventional grafts. Patient demographics were as follows: average age, 78 years; 36 male and 11 female; and 4.1 comorbid medical conditions per patient. The endovascular graft was successfully deployed in all 47 cases; 1 patient experienced a persistent proximal attachment site endoleak after endograft deployment. Endovascular grafts may be used to treat previously failed endovascular and conventional AAA repair procedures with good short- and intermediate-term results. Endovascular treatments in these cases may avoid the difficulties of aortic reoperation or AAA repair in the setting of prior endovascular aortic grafting.

Type III and IV thoracoabdominal aortic aneurysm repair: Results of a trifurcated/two-graft technique

Objective: Thoracoabdominal aortic aneurysm (TAA) repair continues to present a surgical challenge because of obligate intraoperative visceral, renal, and spinal cord ischemia. A novel two-graft technique with a trifurcated graft for sequential visceral revascularization followed by a second graft for inline aneurysm reconstruction minimizes this endorgan ischemia. We herein present our updated experience with this approach for repair of type III and type IV TAAs. Methods: Thirty-two patients (mean age, 70 years) underwent nonemergent repair of extent III (12 patients) and IV (20 patients) TAAs between March 1996 and October 2001. Repair was achieved with a trifurcated graft for uninvolved descending thoracic aorta-to-celiac/superior mesenteric/renal artery bypass with an additional tube or bifurcated graft for inline aneurysm reconstruction. Adjunctive cerebrospinal fluid drainage was used in the last six patients. Six patients had a solitary kidney, and six had previous infrarenal abdominal aortic aneurysm repair. Results: Mean visceral ischemia times were as follows: celiac artery, 12 minutes; superior mesenteric artery, 12 minutes; left renal artery, 10 minutes; and right renal artery, 33 minutes. The creatinine level at discharge was not significantly different from the preoperative level (1.7 versus 1.3; P = .10). Two patients (6.3%) had transient renal failure; however, the permanent renal failure rate was zero. No patient with a solitary kidney had renal dysfunction develop. Paraplegia occurred in two patients (6.3%), one of whom had prior abdominal aortic aneurysm repair and neither of whom had cerebrospinal fluid drainage. Prolonged ventilatory support (>2 days) was necessitated in six patients (19%). The perioperative mortality rate was 6.3% (two patients). The mean follow-up period was 22 months, with a life-table survival rate of 76% at 36 months. Maintenance of preoperative functional status was achieved in 92% (23/25 patients) of long-term survivors. Conclusion: Type III and IVTAA repair with a trifurcated graft for sequential visceral revascularization followed by a second graft for inline aneurysm reconstruction provides short visceral, renal, and spinal cord ischemia times and leads to low rates of endorgan ischemic damage and paraplegia. Preoperative functional status is maintained in most survivors. These results compare favorably with other methods of TAA repair, and this technique presents a useful option in thoracoabdominal aortic reconstruction. (J Vasc Surg 2002;36:211-6.)

Screening for Abdominal Aortic Aneurysm During Transthoracic Echocardiography in a Hypertensive Patient Population

This study was undertaken to determine the utility of transthoracic echocardiography as a screening test for occult abdominal aortic aneurysm in hypertensive patients older than 50 years of age. Longitudinal and transverse images of the abdominal aorta were obtained during the subcostal portion of the transthoracic echocardiogram. Abdominal aortic aneurysm was defined as an abdominal aortic dimension (antero-posterior or lateral) G3.0 cm. Exclusion criteria included prior abdominal aortic aneurysm repair, known abdominal aortic aneurysm, or inadequate images of the abdominal aorta (nine patients). Two hundred patients (107 men, 93 women; mean age 71 years, range 51 to 92 years) met the study inclusion criteria. An occult abdominal aortic aneurysm was identified in 13 patients (6.5%). Sixty-nine percent of the abdominal aortic aneurysm patients were men, with a mean age of 73 years and a mean duration of hypertension of 11 years. Seventy-seven percent had a history of tobacco use, and 15% had a positive family history of abdominal aortic aneurysm. All aneurysms were infrarenal in location, with abdominal aortic aneurysm diameter ranging from 3.0 to 5.2 cm (mean 3.9 cm). Laminated thrombus was present in six patients (46%), and in one patient a right common iliac artery aneurysm was also detected. Imaging of the abdominal aorta during transthoracic echocardiography required an average of 6.7 minutes (range 4 to 10 minutes). In conclusion, the abdominal aorta could be accurately imaged in the majority of patients (96%) undergoing transthoracic echocardiography in this study. The incidence of occult abdominal aortic aneurysm in hypertensive patients older than 50 years of age is significant (6.5%). Screening for occult abdominal aortic aneurysm in this patient population should be a routine extension of the transthoracic echocardiogram. (J Am Soc Echocardiogr 1997;10:722-7.)