Coil embolization of persistent false lumen after type A dissection repair.

A 44-year-old man with a type A dissection repair 5 years earlier presented with progressive enlargement of the residual arch and thoracic aorta. Flow into the false lumen from the distal aortic suture line was evident on contrast-enhanced computed tomography. Through a redo hemisternotomy, the false lumen was accessed directly. An Amplatzer plug was deployed within the narrowed neck of the false lumen proximal to the enlarged false lumen within descending aorta. Interlocking coils were deployed proximal to the Amplatzer plug, resulting in thrombosis of the false lumen.

Role of statin therapy and angiotensin blockade in patients with asymptomatic moderate carotid artery stenosis.

BACKGROUND: The purpose of this study was to evaluate the 10-year outcome of patients presenting with asymptomatic moderate carotid artery stenosis, and to determine which factors correlate with progression of disease to stroke or revascularization. METHODS: A retrospective review of all new patients presenting with asymptomatic moderate carotid artery stenosis from July 1998 to December 2001 was undertaken. Patients were consecutively identified and included by using duplex ultrasonography to identify moderate carotid disease. Variables were recorded for all patient encounters through June 2010. The primary end point was occurrence of ipsilateral cerebrovascular stroke or revascularization event (SORE). Statin therapy and angiotensin blockade (STAB) were categorized as follows: STAB(0)-medical treatment with neither statin therapy nor angiotensin blockade, STAB(1)-treatment with only one of the two, STAB(2)-treatment with both. An amortized cost model analyzed the cost of SORE-free survival. RESULTS: Over a 42-month period, 468 carotids in 366 patients with an average age of 69.0 ± 8.7 years were evaluated. Over a mean follow-up of 6.6 ± 2.7 years, SORE occurred in 150 (32.1%) carotid arteries. Hyperlipidemia was predictive of SORE (hazard ratio [HR]: 1.543, 95% confidence interval [CI]: 1.053-2.262, P = 0.03). Medical therapies protective against SORE were beta-blockade (HR: 0.612, 95% CI: 0.435-0.861, P < 0.05), STAB(1) (HR: 0.487, 95% CI: 0.336-0.706, P < 0.01), and STAB(2) (HR: 0.149, 95% CI: 0.089-0.248, P < 0.01). At 10 years, SORE-free survival in STAB(2) was 82.7% ± 4.6%, STAB(1) was 56.3% ± 5.0%, and STAB(0) was 29.3% ± 5.4% (P < 0.01). The cost per SORE-free year in STAB(2) was $1,695.40 ± $275.60, STAB(1) was $3,916.80 ± $605.44, and STAB(0) was $4,126.40 ± $427.23 (P < 0.01). CONCLUSION: These data demonstrate the clinical and financial advantage of using both statin therapy and angiotensin pathway blockage in patients with asymptomatic moderate carotid artery stenosis.

Impact of operative indication and surgical complexity on outcomes after thoracic endovascular aortic repair at National Surgical Quality Improvement Program Centers.

INTRODUCTION: Thoracic endovascular aortic repair (TEVAR) devices are increasingly being utilized to treat aortic pathologies outside of the original Food & Drug Administration (FDA) approval for nonruptured descending thoracic aorta aneurysms (DTAs). The objective of this study was to evaluate the outcomes of patients undergoing TEVAR, elucidating the role of surgical and pathologic variables on morbidity and mortality. METHODS: National Surgical Quality Improvement Program (NSQIP) data were reviewed for all patients undergoing endovascular thoracic aorta repair from 2005 to 2007. The patients' operative indication and surgical complexity were used to divide them into study and control populations. Comorbid profiles were assessed utilizing a modified Charlson Comorbidity Index (CCI). Thirty-day occurrences of mortality and serious adverse events (SAEs) were used as study endpoints. Univariate and multivariate models were created using demographic and clinical variables to assess for significant differences in endpoints (P ≤ .05). RESULTS: A total of 440 patients undergoing TEVAR were identified. When evaluating patients based on operative indication, the ruptured population had increased mortality and SAE rates compared to the nonruptured DTA population (22.6% vs 6.2%;P < .01 and 35.5% vs 9.1%;P < .01, respectively). Further analysis by surgical complexity revealed increased mortality and SAE rates when comparing the brachiocephalic aortic debranching population to the noncovered left subclavian artery population (23.1% vs 6.5%; P = .02 and 30.8% vs 9.1%; P < .01, respectively). Multivariate analysis demonstrated that operative indication was not a correlate of mortality or SAEs (odds ratio [OR], 0.95; P = .92 and OR, 1.42; P = .39, respectively); however, brachiocephalic aortic debranching exhibited a deleterious effect on mortality (OR, 8.75; P < .01) and SAE rate (OR, 6.67; P = .01). CONCLUSION: The operative indication for a TEVAR procedure was not found to be a predictor of poor patient outcome. Surgical complexity, specifically the need for brachiocephalic aortic debranching and aortoiliac conduit, was shown to influence the occurrence of SAEs in a multivariate model. Comparative data, such as these, illustrate real-world outcomes of patients undergoing TEVAR outside of the original FDA-approved indications. This information is of paramount importance to various stakeholders, including third-party payers, the device industry, regulatory agencies, surgeons, and their patients.

Examining the myth of the "July Phenomenon" in surgical patients.

BACKGROUND: The objective of this study is to evaluate morbidity and mortality rates in surgical patients at the beginning of the academic year. METHODS: The National Surgical Quality Improvement Program database was utilized to gather data on the 10 most common inpatient operative procedures from 2005-2007. Study end points included mortality, serious adverse events (SAE), and all morbidities. Statistical analysis of outcomes was conducted examining the total population, and then stratified by operation to assess for significant differences in end points (P < .05). RESULTS: A total of 89,473 patients were identified. During the first academic quarter, the mortality rate was no different in the study group than the control group (2.0% vs 2.2%, P = .793). Overall SAE and morbidity rates were similar between populations (11.5% vs 11.4%, P = .697 and 18.3% vs 17.8%, P = .076, respectively). When stratified by operation, "artery bypass graft" (3.7% vs 2.9%, P = .039) and "repair bowel opening" (1.1% vs 0.6%, P = .033) subsets had increases in mortality rate. Multivariate analysis confirmed the deleterious effect of first quarter admission in only the "artery bypass graft" subset (OR = 1.35, CI 1 = .023-1.774). CONCLUSION: By in large, these data refute the "July Phenomenon." Multivariate analysis revealed patient disease to have a greater impact than timing of operation in the "repair bowel opening" subset. The "artery bypass graft" population was affected by timing of operation and the very small effect on mortality (<1%) may reflect new surgery residents being unfamiliar with the management of complex cardiovascular disease.

A contemporary rural trauma center experience in blunt traumatic aortic injury.

INTRODUCTION: Traumatic aortic injury (TAI) is a rare yet highly lethal injury associated with blunt force deceleration injury. The adoption of thoracic endovascular aortic repair (TEVAR) has become a safer option than traditional open repair. The purpose of this study is to review a rural trauma center experience with TAI. METHODS: A retrospective analysis was performed, reviewing all patients who presented with TAI between 2000 and 2009. Clinical, anatomical, and procedural variables of all cases were systematically reviewed. Clinical endpoints included mortality, and aortic-related mortality, and hospital length of stay. The study population was stratified by those that underwent surgical repair (SR) and those managed medically (MM). RESULTS: Fifty-six patients presented with blunt TAI; 35 patients (62.5%) were surgically repaired (22 open, 13 TEVAR), while 21 (37.5%) were MM. The only difference in comorbidities was a higher rate of coronary artery disease in MM. Mean hospital arrival time (SR, 188.6 ± 30.3 minutes, MM, 253 ± 65.3 minutes), aortic injury grade (SR, 2.7 ± 0.1; MM, 2.3 ± 0.2), and injury severity score were not significantly different between the groups. Head Abbreviated Injury Score (AIS) was worse in the MM group, while chest AIS was worse in the SR group (P < .05). There were nine (42.9%) deaths in the MM group, while there were only two (5.7%) in the SR group (P < .001). There was no significant difference in aortic-related mortality. Mean follow-up time was not statistically different. CONCLUSION: These data provide a group of stable patients to examine the management of TAI in the endovascular era. The low aortic-related mortality in the MM group demonstrates that there is time for a thorough evaluation in patients sustaining TAI who arrive without hemodynamic instability.

The impact of socioeconomic factors on outcome and hospital costs associated with femoropopliteal revascularization.

INTRODUCTION: Within the context of healthcare system reform, the cost efficacy of lower extremity revascularization remains a timely topic. The impact of an individual patient's socioeconomic status represents an under-studied aspect of vascular care, especially with respect to longitudinal costs and outcomes. The purpose of this study is to examine the relationship between socioeconomic status and clinical outcomes as well as inpatient hospital costs. METHODS: A retrospective femoropopliteal revascularization database, which included socioeconomic factors (household income, education level, and payor status), in addition to standard demographic, clinical, anatomical, and procedural variables were analyzed over a 3-year period. Patients were stratified by income level (low income [LI] <200% federal poverty level [$42,400 for a household of 4], and higher income [HI] >200% federal poverty level) and revascularization technique (open vs endovascular) and analyzed for the endpoints of primary assisted patency, amortized cost-per-day of patency, and limb salvage. Data were analyzed with univariate and multivariate techniques. RESULTS: A total of 187 cases were identified with complete data for analysis, 146 in the LI and 41 in the HI cohorts. LI patients differed from HI patients by mean age (66.2 +/- 1.0 vs 61.8 +/- 1.5 years, P = .04), high school graduate rate (51.4% vs 85.4%, P < .001), presence of tissue loss (30.1% vs 14.6%, P = .05), female gender (43.7% vs 22.0%, P = .01) and preoperative statin use (45.8% vs 75.6%, P < .001). There were no differences with respect to other comorbidities including smoking status, presence of diabetes, renal insufficiency, anatomic factors or treatment modality (open vs endovascular). Ninety-seven patients underwent endovascular revascularization. The following outcomes were noted in the endovascular subset of LI and HI patients respectively: primary assisted patency (66% vs 71%, P = NS) and 12-month cost-per-day of patency ($166.30 +/- 77.40 vs $22.45 +/- 12.45, P = .05). Ninety-eight patients underwent open revascularization, with the following outcomes in LI and HI patients respectively: primary assisted patency (78% vs 86%, P = NS) and 12-month cost-per-day of patency ($319.43 +/- 225.44 vs $40.47 +/- 4.63, P = .07). Of the 77 patients with critical limb ischemia, 19 underwent eventual amputation. Multivariate analysis demonstrated that income above 100% of the federal poverty line was protective against limb loss (odds ratio 0.06, 95% confidence interval 0.01-0.51, P < .001). CONCLUSION: Income level correlates with advanced presentation, advanced age, and lack of statin use. Although primary assisted patency rate is not affected by income status, an increased cost-per-day of patency and inferior limb salvage is found in lower income patients.

Preoperative statin therapy is associated with improved outcomes and resource utilization in patients undergoing aortic aneurysm repair.

INTRODUCTION: This study hypothesized that preoperative statin therapy would have a protective effect on patients undergoing elective abdominal aortic aneurysm (AAA) repair and that the risk-reduction effect of these agents would result in a reduction in subsequent total hospital costs. METHODS: All patients who underwent an elective endovascular AAA repair (EVAR) or open AAA repair (OAR) between 2004 and 2007 were retrospectively reviewed. Clinical end points included postoperative days, length of hospital stay, postoperative complications (myocardial infarction, stroke, renal failure, hemorrhage, pneumonia, urinary tract infection, wound infection), and 30-day mortality. The financial end point was total hospital cost associated with the procedure. RESULTS: We identified 401 patients, consisting of 173 EVAR patients (43%) and 228 OAR (57%). Despite a higher Society for Vascular Surgery risk score, the EVAR statin cohort had significantly reduced postoperative days (1.9 +/- 0.2 vs 2.3 +/- 0.3, P < .05) and hospital length of stay (2.3 +/- 0.3 vs 2.8 +/- 0.4, P < .05) compared with the nonstatin EVAR cohort. Postoperative complications (4.4% vs 14.7%, P < .05) and the mortality rate (0.0% vs 5.9%, P < .05) were significantly decreased in the OAR statin cohort compared with the nonstatin OAR cohort and trended to be decreased in the EVAR statin group. Statin therapy translated into a lower total cost per patient of $3,205 for EVAR and $3,792 for OAR (P < .05). CONCLUSION: With respect to both clinical outcome measures and subsequent resource utilization, statin therapy is associated with a beneficial effect in patients undergoing elective AAA repair. These data suggest that preoperative statin therapy should be an integral part of the risk optimization for patients undergoing AAA repair.

Evolution of bacterial arteritis into a mycotic aortic aneurysm.

Arteritis and mycotic aneurysms have been well described for more than 100 years. The authors report a case of bacterial arteritis that presented with pneumatosis of the aortic wall and that evolved over 1 week into an infected abdominal aortic aneurysm. This case documents the rapid progression from arteritis to mycotic aneurysm, highlighting the need for close radiologic follow-up and aggressive medical and surgical management.

Endovascular stent exclusion of a hepatic artery pseudoaneurysm.

Presented is a patient with an iatrogenic hepatic artery pseudoaneurysm that was treated by endovascular stent grafting. Endovascular stent grafting of a hepatic artery pseudoaneurysm offers a safe and potentially less morbid alternative to an open repair. The report stresses the necessity of careful preoperative evaluation with angiography to determine the feasibility of the procedure. An aggressive approach to treating hepatic artery pseudoaneurysms is advocated because of the poor correlation between size and their tendency to rupture. With an increasing rate of diagnosis of visceral artery aneurysms in elderly, debilitated patients, endovascular repair is anticipated to have an increasing role and should be considered a first-line therapy in anatomically suitable candidates.

Effects of intratracheal tumor necrosis factor-alpha plasmid vector on lipopolysaccharide lethality and lung injury in mice.

Bacterial lipopolysaccharide (LPS) causes acute lung injury (ALI) and contributes to inflammation in the acute respiratory distress syndrome (ARDS) and sepsis, making mechanisms of resistance to LPS critically important in clinical settings. The authors postulated that intratracheal administration of a plasmid (pcDNA3. 0-rTNFalpha) encoding rat tumor necrosis factor-alpha (TNF-alpha) would increase resistance of mice to LPS-induced ALI or mortality. They investigated the time course and dose-response for development of LPS-induced ALI in C57/BL6 mice and sought possible protective effects of 100 microg pcDNA3.0-rTNFalpha intratracheally 1, 2, or 3 weeks before LPS challenge. Lung myeloperoxidase (MPO) activity and alveolar lavage fluid (BALF) cell counts increased significantly 48 hours after intraperitoneal (IP) LPS challenges. After pcDNA3.0-rTNFalpha pretreatment, mice challenged with LPS had lower lung/body weight ratios than mice treated with pcDNA3.0; however, other indices of lung injury did not differ. Survival of mice challenged with lethal IP LPS 2 weeks after intratracheal pcDNA3.0-rTNFalpha vector improved significantly, compared to mice pretreated with the control vector, pcDNA3.0. However, pcDNA3.0-pretreated mice tolerated LPS challenge less well than saline-pretreated controls. LPS causes neutrophilic lung injury and mortality, but pcDNA3.0-TNFalpha does not prevent ALI due to LPS. Intratracheal pcDNA3.0-rTNFalpha pretreatment significantly improves survival of mice after LPS challenge, compared to those pretreated with pcDNA3.0.

p38mapk and MEK1/2 inhibition contribute to cellular oxidant injury after hypoxia.

Lung epithelial cells produce increased reactive oxygen species (ROS) after hypoxia exposure, and they are more susceptible after hypoxia to injury by agents that generate superoxide [O2-; e.g., 2,3-dimethoxy-1,4-naphthoquinone (DMNQ)]. Cellular GSH and MnSOD both decrease in hypoxic lung epithelial cells, altering the redox state. Because ROS participate in signaling pathways involved in cell death or survival, we tested the hypothesis that mitogen-activated protein kinases (MAPK) were involved in a protective response against cellular injury during reoxygenation. Human lung epithelial A549 cells were incubated in hypoxia (<1% O2 for 24 h) and then reoxygenated by return to air. p38mapk and MKK3 phosphorylation both decreased after hypoxia. During reoxygenation, cells were incubated with DMNQ (0-50 microM), a redox cycling quinone that produces O2-. Hypoxia preexposure significantly increased epithelial cell lysis resulting from DMNQ. Addition of the p38mapk inhibitors SB-202190 or SB-203580 markedly increased cytotoxicity, as did the mitogen/extracellular signal-regulated kinase (MEK) 1/2 inhibitor PD-98059 (all 10 microM), suggesting a protective effect of downstream molecules activated by the kinases. Transfection of A549 cells with a dominant active MKK3 plasmid (MKK3[Glu]) partially inhibited cytolysis resulting from DMNQ, whereas the inactive MKK3 plasmid (MKK3[Ala]) had less evident protective effects. Stress-related signaling pathways in epithelial cells are modulated by hypoxia and confer protection from reoxygenation, since hypoxia and chemical inhibition of p38mapk and MEK1/2 similarly increase cytolysis resulting from O2-.

Mitochondrial complex I, aconitase, and succinate dehydrogenase during hypoxia-reoxygenation: modulation of enzyme activities by MnSOD.

Both NADH dehydrogenase (complex I) and aconitase are inactivated partially in vitro by superoxide (O2-.) and other oxidants that cause loss of iron from enzyme cubane (4Fe-4S) centers. We tested whether hypoxia-reoxygenation (H-R) by itself would decrease lung epithelial cell NADH dehydrogenase, aconitase, and succinate dehydrogenase (SDH) activities and whether transfection with adenoviral vectors expressing MnSOD (Ad.MnSOD) would inhibit oxidative enzyme inactivation and thus confirm a mechanism involving O2-. Human lung carcinoma cells with alveolar epithelial cell characteristics (A549 cells) were exposed to <1% O2-5% CO2 (hypoxia) for 24 h followed by air-5% CO2 for 24 h (reoxygenation). NADH dehydrogenase activity was assayed in submitochondrial particles; aconitase and SDH activities were measured in cell lysates. H-R significantly decreased NADH dehydrogenase, aconitase, and SDH activities. Ad.MnSOD increased mitochondrial MnSOD substantially and prevented the inhibitory effects of H-R on enzyme activities. Addition of alpha-ketoglutarate plus aspartate, but not succinate, to medium prevented cytotoxicity due to 2,3-dimethoxy-1,4-naphthoquinone. After hypoxia, cells displayed significantly increased dihydrorhodamine fluorescence, indicating increased mitochondrial oxidant production. Inhibition of NADH dehydrogenase, aconitase, and SDH activities during reoxygenation are due to excess O2-. produced in mitochondria, because enzyme inactivation can be prevented by overexpression of MnSOD.