Out with the old: Single center experience with transvenous extraction of leads older than 15 years.

BACKGROUND: Lead dwell time is the single strongest predictor of failure and complications in transvenous lead extraction. OBJECTIVES: To report the success rate and complications of transvenous lead extractions with implant dwell time of at least 15 years. METHODS: Procedural and patient data were prospectively collected into a database. The excimer laser was the primary method for lead extraction with the use of mechanical rotational sheaths and femoral snares at operator discretion. RESULTS: A total of 442 patients between 2011 and 2020 underwent lead extraction (705 leads) primarily for infection or device failure at our high-volume center. Forty-one patients with 71 leads > 15 years old were included in this cohort. Mean patient age was 53.5 ± 18.5 years, 67.5% were male. Mean lead dwell time was 19.6 ± 4.4 years. Thirty-six of 41 (88%) patients had successful extraction of all leads compared to 96% in the remaining 401 patients, p value.004. Of the five patients without fully successful extractions two of these patients had abandoned leads (three total) that were clinically significant. There were two (4.9%) major complications in the very old lead group and six (1.5%) in the other group. In the very old lead group, one patient experienced right atrial appendage perforation requiring surgical repair and recovered well. One patient experienced new complete heart block requiring 2 min of CPR but did well thereafter. There was no procedure-related mortality. CONCLUSIONS: Despite challenges posed by older leads, very old leads can be safely and effectively extracted with low complication rates.

Hospital Care for Adult Patients with Congenital Heart Diseases.

OBJECTIVE: The ideal type of hospital to care for adult congenital heart disease (ACHD) patients is not well known. Hospital competitiveness, clinical volume and market structure can influence clinical outcomes. We sought to understand how hospital competitiveness affects clinical outcomes in ACHD patients in the era prior to the Adult Congenital Heart Association accreditation program. METHODS: Patient discharges with ACHD diagnosis codes were filtered between 2006-2011 from an all-payer inpatient healthcare database. Hospital-level data was linked to market structure patient flow. A common measure of market concentration used to determine market competitiveness-the Herfindahl-Hirschman Index (HHI)-was stratified into: more competitive (HHI ≤25th percentile), moderately competitive (HHI 25th to <75th percentile), and less competitive (HHI ≥75th percentile) hospital. Any complication, home discharge and mortality were analyzed with clustered mixed effects logistic regression. The combined impact of HHI and any complication on mortality by interaction was assessed. RESULTS: A total of 67,434 patient discharges were isolated. More competitive hospitals discharged the least number of patients (N = 15,270, 22.6%) versus moderately competitive (N = 36,244, 53.7%) and less competitive (N = 15,920, 23.6%) hospitals. The adjusted odds of any complication or home discharge were not associated with hospital competitiveness strata. Compared to more competitive hospitals, mortality at moderately competitive hospitals (Adjusted Odds Ratio (AOR) 0.79, 95% CI: 0.66-0.94) and less competitive hospitals (AOR 0.79, 95% CI: 0.63-0.98) were lower (p = 0.025). Age, race, elective admission, transfer status, and payer mix were all significantly associated with adjusted odds of any complication, home discharge and mortality (p ≤ 0.05). Having any complication independently increased the adjusted odds of mortality more than 6-fold (p < 0.001), and this trend was independent of HHI strata. Failure to rescue an ACHD patient from mortality after having any complication is highest at less competitive hospitals. Sensitivity analysis which excluded the transfer status variable, showed that any complication (p = 0.047) and mortality (p = 0.01) were independently associated with HHI strata. CONCLUSIONS: Whether lower competition allow hospitals to focus more on quality of care is unknown. Hospital competitiveness and outcome seem to have an inverse trend relationship among ACHD patients. Since medical care is frequently provided away from the home area, hospital selection is an important issue for ACHD patients. Further research is needed to determine why competitiveness is linked to surgical outcomes in this population.

Expanding the Team: Optimizing the Multidisciplinary Management of Drug Use-Associated Infective Endocarditis.

Amidst a substance use epidemic, hospitalizations and valve surgeries related to drug use-associated infective endocarditis (DU-IE) rose substantially in the last decade. Rates of reoperation and mortality remain high, yet in many hospitals patients are not offered valve surgery or evidence-based addiction treatment. A multidisciplinary team approach can improve outcomes in patients with infective endocarditis; however, the breadth of expertise that should be incorporated into this team is inadequately conceptualized. It is our opinion that incorporating addiction medicine services into the team may improve outcomes in DU-IE. Here, we describe our experience incorporating addiction medicine services into the multidisciplinary management of DU-IE and share implications for other hospitals and health systems looking to improve care for people with DU-IE.

Racial Disparity: The Adult Congenital Heart Disease Surgery Perspective.

The influence of race and ethnicity on clinical outcomes in medicine are widely acknowledged. However, the effect of race on adult congenital heart disease (ACHD) surgery is not known. We sought to evaluate the possible association between race and outcomes following ACHD operations. Discharge records for patients who underwent ACHD surgery between 2005 and 2014, were isolated from an all-payer voluntary database in the United States. Hierarchical case-mix regression models and sensitivity analyses examined any complication, in-hospital mortality, and discharge disposition (home/non-home) by race (white-WP, black-BP, non-white non-black-NWNB). Of the 174,370 patients (WP: 80.8%, BP: 5.8%, NWNB: 13.4%), black patients were youngest to undergo surgery (WP: 57.9 ± 15.8 years, BP: 50.2 ± 16.1 years, NWNB: 51.6 ± 16.9 years, P < 0.0001), the most likely to have a comorbidity (WP: 70.3%, BP: 74.3%, NWNB: 68.6%, P < 0.0001), and most likely to have had a post-operative cardiac complication (WP: 9.4%, BP: 15.3%, NWNB: 10.9%, P < 0.0001). BP had similar odds of having any complication (AOR = 0.99, 95%CI = 0.94-1.04), while NWNB had significantly decreased odds of a major complication (AOR = 0.90, 95%CI = 0.87-0.93). BP had equivalent in-hospital mortality compared to WP (AOR = 1.03, 95%CI = 0.91-1.18), while NWNB had significantly increased odds of in-hospital mortality (AOR = 1.29, 95%CI = 1.18-1.41). Among survivors, BP were less likely to discharge home (AOR = 0.88, 95%CI = 0.82-0.94), and NWNB were more likely to discharge home than WP (AOR = 1.26, 95%CI = 1.19-1.33). Race and clinical outcomes are associated among patients undergoing surgery for ACHD. Understanding why and how these factors are impactful will help improve care for this complex population.

Transvenous management of cardiac implantable electronic device late lead perforation.

INTRODUCTION: Late lead perforation (LLP), defined as perforation ≥30 days from cardiac implantable electronic device implant, is a rare diagnosis and little data exist regarding management practices and outcomes. The purpose of this study was to evaluate the occurrence, safety, and efficacy of transvenous management of clinically significant LLP. METHODS: The electronic medical records of a single-center tertiary hospital were reviewed for all patients who were referred for LLP or its sequelae. RESULTS: Eleven consecutive patients were identified from October 2011 to December 2018 with clinically significant LLP. Patients most often presented with pericardial symptoms with the exception of one asymptomatic patient. The median time from lead implant to intervention for LLP was 246 days. Nine patients were managed with an initial transvenous approach, with one requiring sternotomy (lead 6.3 years old). Two patients had a surgical approach, one performed at an outside hospital with subsequent death and another had a mini-thoracotomy, but the lead was removed percutaneously with no surgical repair. In this small cohort, there was no association between the lead extending beyond the parietal pericardium and surgical repair (P = .99). CONCLUSION: Our single-center experience suggests that LLP can be initially managed with a cautious transvenous approach in most patients, but intraprocedural ultrasound for pericardial monitoring and a rescue plan with immediate surgical back up is mandatory.

Near-complete aortic mechanical valve dehiscence due to endocarditis reinfection.

Prosthetic valve infective endocarditis (IE) is one of the most serious postimplantation complications. Prosthetic aortic valve IE constitutes 1%-6% of all prosthetic valve IE cases. We present a dramatic echocardiographic case of prosthetic aortic valve IE leading to near-complete valve dehiscence. Echocardiographic evidence of prosthetic aortic valve rocking motion is indicative of significant dehiscence. Aside from IE, other causes and risk factors for prosthetic aortic valve dehiscence include inflammatory and autoimmune vasculitides, concomitant ascending aorta aneurysm, and aortic root calcification.

B2 cells suppress experimental abdominal aortic aneurysms.

Recent reports of rupture in patients with abdominal aortic aneurysm (AAA) receiving B-cell depletion therapy highlight the importance of understanding the role of B cells (B1 and B2 subsets) in the development of AAA. We hypothesized that B2 cells aggravate experimental aneurysm formation. The IHC staining revealed infiltration of B cells in the aorta of wild-type (C57BL/6) mice at day 7 after elastase perfusion and persisted through day 21. Quantification of immune cell types using flow cytometry at day 14 showed significantly greater infiltration of mononuclear cells, including B cells (B2: 93% of total B cells) and T cells in elastase-perfused aortas compared with saline-perfused or normal aortas. muMT (mature B-cell deficient) mice were prone to AAA formation similar to wild-type mice in two different experimental AAA models. Contradicting our hypothesis, adoptive transfer of B2 cells suppressed AAA formation (102.0% ± 7.3% versus 75.2% ± 5.5%; P < 0.05) with concomitant increase in the splenic regulatory T cell (0.24% ± 0.03% versus 0.92% ± 0.23%; P < 0.05) and decrease in aortic infiltration of mononuclear cells. Our data suggest that B2 cells constitute the largest population of B cells in experimental AAA. Furthermore, B2 cells, in the absence of other B-cell subsets, increase splenic regulatory T-cell population and suppress AAA formation.

5-Lipoxygenase pathway in experimental abdominal aortic aneurysms.

OBJECTIVE: The impact of leukotriene production by the 5-lipoxygenase (5-LO) pathway in the pathophysiology of abdominal aortic aneurysms (AAAs) has been debated. Moreover, a clear mechanism through which 5-LO influences AAA remains unclear. APPROACH AND RESULTS: Aneurysm formation was attenuated in 5-LO(-/-) mice, and in lethally irradiated wild-type mice reconstituted with 5-LO(-/-) bone marrow in an elastase perfusion model. Pharmacological inhibition of 5-LO-attenuated aneurysm formation in both aortic elastase perfused wild-type and angiotensin II-treated LDLr(-/-) (low-density lipoprotein receptor) mice, with resultant preservation of elastin and fewer 5-LO and MMP9 (matrix metalloproteinase)-producing cells. Separately, analysis of wild-type mice 7 days after elastase perfusion showed that 5-LO inhibition was associated with reduced polymorphonuclear leukocyte infiltration to the aortic wall. Importantly, 5-LO inhibition initiated 3 days after elastase perfusion in wild-type mice arrested progression of small AAA. Human AAA and control aorta corroborated these elastin and 5-LO expression patterns. CONCLUSIONS: Inhibition of 5-LO by pharmacological or genetic approaches attenuates aneurysm formation and prevents fragmentation of the medial layer in 2 unique AAA models. Administration of 5-LO inhibitor in small AAA slows progression of AAA. Targeted interruption of the 5-LO pathway is a potential treatment strategy in AAA.

Adenosine 2A receptor modulates inflammation and phenotype in experimental abdominal aortic aneurysms.

Activation of the adenosine 2A receptor (A2AR) reduces inflammation in models of acute injury but contribution in development of chronic abdominal aortic aneurysms (AAAs) is unknown. Elastase perfusion to induce AAA formation in A2AR-knockout (A2ARKO) and C57BL6/J wild-type (WT) mice resulted in nearly 100% larger aneurysms in A2ARKO compared to WT at d 14 (P<0.05), with evidence of greater elastin fragmentation, more immune cell infiltration, and increased matrix metallatoproteinase (MMP) 9 expression (P<0.05). Separately, exogenous A2AR antagonism in elastase-perfused WT mice also resulted in larger aneurysms (P<0.05), while A2AR agonism limited aortic dilatation (P<0.05). Activated Thy-1.2(+) T lymphocytes from WT mice treated in vitro with A2AR antagonist increased cytokine production, and treatment with A2AR agonist decreased cytokine production (P<0.05 for all). Primary activated CD4(+) T lymphocytes from A2ARKO mice exhibited greater chemotaxis (P<0.05). A2AR antagonist increased chemotaxis of activated CD4(+) cells from WT mice in vitro, and A2AR agonist reduced this effect (P<0.05). A2AR activation attenuates AAA formation partly by inhibiting immune cell recruitment and reducing elastin fragmentation. These findings support augmenting A2AR signaling as a putative target for limiting aneurysm formation.

Midterm Outcomes: A Comprehensive Approach to Surgery for Hypertrophic Obstructive Cardiomyopathy.

BACKGROUND: Left ventricular outflow tract (LVOT) obstruction in obstructive hypertrophic cardiomyopathy (HCM) is caused by a constellation of abnormalities. This study reviewed outcomes of a comprehensive approach to correct these abnormalities during surgery. METHODS: This was a single-institution study of patients with HCM who underwent septal myectomy from 2016 to 2023. Their New York Heart Association functional classification and most recent echocardiogram that estimated LVOT gradient and mitral valve function were tracked. RESULTS: The study included 103 patients with a mean age of 54 years (interquartile range, 40-67 years) and common comorbidities: hypertension (50%) and atrial fibrillation (25%). On average, the preprocedure resting echocardiogram showed an LVOT gradient of 36.4 mm Hg and moderate or severe mitral regurgitation in 50.5% of patients. All patients underwent septal myectomy, and associated abnormalities contributing to LVOT obstruction were addressed. Elongation of the anterior leaflet of the mitral valve was typically treated with papillary muscle realignment (72%). Aberrant papillary muscle heads and elongated secondary chordae tendineae contributing to systolic anterior motion were resected (66%). Myocardial bands, including apicoseptal bands contributing to LVOT obstruction, were resected (68%). With an average follow-up of 4 years, 91% of patients were considered to be in New York Heart Association functional class I or II. Long-term echocardiographic follow-up showed a mean peak LVOT gradient of 11 mm Hg (interquartile range, 4-13 mm Hg). Only 1 patient had more than mild mitral regurgitation. CONCLUSIONS: A comprehensive surgical approach to HCM that addresses the entire constellation of abnormalities associated with HCM, including mitral valve anterior leaflet elongation, aberrant or displaced mitral valve subvalvular apparatus, and myocardial bands, leads to outstanding midterm outcomes.

Primary payer status is associated with mortality and resource utilization for coronary artery bypass grafting.

BACKGROUND: Medicaid and uninsured populations are a significant focus of current healthcare reform. We hypothesized that outcomes after coronary artery bypass grafting (CABG) in the United States is dependent on primary payer status. METHODS AND RESULTS: From 2003 to 2007, 1,250,619 isolated CABG operations were evaluated using the Nationwide Inpatient Sample (NIS) database. Patients were stratified by primary payer status: Medicare, Medicaid, uninsured, and private insurance. Hierarchical multiple regression models were applied to assess the effect of primary payer status on postoperative outcomes. Unadjusted mortality for Medicare (3.3%), Medicaid (2.4%), and uninsured (1.9%) patients were higher compared with private insurance patients (1.1%, P<0.001). Unadjusted length of stay was longest for Medicaid patients (10.9 ± 0.04 days) and shortest for private insurance patients (8.0 ± 0.01 days, P<0.001). Medicaid patients accrued the highest unadjusted total costs ($113 380 ± 386, P<0.001). Importantly, after controlling for patient risk factors, income, hospital features, and operative volume, Medicaid (odds ratio, 1.82; P<0.001) and uninsured (odds ratio, 1.62; P<0.001) payer status independently conferred the highest adjusted odds of in-hospital mortality. In addition, Medicaid payer status was associated with the longest adjusted length of stay and highest adjusted total costs (P<0.001). CONCLUSIONS: Medicaid and uninsured payer status confers increased risk adjusted in-hospital mortality for patients undergoing coronary artery bypass grafting operations. Medicaid was further associated with the greatest adjusted length of stay and total costs despite risk factors. Possible explanations include delays in access to care or disparate differences in health maintenance.

Experimental abdominal aortic aneurysm formation is mediated by IL-17 and attenuated by mesenchymal stem cell treatment.

BACKGROUND: Abdominal aortic aneurysm (AAA) formation is characterized by inflammation, smooth muscle activation and matrix degradation. This study tests the hypothesis that CD4+ T-cell-produced IL-17 modulates inflammation and smooth muscle cell activation, leading to the pathogenesis of AAA and that human mesenchymal stem cell (MSC) treatment can attenuate IL-17 production and AAA formation. METHODS AND RESULTS: Human aortic tissue demonstrated a significant increase in IL-17 and IL-23 expression in AAA patients compared with control subjects as analyzed by RT-PCR and ELISA. AAA formation was assessed in C57BL/6 (wild-type; WT), IL-23(-/-) or IL-17(-/-) mice using an elastase-perfusion model. Heat-inactivated elastase was used as control. On days 3, 7, and 14 after perfusion, abdominal aorta diameter was measured by video micrometry, and aortic tissue was analyzed for cytokines, cell counts, and IL-17-producing CD4+ T cells. Aortic diameter and cytokine production (MCP-1, RANTES, KC, TNF-α, MIP-1α, and IFN-γ) was significantly attenuated in elastase-perfused IL-17(-/-) and IL-23(-/-) mice compared with WT mice on day 14. Cellular infiltration (especially IL-17-producing CD4+ T cells) was significantly attenuated in elastase-perfused IL-17(-/-) mice compared with WT mice on day 14. Primary aortic smooth muscle cells were significantly activated by elastase or IL-17 treatment. Furthermore, MSC treatment significantly attenuated AAA formation and IL-17 production in elastase-perfused WT mice. CONCLUSIONS: These results demonstrate that CD4+ T-cell-produced IL-17 plays a critical role in promoting inflammation during AAA formation and that immunomodulation of IL-17 by MSCs can offer protection against AAA formation.

Percutaneous transjugular implantation of MELODY® valve into tricuspid bioprosthesis.

We present the technique of transcatheter balloon expandable (MELODY®) valve-in-valve deployment in a frail octogenarian with a failed previous tricuspid bioprosthesis. In patients who are not candidates for conventional surgery, transcatheter approach provides an alternative that warrants careful consideration.

Substance Use Disorders Are Prevalent in Adults With Congenital Heart Disease and Are Associated With Increased Healthcare Use.

Adults with congenital heart disease (CHD) represent a heterogeneous group with significant long-term health risks. Previous studies have demonstrated a high prevalence of psychiatric disorders among adults with CHD; however, little is known about the frequency of co-morbid substance use disorders (SUDs) in patients with CHD. The Oregon All Payer All Claims (APAC) database for the years 2014 to 2017 was queried for adults aged 18 to 65 years with International Classification of Diseases, Ninth or Tenth Revision codes consistent with CHD. Alcohol and substance use were identified by International Classification of Diseases codes for use or dependence and classified in mutually exclusive categories of none, alcohol only, and other drugs (with or without alcohol). Descriptive statistics were used to characterize prevalence and chi-square tests were used to test for associations between variables. A total of 12,366 adults with CHD were identified. The prevalence of substance use was 15.7%. The prevalence of isolated alcohol use was 3.9%. A total of 19% of patients used tobacco. Insurance type, presence of a concurrent mental health diagnosis, and age were associated with substance use, whereas CHD complexity was not. Cardiovascular co-morbidities were more common in patients with reported substance use. Inpatient and emergency care use were higher in those with SUD. In conclusion, this study of substance and alcohol use among adults with CHD demonstrates high rates of co-morbid SUD, particularly among patients with mental health disorders and Medicaid insurance, associated with increased healthcare utilization. We identify a population in need of targeted interventions to improve long-term health.

Physiologic risk stratification is important to long-term mortality, complications, and readmission in thoracic endovascular aortic repair.

Use of the American Society of Anesthesiologists (ASA) physical status classification is important for periprocedural risk stratification. However, the collective effect after adjustment for the Society for Vascular Surgery (SVS) medical comorbidity grading system on long-term all-cause mortality, complications, and discharge disposition is unknown. We examined these associations in patients after thoracic endograft placement. Data from three thoracic endovascular aortic repair (TEVAR) trials through 5 years of follow-up were included. Patients with acute complicated type B dissection (n = 50), traumatic transection (n = 101), or descending thoracic aneurysm (n = 66) were analyzed. The patients were stratified into three groups according to the ASA class: I-II, III, and IV. Multivariable proportional hazards regression models were used to examine the effect of ASA class on 5-year mortality, complications, and rehospitalizations after adjustment for SVS risk score and potential confounders. The largest proportion of patients treated by TEVAR across the ASA groups (n = 217) was ASA IV (n = 97; 44.7%; P < .001), followed by ASA III (n = 83; 38.2%) and ASA I-II (n = 37; 17.1%). Among the ASA groups, the ASA I-II patients were, on average, 6 years younger than those with ASA III and 3 years older than those with ASA IV (ASA I-II: age, 54.3 ± 22.0 years; ASA III: age, 60.0 ± 19.7 years; ASA IV: age, 51.0 ± 18.4 years; P = .009). Multivariable adjusted 5-year outcome models showed that ASA class IV, independent of the SVS score, conferred an increased risk of mortality (hazard ratio [HR], 3.83; 95% confidence interval [CI], 1.19-12.25; P = .0239) and complications (HR, 4.53; 95% CI, 1.69-12.13; P = .0027) but not rehospitalization (HR, 1.84; 95% CI, 0.93-3.68; P = .0817) compared with ASA class I-II. Procedural ASA class is associated with long-term outcomes among post-TEVAR patients, independent of the SVS score. The ASA class and SVS score remain important to patient counseling and postoperative outcomes beyond the index operation.

Transcatheter arterial revascularization outcomes at vascular and general surgery teaching hospitals and nonteaching hospitals are comparable.

BACKGROUND: Outcomes following transcatheter interventions at vascular and general surgery teaching hospitals (STH) are unknown. We examine whether surgery training programs influence clinically relevant outcomes after commonly performed endovascular procedures. METHODS: Using an all-payer inpatient care database from 2008, we selected adults who underwent either endovascular carotid stenting, endografting of descending thoracic aortic aneurysm, endovascular abdominal aortic aneurysm repair, or peripheral arterial revascularization. Patients were stratified by procedures completed at Surgery Teaching (Participate in Accreditation Council for Graduate Medical Education [ACGME]-accredited vascular and general surgery programs), STH, or nonteaching hospitals (NTH). Hierarchical regression models assessed adverse outcomes and in-hospital mortality among groups. RESULTS: Of the 175,698 records, 44% of the patients were treated at STH, while 56% underwent procedures at NTH. The adjusted odds ratio of any complication or mortality at STH and NTH were similar. Transfers, weekend admissions, and nonelective cases were higher at STH (P < .001, respectively). Paradoxically, STH treated fewer patients with more than three comorbidities compared with NTH (STH: 47% vs NTH: 53%; P < .001). Surgical teaching status did not lower the adjusted odds of mortality for any procedure. Moreover, the occurrence of any complication (adjusted odds ratios, 0.9; 95% confidence interval, .82-1.14; P = .69) and mortality (adjusted odds ratios, 0.9; 95% confidence interval, .74-1.22; P = .67) were equivalent between vascular and general STH. CONCLUSIONS: Following commonly performed transcatheter vascular procedures, and despite more transfers, weekend admissions, and nonelective procedures completed at STH, complications, and mortality were comparable across centers.

Increased JNK in males compared with females in a rodent model of abdominal aortic aneurysm.

BACKGROUND: In humans, there is a 4:1 male:female ratio in the incidence of abdominal aortic aneurysms (AAAs). c-Jun-N-terminal kinase (JNK) is an important upstream regulator of several enzymes involved in AAA formation, including the matrix metalloproteinases (MMPs). The purpose of this study was to determine if there is a gender difference between males and females in JNK during AAA formation. MATERIALS AND METHODS: Male and female C57/B6 mice underwent aortic perfusion with elastase or heat inactivated elastase with aortas harvested at d 3 and 14 for phenotype determination, RT-PCR, Western blot, and zymography. Additionally, in vitro experiments using siRNA were conducted to define JNK regulation of matrix metalloproteinases (MMPs). A t-test was used to compare between groups. RESULTS: Males formed larger AAAs at d 14 compared with females (P < 0.001), with significantly higher levels of JNK1 protein, proMMP9, proMMP2, and active MMP2. At d 3, males had more JNK1 mRNA, protein, and MMP activity. Knockdown of JNK 1 or 2 in vitro decreased MMP activity, while knockdown of JNK 1 and 2 together blocked all MMP activity. CONCLUSION: Alterations in JNK between genders is partially responsible for the differential rates of experimental AAA formation, likely through differential regulation of MMPs.

Differential gender- and species-specific formation of aneurysms using a novel method of inducing abdominal aortic aneurysms.

BACKGROUND: The objective of this study was to test a novel model of inducing abdominal aortic aneurysms (AAAs) in different mouse strains and genders. MATERIALS AND METHODS: Male and female C57BL/6 and B6129 mice (n = 5 per group) underwent periaortic dissection and porcine pancreatic elastase (30 µL) or inactivated elastase application (5 min) to the aorta. Aortic measurements were taken on days 0 and 14. Aortic samples were analyzed for histology and zymography for matrix metalloproteinase (MMP) activity. Comparison statistics were performed using unpaired t-test. RESULTS: AAA phenotype (50% aortic increase) occurred in external elastase-treated males (100%) and females (90%). No control animals developed AAAs. The aortic diameter was larger in C57BL/6 and B6129 elastase-treated versus control males (P = 0.0028 and P < 0.0001, respectively) and females (P < 0.0001 and P = 0.0458, respectively). Histology verified phenotype via disrupted internal elastic laminae. Macrophage counts in elastase-treated animals were >6-fold higher than in controls (all groups significant). MMP9 activity was greater in elastase-treated males and females in C57BL/6 (P = 0.0031, P = 0.0004) and B6129 (P = 0.025, P = 0.2) mice; MMP2 activity was greater in C57BL/6 versus B6129 male elastase-treated mice. CONCLUSIONS: This rodent model produced AAAs in both genders and strains of mice. This model is simple, has little variability, and occurs in the infrarenal aorta, substantiating the external elastase model for future studies.

Hybrid repair of aortic arch aneurysm.

Hybrid repair of thoracic aortic aneurysm has been used with increasing frequency over the past decade, as indications for endovascular therapy have continued to expand. Hybrid techniques may avoid and limit the morbidity and mortality associated with sternotomy or thoracotomy, mechanical circulatory support, and hypothermic arrest. We present the case of a patient with extensive aortic aneurysmal disease initially needing open ascending aortic and subsequent thoracoabdominal repair. However, owing to continued enlargement of the aortic arch, hybrid extrathoracic, extra-anatomic complete aortic arch debranching and transcatheter endografting was ultimately pursued with favorable midterm results.

Lung hernia following robotic-assisted mitral valve repair.

Lung hernia is an uncommon diagnosis characterized by lung tissue protruding through a chest wall defect. It may occur spontaneously, as a congenital defect, as a result of trauma, or as a postsurgical complication. We describe the occurrence of lung hernia and subsequent successful herniorraphy in two patients following robotic-assisted mitral valve repair.