Unroofing of an anomalous right coronary artery originating from the left coronary sinus.

Coronary abnormalities, including the anomalous aortic origin of a coronary artery, coronary fistula and myocardial bridge, are among the most common congenital cardiovascular anomalies. A left coronary artery arising from the right cusp is less common than the right coronary artery arising from the left cusp but is more often found in autopsy series of sudden cardiac deaths. A slit-like/fish-mouth-shaped orifice, acute angle take-off, intramural course, interarterial course and hypoplasia of the proximal coronary artery have all been proposed as reasons for symptoms, ischaemia and sudden cardiac death. Surgical intervention is recommended for those patients with signs or symptoms of myocardial ischaemia. Intervention in asymptomatic patients with an interarterial/intramural left coronary artery from the right sinus of Valsalva is recommended due to the higher calculated risk of sudden cardiac death. In asymptomatic patients with an intramural right coronary artery from the left sinus of Valsalva, provocative testing is recommended. The slit-like orifice is more commonly seen in an anomalous right coronary artery arising from the left sinus, and we believe it is the major factor responsible for myocardial ischaemia. Our unroofing technique focuses on: (i) transecting the endothelial tissue flap to create a neo-ostium; (ii) limiting the flap resection to the intramural portion to avoid extra-aortic incision; and (iii) marsupialization of a neo-ostium with interrupted sutures to reapproximate the endothelium and prevent aortic dissection.

Use of thoracic endovascular aortic repair for management of aortobronchial fistula.

We report the case of a 66-year-old man who had been emergently transferred to our institution with hemoptysis and hemodynamic instability. His computed tomography findings were consistent with the presence of an aortobronchial fistula. The patient had undergone open repair of coarctation of aorta via thoracotomy 20 years previously, and he was not deemed a suitable candidate for open repair. He was successfully treated with thoracic endovascular aortic repair with successful exclusion of the fistula. The patient was discharged home, and the subsequent follow-up imaging study at 12 months showed the graft in a stable position without evidence of infection, pseudoaneurysm, or endoleak. This case has demonstrated the successful use of thoracic endovascular aortic repair for urgent management of an aortobronchial fistula.

Direct Comparison of Outcomes After Transcatheter Aortic Valve Replacement in Veterans and Non-Veterans Using the Transcatheter Valve Therapy Registry.

OBJECTIVES: This study aims to compare veterans and non-veterans undergoing transcatheter aortic valve replacement (TAVR) using data from the Society for Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy (STS/ACC TVT) registry. METHODS: Patients undergoing TAVR at George Washington University (GWU) and veterans treated at Washington DC Veterans Affairs Medical Center (VAMC) who underwent TAVR at GWU from 2014-2020 were included. All patients were reported in the TVT registry. Emergency and valve-in-valve TAVR were excluded. Cohorts were divided based on veteran status. Operators were the same for both groups. Outcomes were compared at 30 days and 1 year. The primary outcome was mortality and secondary outcomes were morbidity metrics. RESULTS: A total of 299 patients (91 veterans, 208 non-veterans) were included. Veterans had higher rates of hypertension (87.9% vs 77.9%; P=.04), diabetes (46.7% vs 28.9%; P<.01), and lung disease (2.4% vs 11.0%; P<.001). Outcomes were not significantly different between veterans and non-veterans, including 30-day mortality (0% vs 2.9%, respectively; P=.18), 1-year mortality (9.8% vs 10.7%, respectively; P=.61), stroke incidence (0% vs 2.5%, respectively; P=.73), median intensive care unit stay (24 hours in both groups), and overall hospital stay (2 days in both groups). CONCLUSIONS: The affiliation between a VAMC and an academic medical center allowed for direct comparison between veterans and non-veterans undergoing TAVR by the same operators using the TVT registry. Despite significantly higher rates of comorbidities, veterans had equivalent outcomes compared with non-veterans. This may be in part due to the comprehensive care that veterans receive in the VAMC and this institution's integrated heart center team.

Correction to: Thoracic endovascular repair of a rare case of leaking aortic arch intramural hematoma secondary to Giant cell arteritis.

'In the published article (Salaskar et al. 2019) the statement under the subheading 'Consent for publication' is incorrect.

Thoracic endovascular repair of a rare case of leaking aortic arch intramural hematoma secondary to Giant cell arteritis.

BACKGROUND: Traditionally thoracic aortic aneurysms (TAA) secondary to Giant Cell Arteritis (GCA) were treated with resection and open repair. However no prior studies have reported an aortic intramural hematoma (IMH) as a presentation of GCA or outcome of thoracic endovascular aortic repair (TEVAR) in TAA or IMH secondary to GCA. CASE PRESENTATION: A 59 year old female, nonsmoker, non-hypertensive, non-diabetic with a known history of GCA, temporal arteritis on prednisone presented with shortness of breath & chest pain. Chest CT revealed aortic arch IMH and large left hemothorax. CTA confirmed distal aortic arch focal dilation, a focal intimal irregularity in the distal aortic arch and extensive IMH without any active extravasation or signs of aortitis. Patient underwent an urgent TEVAR without oversizing the aortic landing zones. Post TEVAR aortogram showed exclusion of the site of IMH origin and dilated aortic arch segment by the stent and absence of active extravasation. One month post-TEVAR CTA showed patent stent graft with resolution of IMH and hemothorax. One year after TEVAR, patient remained asymptomatic. CONCLUSION: GCA can present as an IMH secondary to underlying chronic vasculitis. When endovascular repair is considered, great care should be taken not to grossly oversize aortic landing zones.

Hemiarch and Total Arch Surgery in Patients With Previous Repair of Acute Type I Aortic Dissection.

BACKGROUND: We examined our contemporary experience with hemiarch and total arch replacement in patients with previous acute type I aortic dissection. METHODS: Over an 8.5-year period, 137 consecutive patients (median age 58 years, interquartile range, 50 to 67) underwent hemiarch or total transverse aortic arch replacement a median of 7.7 years (range, 67 days to 32 years; interquartile range, 2.8 to 12.3 years) after previous acute type I aortic dissection repair. Interventions involving only the aortic root, aortic valve, descending aorta, or thoracoabdominal aorta were excluded. Multivariate analysis of 20 potential preoperative and intraoperative risk factors was performed to examine early death, neurologic deficit, composite endpoint (operative death, permanent neurologic deficit, or hemodialysis at discharge), and long-term mortality. RESULTS: Total arch replacement was performed in 103 patients (75.2%), hemiarch replacement in 34 (24.8%), and elephant trunk procedures in 77 (56.2%). Thirty-one repairs (22.6%) were emergent or urgent. There were 16 operative deaths (11.7%), 4 permanent strokes (3.6%), and 21 (15.3%) instances of the composite endpoint. In the multivariate analysis, congestive heart failure and cardiopulmonary bypass time independently predicted operative mortality (p = 0.0027, p = 0.018). Emergency operation approached significance for stroke (p = 0.088). Predictors of long-term mortality (during a median follow-up period of 5.1 years, 95% confidence interval: 4.4 to 5.8) were female sex (p = 0.0036), congestive heart failure (p = 0.0045), and circulatory arrest time (p = 0.0013); preoperative pulmonary disease approached significance (p = 0.074). Five-year survival was 73.2%. CONCLUSIONS: In patients with previous acute type I aortic dissection repair, hemiarch and total arch operations have respectable morbidity and survival rates. Congestive heart failure predicts operative death, long-term mortality, and our adverse event endpoint. Cardiopulmonary bypass time predicts operative mortality, and female sex and circulatory arrest time predict long-term mortality.

Cellular and molecular basis of Venous insufficiency.

Chronic venous disease (CVD) has a range of clinical presentations, including tortuous, distended veins in lower extremities, increasing skin pigmentation, and in severe cases ulceration of the affected skin. Venous insufficiency, a precursor to CVD characterized by improper return of blood from the lower extremities to the heart, must be studied in its earliest stages at a time when preventative measures could be applied in man. This underscores the need for basic research into biomarkers and genetic predisposing factors affecting the progression of venous disease. Investigation over the past decade has yielded insight into these specific genetic, cellular and molecular mechanisms underlying the development of venous disease. Among the many advances include the elucidation of an increasing role for matrix metalloproteinases as important mediators of the degenerative process involved with venous insufficiency. This may be preceded by an inflammatory process which further contributes to venular degeneration and endothelial dysfunction seen in advanced presentation of disease. Furthermore, genomic analyses have shed light upon temporal expression patterns of matrix remodeling proteins in diseased tissue samples. In this review we examine some of the current findings surrounding cellular, molecular and genetic advances in delineating the etiology of chronic venous disease.

Matrix metalloproteinase-1-mediated up-regulation of vascular endothelial growth factor-2 in endothelial cells.

Matrix metalloproteinase-1 (MMP-1) is a collagenase that is highly active in extracellular matrix and vascular remodeling, angiogenesis, and tumor progression. Vascular endothelial growth factor receptor-2 (VEGFR2), the main receptor for VEGF-A, is expressed on endothelial cells and promotes cell survival, proliferation, and other functions. Although MMP-1 and VEGFR2 co-exist in many normal and pathophysiological conditions, the effect of MMP-1 on cellular VEGFR2 that can promote the above processes is unknown. In this study we test the hypothesis that stimulation of endothelial cells with MMP-1 increases their levels of VEGFR2. The increased VEGFR2 is then available to bind VEGF-A, resulting in increased response. Indeed we found that endothelial cells incubated with active MMP-1 had higher mRNA and protein levels of VEGFR2. Furthermore, VEGF-A-dependent phosphorylation of intracellular signaling molecules and endothelial proliferation were elevated after MMP-1 treatment. MMP-1 caused activation of the nuclear factor-κB (NF-κB) pathway (p65/RelA) in endothelial cells, and this response was dependent upon activation of protease activated receptor-1 (PAR-1). Chromatin immunoprecipitation was used to confirm NF-κB-mediated active transcription of the VEGFR2 (KDR) gene. Elevation in VEGFR2 after MMP-1 stimulation was inhibited by PAR-1 knockdown and NF-κB specific inhibition. We conclude that MMP-1 promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 and activation of NF-κB. These results suggest a mechanism by which MMP-1 may prime or sensitize endothelial cell functions.

Acute venous occlusion enhances matrix metalloprotease activity: Implications on endothelial dysfunction.

Venous hypertension is associated with microvascular inflammation, restructuring, and apoptosis, but the cellular and molecular mechanisms underlying these events remain uncertain. In the present study, we tested the hypothesis that elevated venous pressure and reduction of shear stress induce elevated enzymatic activity. This activity in turn may affect endothelial surface receptors and promote their dysfunction. Using a rodent model for venous hypertension using acute venular occlusion, microzymographic techniques for enzyme detection, and immunohistochemistry for receptor labeling, we found increased activity of the matrix metalloproteases (MMPs) -1, -8, and -9 and tissue inhibitors of metalloproteases (TIMPs) -1 and -2 in both high- and low-pressure regions. In this short time frame, we also observed that elevated venule pressure led to two different fates for the vascular endothelial growth factor receptor-2 (VEGFR2); in higher-pressure upstream regions, some animals exhibited higher VEGFR2 expression, while others displayed lower levels upstream compared to their downstream counterparts with lower pressure. VEGFR2 expression was, on average, more pronounced upon application of MMP inhibitor, suggesting possible cleavage of the receptor by activated enzymes in this model. We conclude that venous pressure elevation increases enzymatic activity which may contribute to inflammation and endothelial dysfunction associated with this disease by influencing critical surface receptors.