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Cadaveric tissue-perfusion models are well established in the fields of structural heart and peripheral vascular disease; however, less consideration has been given toward coronary artery disease despite comparable prevalence and morbidity. Two tissue-perfusion models were developed to address this need. The first, an intact heart model, allows simulation of percutaneous coronary interventional procedures. The second focuses upon isolated arteries, allowing quantification of simulated procedures. Both models were applied for clinical training and for investigations into medical device behavior. The manner of preparation facilitates access to clinically relevant disease, thus providing a platform to further research on coronary artery disease.

Objectives: Prosthetic leaflet thrombosis is a growing concern in transcatheter aortic valve replacement (TAVR). Given the uncertainty of best practices for antiplatelet and anticoagulation therapies in the post-TAVR period, additional evidence regarding the impact of anticoagulation on prosthetic valve function after TAVR is needed., Methods: Patients undergoing native-valve TAVR at a single academic institution between 2012 and 2015 were analyzed based on any anticoagulant use at hospital discharge post TAVR. Changes in prosthetic valve peak velocity and mean gradient were assessed based on transthoracic echocardiograms performed immediately following valve implant and at 4-week follow-up. Multivariate regression analyses were performed to explore the impact of anticoagulation status on early TAVR valve performance., Results: For 403 patients, there were no available data to analyze. Of those, 29.6% were discharged on anticoagulation. Following TAVR, the average mean prosthetic valve gradient was 11.8 ± 5.6 mm Hg and peak velocity was 2.33 ± 0.52 m/s. There were no significant differences between anticoagulated and non-anticoagulated groups in the mean or peak gradients or velocity immediately following implant or at 4 weeks, which remained true following multivariate adjustment (P=.80 for delta mean gradient; P=.91 for delta peak velocity)., Conclusion: Our data suggest that the absence of anticoagulation is not associated with short-term degradation in TAVR performance and do not support the routine use of anticoagulation following native-valve TAVR.

The inability to reposition or retrieve balloon-expandable transcatheter aortic valves once they have been deployed requires implantation of the valve in the descending aorta or open surgical procedures to extract the valve. We describe the challenging transfemoral delivery of an Edwards Lifesciences Sapien valve wherein we had difficulty crossing the aortic valve and the guidewire position was compromised. We performed a transapical puncture to snare the guidewire and create a left ventricular to femoral wire rail, allowing us to deliver the transfemoral transcatheter valve, salvaging a situation where we would have been required to implant the valve in the descending aorta. We believe this is the first time this technique has been reported and represents an important method to facilitate delivery of transcatheter valves where guidewire support is insufficient or lost.

Published mortality models for percutaneous coronary intervention (PCI), including the Clinical Outcomes Assessment Program (COAP) model, have not considered the effect of out-ofhospital cardiac arrest. The primary objective of this study was to determine if the inclusion of out-of-hospital cardiac arrest altered the COAP mortality model for PCI. The COAP PCI database contains extensive demographic, clinical, procedural and outcome information, including out-of-hospital cardiac arrest, which was added to the data collection form in 2006. This study included 15,586 consecutive PCIs performed in 31 Washington State hospitals in 2006. Using development and test sets, the existing COAP PCI logistic regression mortality model was examined to assess the effect of out-of-hospital arrest on in-hospital mortality. Overall, 2% of individuals undergoing PCI had cardiac arrest prior to hospital arrival. Among 8 hospitals with PCI volumes < 120 cases per year, 4 had cardiac arrest volumes that exceeded 10% of total volume, whereas none of the centers with > 120 cases per year did. In-hospital mortality was 19% in the arrest group and was 1.0% in remaining procedures (p < 0.0001). In the new multivariate model, out-of-hospital cardiac arrest was highly associated with mortality (odds ratio = 5.50; 95% confidence interval [CI] = 3.28-9.25). When evaluated in the test set, the new model had excellent discrimination (c-statistic = 0.89; 95% CI = 0.85-0.93). Out-of-hospital cardiac arrest is an important determinant of risk-adjusted in-hospital mortality for PCI, particularly for hospitals with low volumes and relatively high volumes of cardiac arrest cases.

Restenosis remains a vexing problem in patients undergoing percutaneous coronary interventions (PCI). This phenomenon is related to a combination of events, including elastic recoil, negative remodeling and fibrointimal tissue proliferation. While stenting (bare metal and drug eluting) has made a dramatic impact in preventing recoil and remodeling, restenosis still occurs. Once restenosis occurs, it presents its own set of challenges due to the excess tissue proliferation. Major predicators of restenosis include diabetes, small stent diameter and long stented lesions. Vascular brachytherapy is the only proven therapy associated with a significant reduction in angiographic restenosis and the need for target vessel revascularization for the treatment of in-stent restenosis.