Outcomes after stent graft therapy for dissection-related aneurysmal degeneration in the descending thoracic aorta.

OBJECTIVE: Stent graft therapy has emerged as an alternative to open surgery in the management of chronic dissection-related aneurysmal degeneration (DRAD) in the descending thoracic aorta (DTA). The incidence of perioperative complications, need for secondary aortic intervention (SAI), and rate of aneurysmal false-lumen thrombosis have not been thoroughly described. METHODS: Perioperative and midterm outcomes in patients who underwent stent graft therapy for chronic DRAD DTA at a single institution between January 2006 and September 2013 were retrospectively analyzed. Preoperative anatomic factors, including the number of visceral and renal side branches off the false lumen, and false lumen volume, were analyzed for their ability to predict treatment failure. Treatment failure was defined as death, need for a SAI, and failure to achieve thrombosis of the DRAD DTA. Treatment success was defined as thrombosis of the false lumen in the area of the DRAD DTA with stability or a decrease in the maximum diameter of the DRAD DTA. RESULTS: During the study period, 47 patients underwent stent graft therapy for chronic DRAD DTA. Patients were a mean age of 58.3 ± 11.7 years, 74.5% (n = 35) were male, and 14.9% (n = 7) had a history of connective tissue disease. The left subclavian artery was covered in 48.9% (n = 23), and revascularization was performed in 87.0% (n = 20). Spinal drains were used in 74.5% (n = 35). Spinal cord ischemia developed in 6.4% (n = 3), which resolved in two and improved in one. No retrograde aortic dissections occurred. The 30-day mortality was 4.3% (n = 2); one death was in a patient with rupture. Mean clinical follow-up was 35.1 ± 20.9 months. The 5-year Kaplan-Meier survival was 89% ± 5%. Treatment failure occurred in 18 patients (38.3%): 9 required SAIs, 6 did not have thrombosis of the false lumen in the area of the DRAD DTA, and 4 died, with 1 patient dying during a SAI. No preoperative anatomic factor predicted treatment failure. The 5-year freedom from treatment failure was 54% ± 9%. Including the nine patients who underwent SAI, treatment success was achieved in 85.2% of patients. CONCLUSIONS: In this single-center experience of stent graft therapy for chronic DRAD DTA, treatment success was achieved in 85% of patients after a SAI rate of 20%. No preoperative anatomic factor predicted treatment failure, which occurred in almost 40% of the patients. Identifying predictors of treatment failure may improve future outcomes.

Regulation and actions of activin A and follistatin in myocardial ischaemia-reperfusion injury.

Activin A, a member of the transforming growth factor-ß superfamily, is stimulated early in inflammation via the Toll-like receptor (TLR) 4 signalling pathway, which is also activated in myocardial ischaemia-reperfusion. Neutralising activin A by treatment with the activin-binding protein, follistatin, reduces inflammation and mortality in several disease models. This study assesses the regulation of activin A and follistatin in a murine myocardial ischaemia-reperfusion model and determines whether exogenous follistatin treatment is protective against injury. Myocardial activin A and follistatin protein levels were elevated following 30 min of ischaemia and 2h of reperfusion in wild-type mice. Activin A, but not follistatin, gene expression was also up-regulated. Serum activin A did not change significantly, but serum follistatin decreased. These responses to ischaemia-reperfusion were absent in TLR4(-/-) mice. Pre-treatment with follistatin significantly reduced ischaemia-reperfusion induced myocardial infarction. In mouse neonatal cardiomyocyte cultures, activin A exacerbated, while follistatin reduced, cellular injury after 3h of hypoxia and 2h of re-oxygenation. Neither activin A nor follistatin affected hypoxia-reoxygenation induced reactive oxygen species production by these cells. However, activin A reduced cardiomyocyte mitochondrial membrane potential, and follistatin treatment ameliorated the effect of hypoxia-reoxygenation on cardiomyocyte mitochondrial membrane potential. Taken together, these data indicate that myocardial ischaemia-reperfusion, through activation of TLR4 signalling, stimulates local production of activin A, which damages cardiomyocytes independently of increased reactive oxygen species. Blocking activin action by exogenous follistatin reduces this damage.

Role of cytokine hemoadsorption in cardiopulmonary bypass-induced ventricular dysfunction in a porcine model.

Little is known about the effect of cardiopulmonary bypass alone on cardiac function; in an attempt to illuminate this relationship and test a possible mechanism, we used Cytosorb, a device capable of removing virtually all types of circulating cytokines to test the hypothesis that hemoadsorption of cytokines during bypass attenuates bypass-induced acute organ dysfunction. Twelve Yorkshire pigs (50-65 kg) were instrumented with a left ventricular conductance catheter. Baseline mechanics and cytokine expression (tumor necrosis factor [TNF], interleukin-6 [IL-6], and interleukin-10) were measured before and hourly after 1 hour of normothermic cardiopulmonary bypass. Animals underwent bypass without (cardiopulmonary bypass [CPB], n = 6) or with (CPB+HA, n = 6) the CytosorbTM device. Data were compared with "historical" controls (n = 6) that were similarly instrumented but underwent observation instead of bypass. Five hours after separation from bypass (or observation), animals were euthanized. Myocardial water content was determined postmortem. Neither TNF nor IL-6 was significantly elevated in either experimental group versus controls at any time point. Preload recruitable stroke work and dP/dtmax were significantly depressed immediately after separation from bypass in both CPB+HA and CPB and remained depressed for the duration of the experiment. Although Tau remained unchanged, dP/dTmin was significantly diminished in both bypass groups at all time points after separation from bypass. Cytokine hemoadsorption had no effect on any measurable index of function. Differences in postmortem data were not evident between groups. One hour of normothermic CPB results in a significant and sustained decline in left ventricular function that appears unrelated to changes in cytokine expression. Because we did not appreciate a significant change in cytokine concentrations postbypass, the capacity of cytokine hemoadsorption to attenuate CPB-induced ventricular dysfunction could not be assessed.

Is Porcine Small Intestinal Submucosal Extracellular Matrix (ECM) a Suitable Material for Right Ventricular Outflow Tract Reconstruction in Association With Pulmonary Valve Replacement?

Pulmonary valve replacement (PVR) with right ventricular outflow tract (RVOT) reconstruction is a common congenital cardiac operation. Porcine submucosal intestinal-derived extracellular matrix (ECM) patches have been used for RVOT reconstruction. We present 2 adult patients with Tetralogy of Fallot who underwent PVR with RVOT reconstruction utilizing ECM. Both cases required reoperation due to patch dehiscence causing a large paravalvular leak. One patient also had a pseudoaneurysm associated with ECM dehiscence. There may be a propensity for ECM dehiscence in this application and, based on these cases, we recommend avoidance of ECM in RVOT reconstruction with PVR. PVR patients repaired with ECM should be monitored for this complication.

Protease-activated receptor 2 deficiency reduces cardiac ischemia/reperfusion injury.

OBJECTIVE: To investigate the effect of protease-activated receptor (PAR) 2 deficiency on ischemia/reperfusion (I/R) injury-induced infarct size, inflammation, heart remodeling, and cardiac function. METHODS AND RESULTS: PAR-2 signaling enhances inflammation in different diseases. The effect of PAR-2 deficiency in cardiac I/R injury is unknown. PAR-2(-/-) mice and wild-type littermates were subjected to 30 minutes of ischemia and up to 4 weeks of reperfusion. Infarct size, oxidative/nitrative stress, phosphorylation of mitogen-activated protein kinases, and inflammatory gene expression were assessed 2 hours after reperfusion. Changes in heart size and function were measured by echocardiography up to 4 weeks after reperfusion. Infarct size was significantly reduced in hearts of PAR-2(-/-) mice compared with wild-type littermates. In addition, oxidative/nitrative stress, phosphorylation of mitogen-activated protein kinase, and expression of proinflammatory genes were significantly attenuated in injured hearts of PAR-2(-/-) mice. Finally, PAR-2(-/-) mice were protected from postinfarction remodeling and showed less impairment in heart function compared with wild-type littermates up to 4 weeks after I/R injury. CONCLUSIONS: PAR-2 deficiency reduces myocardial infarction and heart remodeling after I/R injury.

Consensus statement: minimal criteria for reporting the systemic inflammatory response to cardiopulmonary bypass.

The lack of established cause and effect between putative mediators of inflammation and adverse clinical outcomes has been responsible for many failed anti-inflammatory interventions in cardiopulmonary bypass (CPB). Candidate interventions that impress in preclinical trials by suppressing a given inflammation marker might fail at the clinical trial stage because the marker of interest is not linked causally to an adverse outcome. Alternatively, there exist examples in which pharmaceutical agents or other interventions improve clinical outcomes but for which we are uncertain of any antiinflammatory mechanism. The Outcomes consensus panel made 3 recommendations in 2009 for the conduct of clinical trials focused on the systemic inflammatory response. This panel was tasked with updating, as well as simplifying, a previous consensus statement. The present recommendations for investigators are the following: (1) Measure at least 1 inflammation marker, defined in broad terms; (2) measure at least 1clinical end point, drawn from a list of practical yet clinically meaningful end points suggested by the consensus panel; and(3) report a core set of CPB and perfusion criteria that maybe linked to outcomes. Our collective belief is that adhering to these simple consensus recommendations will help define the influence of CPB practice on the systemic inflammatory response, advance our understanding of causal inflammatory mechanisms, and standardize the reporting of research findings in the peer-reviewed literature.

The Surgeon as Educator.

Surgical education in 2019 faces may challenges to maintain the high standards of excellence achieved in prior generations of learners and trainers in cardiothoracic surgery. This compendium hopes to review the current and future strategies in surgical education. The topics include the adult learner, assessing competence, providing formative feedback, developing strategies to minimize implicit bias, optimizing education in the operating room, effective classroom teaching, the future of e-learning, the alternative curriculum, teaching mentorship and coaching, deliberate practice and simulation, faculty development, the potential roles of virtual and augmented reality, and the impact artificial intelligence might have on surgical education in the future.

Flipping the Classroom: How to Optimize Learning in the Didactic Setting.

Classic classroom education emphasizes the teacher imparting knowledge, experience, or wisdom (pedagogy). Adult educational theory indicates learning is optimized in an experiential setting, where the learner prepares, the session is case based, and the responsibility of the educator is to teach what the learner does not know. This is referred to as "flipping the classroom." Flipping the classroom is not simple, as the historical educational culture often changes; and, at least early in the transition process, different expectations, preparation, or training are essential for both the learner and educator for this approach to be effective.

Improved Outcomes of Heart Transplantation in Adults With Congenital Heart Disease Receiving Regionalized Care.

BACKGROUND: The number of adult congenital heart disease (CHD) patients undergoing heart transplantation is increasing rapidly. CHD patients have higher surgical risk at transplantation. High-volume adult CHD transplant centers may have better transplant outcomes. OBJECTIVES: This study aimed to evaluate the effect of center CHD transplant volume and expertise on transplant outcomes in CHD patients. METHODS: The authors studied heart transplantations in CHD patients age ≥18 years using the United Network of Organ Sharing (UNOS) database for the primary outcomes of waitlist mortality and post-transplant outcomes at 30 days and 1 year. Transplant centers were assessed by status as the highest CHD transplant volume center in a UNOS region versus all others, presence of Adult Congenital Heart Association accreditation, and adult versus pediatric hospital designation. RESULTS: Between January of 2000 and June of 2018, 1,746 adult CHD patients were listed for transplant; 1,006 (57.6%) of these underwent heart transplantation. After adjusting for age, sex, listing status, and inotrope requirement, waitlist mortality risk was lower at Adult Congenital Heart Association accredited centers (hazard ratio: 0.730; p = 0.020). Post-transplant 30-day mortality was lower at the highest volume CHD transplant center in each UNOS region (hazard ratio: 0.706; p = 0.014). CONCLUSIONS: Designated expertise in CHD care is associated with improved waitlist outcomes for CHD patients listed for transplantation. Post-transplant survival was improved at the highest volume regional center. These findings suggest a possible advantage of regionalization of CHD transplantation.

Protease-activated receptor-1 contributes to cardiac remodeling and hypertrophy.

BACKGROUND: Protease-activated receptor-1 (PAR-1) is the high-affinity receptor for the coagulation protease thrombin. It is expressed by a variety of cell types in the heart, including cardiomyocytes and cardiac fibroblasts. We have shown that tissue factor (TF) and thrombin contribute to infarct size after cardiac ischemia-reperfusion (I/R) injury. Moreover, in vitro studies have shown that PAR-1 signaling induces hypertrophy of cardiomyocytes and proliferation of cardiac fibroblasts. The purpose of the present study was to investigate the role of PAR-1 in infarction, cardiac remodeling, and hypertrophy after I/R injury. In addition, we analyzed the effect of overexpression of PAR-1 on cardiomyocytes. METHODS AND RESULTS: We found that PAR-1 deficiency reduced dilation of the left ventricle and reduced impairment of left ventricular function 2 weeks after I/R injury. Activation of ERK1/2 was increased in injured PAR-1(-/-) mice compared with wild-type mice; however, PAR-1 deficiency did not affect infarct size. Cardiomyocyte-specific overexpression of PAR-1 in mice induced eccentric hypertrophy (increased left ventricular dimension and normal left ventricular wall thickness) and dilated cardiomyopathy. Deletion of the TF gene in cardiomyocytes reduced the eccentric hypertrophy in mice overexpressing PAR-1. CONCLUSIONS: Our results demonstrate that PAR-1 contributes to cardiac remodeling and hypertrophy. Moreover, overexpression of PAR-1 on cardiomyocytes induced eccentric hypertrophy. Inhibition of PAR-1 after myocardial infarction may represent a novel therapy to reduce hypertrophy and heart failure in humans.

Characteristics of extracoronary vascular disease in heart transplant recipient.

BACKGROUND: Heart transplant candidates carry many of risk factors for vascular disease, and in addition, recipients continue to accumulate them following heart transplantation (HTx). However, very limited information is available on this entity. This study was designed to address characteristics of extracoronary vascular disease in heart transplant recipients. METHODS: This is a nonconcurrent cohort study of 402 patients who received HTx at the University of Washington between 1985 and 2004. Pretransplant arterial evaluation included carotid, lower extremity, and renal artery duplex studies. CT angiogram was obtained when indicated. Patients with severe arterial disease were excluded from the transplant list. Posttransplant vascular evaluation was done with the patient's history and physical examination. RESULTS: Median follow-up was 5.5 years. Seventy vascular diseases were detected in 49 patients (12% of study population). Patients with pretransplant vascular disease, compared to those without, were older at the HTx, carried the diagnosis of ischemic cardiomyopathy more commonly, and had more comorbidities including history of smoking, alcohol drinking, chronic obstructive pulmonary disease, and prior heart operations. The prevalence of vascular disease was 6% prior to HTx and it cumulatively increased up to 17% at 17 years after HTx. Nineteen percent of these diseases were the result of arterial traumas mostly caused by medical interventions. Fourteen patients developed abdominal aortic aneurysm (AAA) with two deaths. CONCLUSIONS: It is important for care providers to be aware of the high probability of vascular disease, to be familiar with vascular disease, and to provide appropriate prophylactic and therapeutic measures when evaluating this patient population.

Consensus statement: Defining minimal criteria for reporting the systemic inflammatory response to cardiopulmonary bypass.

The causal factors of the systemic inflammatory response to cardiopulmonary bypass (CPB) were correctly identified in the early 1990 s: "... activation of complement, coagulation, fibrinolytic, and kallikrein cascades, activation of neutrophils with degranulation and protease enzyme release, oxygen radical production, and the synthesis of various cytokines from mononuclear cells" [Butler 1993]. Why therefore have clinical advances to curb the systemic inflammatory response proven such a disappointment? Part of the problem is that cardiac surgery has never taken intellectual ownership of this issue, borrowing its diagnosis from critical care medicine and failing to define the minimal criteria that should be measured when reporting on the systemic inflammatory response. An evidence based review of the current literature by many of the coauthors on this paper found that the majority of studies on the systemic inflammatory response did not measure a single one of the causal factors listed above - thus hindering our ability to identify mechanisms of causation and identify drug targets [Landis 2008]. A panel of experts convened at the Outcomes XII meeting, Barbados 2008, drafted the present consensus document in order to provide a framework to guide future studies and interdictions of the systemic inflammatory response. Herein, we have recommended: 1) mandatory reporting of minimal CPB and perfusion criteria that may affect outcomes, 2) reporting of a minimal set of causal inflammatory markers linked to adverse sequelae, and 3) reporting of at least one clinical end-point of organ injury, from a list of endpoints and markers of organ injury that balance practicality with clinical meaningfulness. It is our collective belief that this document will serve as a foundation for furthering our understanding of the influence of CPB practice with the systemic inflammatory response by standardizing the reporting of research findings in the peer-reviewed literature.

Development of a 3-D printing-based cardiac surgical simulation curriculum to teach septal myectomy.

OBJECTIVE: We sought to develop a 3-D printing-based simulator for teaching extended septal myectomy to trainees in cardiothoracic surgery (clinical postgraduate year 4-7). This procedure is difficult to teach because of generally unfamiliar and highly variable anatomy, limited visibility for the assistant, and significant potential complications. METHODS: A curriculum using multimedia didactics and 3-D print-based patient-specific surgical simulation was implemented. Six identical 3-D prints were constructed for each of 5 consecutive patients. Preoperative septal myectomy was performed on each printed heart by an attending surgeon and 5 residents. Model myectomy specimen volumes were measured according to liquid displacement. All print resections were videotaped and blindly evaluated by 3 attending surgeons. Pre- and post-test evaluations, and a survey tool were also used to evaluate the curriculum. RESULTS: Baseline myectomy resection volumes differed significantly (attending 15 cm3 vs resident 3.1 cm3; P < .05). Residents resected increasingly larger volumes of tissue over the course of the study. Initial resection volume (compared with faculty) increased by 0.82 cm3 per resection (95% confidence interval, 0.37-1.3 cm3; P < .0001). Total resection volume (compared with faculty) increased by 3.6 cm3 per resection (95% confidence interval, 2.4-4.9 cm3; P < .0001). The residents' survey assessment of the simulator was favorable. CONCLUSIONS: A patient-specific 3-D printing-based simulation module shows promise as a tool to augment and improve cardiothoracic resident training in septal myectomy. The residents were quickly able to perform resections on par with the attending. Residents rated the simulator favorably. Each resident benefited by experiencing the variable anatomy of 5 separate patient-specific models.

Long-Term Right Ventricular Assist Device Therapy in an Adult with Pulmonary Atresia/Intact Ventricular Septum.

Durable ventricular assist device (VAD) support is uncommonly employed in adult congenital heart disease and often involves supporting a systemic right ventricle (RV). Ventricular assist device support of a subpulmonic RV is even more unusual.

Does cramming work? Impact of National Web-Based Thoracic Surgery Curriculum login frequency on thoracic surgery in-training exam performance.

OBJECTIVE: Web-based curricula provide login data that can be advantageously used to characterize and analyze study habits. We sought to compare thoracic surgical trainee In-Training Examination percentiles with regard to their study habits (ie, cramming), as characterized by curriculum login frequency to the national Web-based Thoracic Surgery Curriculum. Furthermore, we then aimed to characterize the curriculum login frequency of trainees as stratified by their performance on the In-Training Examination and their improvement on the In-Training Examination over subsequent years. METHODS: We performed a retrospective review of trainees who accessed the curriculum before the 2014 In-Training Examination, with curriculum login data collected from site analytics. Scores were compared between trainees who crammed (≥30% increase in logins in the month before the In-Training Examination) and those who did not. Trainees were stratified on the basis of 2014 In-Training Examination percentile and improvement in percentile from 2013 to 2014 into high, medium, and low scorers and improvers. RESULTS: Of 256 trainees who took the 2014 In-Training Examination, 63 (25%) met criteria as crammers. Crammers increased total study sessions immediately before the In-Training Examination (P < .001), but without impact on 2014 In-Training Examination percentile (P = .995) or year-to-year improvement (P = .234). Stratification by In-Training Examination percentile demonstrated that highest scoring trainees used the curriculum more frequently in the final month than medium-range scorers (P = .039). When stratified by extent of year-to-year improvement, those who improved the most accessed the curriculum significantly more often in the last month compared with baseline (P = .040). Moreover, those with greatest improvement logged in more in the final month than those with least improvement (P = .006). CONCLUSIONS: Increasing the frequency of study periods on the national Web-based thoracic surgery curriculum before the In-Training Examination may have a unique benefit to trainees who initially score low to allow them to significantly improve their subsequent year In-Training Examination performance.

Inhibition of Toll-like receptor 4 with eritoran attenuates myocardial ischemia-reperfusion injury.

BACKGROUND: We previously reported that the functional mutation of Toll-like receptor 4 (TLR4) in C3H/HeJ mice subjected to myocardial ischemia-reperfusion (MI/R) injury resulted in an attenuation of myocardial infarction size. To investigate the ligand-activating TLR4 during MI/R injury, we evaluated the effect of eritoran, a specific TLR4 antagonist, on MI/R injury, with the goal of defining better therapeutic options for MI/R injury. METHODS AND RESULTS: C57BL/6 mice received eritoran (5 mg/kg) intravenously 10 minutes before 30 minutes of in situ of transient occlusion of the left anterior descending artery, followed by 120 minutes of reperfusion. Infarct size was measured using triphenyltetrazoliumchloride staining. A c-Jun NH(2)-terminal kinase (JNK) activation was determined by Western blotting, nuclear factor (NF)-kappaB activity was detected by gel-shift assay, and cytokine expression was measured by ribonuclease protection assay. Mice treated with eritoran developed significantly smaller infarcts when compared with mice treated with vehicle alone (21.0+/-6.4% versus 30.9+/-13.9%; P=0.041). Eritoran pretreatment resulted in a reduction in JNK phosphorylation (eritoran versus vehicle: 3.98+/-0.81 versus 7.01+/-2.21-fold increase; P=0.020), less nuclear NF-kappaB translocation (2.70+/-0.35 versus 7.75+/-0.60-fold increase; P=0.00007), and a decrease in cytokine expression (P<0.05). CONCLUSIONS: We conclude that inhibition of TLR4 with eritoran in an in situ murine model significantly reduces MI/R injury and markers of an inflammatory response.

Is pre-transplant vascular disease a risk factor for mortality and morbidity after heart transplantation?

BACKGROUND: Severe vascular disease is a relative contraindication to heart transplantation (HTx). We addressed the effect of vascular disease on HTx outcomes. METHODS: This is a nonconcurrent cohort study of 402 patients who received HTx at our institution between 1985 and 2004. Pre-transplant vascular evaluation included carotid, lower extremity, and renal artery duplex studies, and CT angiogram when indicated. Patients with severe and nontreatable vascular disease were excluded. Patients were divided into Group 1: those with pre-transplant vasculopathy, and Group 2: those without pre-transplant vasculopathy. Group 1 had 24 patients with 25 vascular lesions: 1 aortic dissection, 2 abdominal aortic aneurysm (AAA)'s, 5 carotid artery stenoses, 1 renal artery stenosis, and 16 peripheral vascular lesions. Interventions were performed to 15 lesions prior to HTx and to 2 lesions after HTx. RESULTS: Median follow-up was 5.5 years. Group 1 had higher incidence of ischemic cardiomyopathy (p<0.001), hypertension (p=0.028), chronic obstructive pulmonary disease (COPD) (p=0.004), and smoking history (p<0.001). There were no differences in sex, hyperlipidemia, diabetes, stroke, or renal dysfunction. Multivariate analysis revealed odds of post-transplant death in Group 1 was 1.4 (95% CI: 0.48-4.1, p=0.54) times greater than that in Group 2. Cox proportional hazards model for survival showed a 50% increase in the hazard of death in patients with pre-transplant vasculopathy, but without statistical significance. Group 1 had higher incidence of post-transplant stroke (p=0.001) but no difference in allograft coronary atherosclerosis. CONCLUSIONS: Pre-transplant vascular disease seems to have negative effect on outcomes after HTx. Larger scale study is needed for further evaluation.

Early outcomes in patients undergoing transcatheter versus surgical pulmonary valve replacement.

OBJECTIVES: To identify predictors of morbidity and mortality in patients undergoing either transcatheter pulmonary valve replacement (TPVR) or surgical pulmonary valve replacement (SPVR) in an effort to quantify any early benefit of TPVR over SPVR. METHODS: Using a risk-adjusted propensity score model, we compare early major morbidity and mortality between patients undergoing SPVR and TPVR at our institution between January 2006 and January 2014. RESULTS: 145 patients in the SPVR cohort and 78 patients in the TPVR cohort were included. Primary pulmonary regurgitation was more common in the SPVR group (76.6% vs 23.1%, p<0.001) and primary pulmonary stenosis was more common in the TPVR group (9.7% vs 44.9%, p< 0.001). In unadjusted analysis, major morbidity and mortality occurred in 11.7% of SPVR patients versus 3.8% of TPVR patients (p=0.04). However, following risk adjustment and inclusion of a propensity score, no significant difference was seen between the two modalities. A larger right ventricular end-diastolic dimension (RVEDVI) was the only preoperative variable associated with the primary end point (OR 1.013/10 mL/m2 increase, p=0.03). Hospital length of stay was significantly longer in patients undergoing SPVR (6.9±1.0 days SPVR vs 1.2±0.3 days TPVR, p<0.0001), with similar hospital costs between groups (mean: US$44 660±5071 SPVR vs US$48 355±1000 TPVR, p=0.7). CONCLUSIONS: Following risk adjustment, no significant differences were observed between SPVR and TPVR strategies. TPVR was associated with a shorter hospitalisation; however, total hospitalisation costs were similar between groups.

Scan, plan, print, practice, perform: Development and use of a patient-specific 3-dimensional printed model in adult cardiac surgery.

OBJECTIVE: Static 3-dimensional printing is used for operative planning in cases that involve difficult anatomy. An interactive 3D print allowing deliberate surgical practice would represent an advance. METHODS: Two patients with hypertrophic cardiomyopathy had 3-dimensional prints constructed preoperatively. Stereolithography files were generated by segmentation of chest computed tomographic scans. Prints were made with hydrogel material, yielding tissue-like models that can be surgically manipulated. Septal myectomy of the print was performed preoperatively in the simulation laboratory. Volumetric measures of print and patient resected specimens were compared. An assessment tool was developed and used to rate the utility of this process. Clinical and echocardiographic data were reviewed. RESULTS: There was congruence between volumes of print and patient resection specimens (patient 1, 3.5 cm3 and 3.0 cm3, respectively; patient 2, 4.0 cm3 and 4.0 cm3, respectively). The prints were rated useful (3.5 and 3.6 on a 5-point Likert scale) for preoperative visualization, planning, and practice. Intraoperative echocardiographic assessment showed adequate relief of left ventricular outflow tract obstruction (patient 1, 80 mm Hg to 18 mm Hg; patient 2, 96 mm Hg to 9 mm Hg). Both patients reported symptomatic improvement (New York Heart Association functional class III to class I). CONCLUSIONS: Three-dimensional printing of interactive hypertrophic cardiomyopathy heart models allows for patient-specific preoperative simulation. Resection volume relationships were congruous on both specimens and suggest evidence of construct validity. This model also holds educational promise for simulation of a low-volume, high-risk operation that is traditionally difficult to teach.