PDA Stent Placement *6: High-Impact Limitations of Angiography to Delineate a Complex PDA.

This is a case of an infant with duct-dependent pulmonary circulation, who required 6 stents delivered over three procedures to fully stent the arterial duct, which originated in a very unusual fashion. The attainable angiographic projections were unable to profile its origin, and only a CT scan was ultimately able to delineate the (stenotic) ductal origin from the aorta.

Single-Stage Surgical Management of Atrioventricular Septal Defects with Coarctation of the Aorta.

Surgical options for coarctation of aorta (CoA) with atrioventricular septal defect (AVSD) include single-stage repair vs. staged approach with neonatal CoA repair and delayed AVSD repair. The durability of left atrioventricular valve (LAVV) function after neonatal repair is questioned, and the optimal approach remains controversial. Eighteen CoA-AVSD patients who underwent single-stage repair 2005-2015 by a single surgeon were retrospectively analyzed. Fifteen patients had complete and three had partial AVSD. Birth weight was 3.19 kg (2.17-4.08). Age at surgery was 16 days (6-127). One- and ten-year survival were 80% and 69%. Freedom from reintervention was 60% and 40% at one and ten-year respectively. Reinterventions included relief of left ventricular outflow tract obstruction (LVOTO) (n = 4), repair of cleft LAVV (n = 3), and LAVV and aortic valve replacement (n = 1). Freedom from LAVV reintervention was 85.6% and 66% at 1 and 10 years respectively. There were four deaths: two post-operative and two following hospital discharge. Mortality was due to sepsis in three patients, and heart failure related to LVOTO and LAVV insufficiency in one. At 68-month (0.6-144) follow-up the majority had mild or less LAVV regurgitation, and all had normal LV dimension and systolic function. There was no recurrent arch obstruction. Single-stage surgical repair of CoA-AVSD is feasible and reasonable. Survival and freedom from reintervention in our cohort approximate those outcomes of two-stage repair with durable left AV valve function and no recurrent arch obstruction. These patients are frequently syndromic and demonstrate mortality risk from non-cardiac causes. Consideration of a single-staged approach is warranted for appropriate patients with CoA-AVSD.

A comprehensive strategy in donor acceptance: Impact on pediatric waitlist and heart transplant outcomes.

Significant inter- and intra-center practice variability is present in pediatric donor heart acceptability. This may contribute to variation in the donor refusal rate and may impact waitlist time, morbidity, mortality, and transplant rates. In order to reduce practice variability, our center developed and implemented a comprehensive strategy regarding donor acceptance in September 2017. The aim of this study was to assess the impact of this strategy on waitlist time and outcomes as well as early post-transplant outcomes. We performed a single-center, retrospective analysis of all pediatric (<18 years) patients listed for single-organ heart transplant at our center from September 2015 to September 2018. Patients were divided into those listed before (Group 1) and after implementation of the comprehensive strategy (Group 2). The primary end-point was waitlist time. Secondary end-points included waitlist removal due to death or clinical deterioration, donor refusals per listed patient, early post-transplant outcomes (graft failure, mechanical ventilation time, inotropic support, length of hospital stay) and 1-year post-transplant survival. Of 78 listed patients, 54 were transplanted (29 in Group 1), 9 were removed due to death or clinical deterioration (7 in Group 1) and 15 were removed due to clinical improvement (12 in Group 1). The waitlist time was significantly shorter in Group 2 (17 days, IQR 7-53) vs Group 1 (90 days, IQR 14-162); P = .006. The number of donor refusals was lower in Group 2 (1, IQR 0-2.2) vs Group 1 (4, IQR 2-19); P < .001. The percentage of refused donors with normal function (Left ventricular ejection fraction > 50%) was lower in Group 2 vs Group 1 (53% vs 84%; P < .001). Difference in removal from the waitlist for death or deterioration in Group 2 vs Group 1 (n = 2, 7% vs n = 7, 20%, P = .18) did not reach statistical significance. There was no difference in post-transplant outcomes between groups. The waitlist time and donor refusals significantly decreased after implementation of a comprehensive donor acceptance strategy without impacting transplant outcomes. This analysis supports the need for a comprehensive approach to donor organ acceptance within a pediatric transplant center.

Mitral Valve Surgery in the First Year of Life.

Data are limited on outcomes associated with mitral valve surgery in infants. Prior studies report high mortality and increased risk for late cardiac failure particularly for those with mitral stenosis. We sought to evaluate outcomes in patients with mitral stenosis (MS) or regurgitation (MR) who had mitral valvuloplasty or replacement in the first year of life. A retrospective analysis of all patients in a single institution who underwent mitral valvuloplasty or replacement in their first year of life from 2004 to 2016 (n = 25), excluding patients with single ventricle pathology or those undergoing surgery for atrioventricular canal defect, was carried out. Median age and weight at surgery were 76.5 days (range 2-329) and 4.5 kg (range 3.0-10.1), respectively. The primary mitral pathology was MR in 16 and MS in 9 patients. Median follow-up among living patients was 4 years (range 106 days-12.3 years). Overall survival was 96% at 30 days and 87.8% at 1, 5, and 10 years. There were three early deaths (12%), all within 6 weeks of surgery. There were no late deaths. Three patients required valve replacement, 1 of which had a primary mitral valve replacement and died within 30 days of surgery. Re-intervention-free survival (surgical and catheter based) was 83.8%, 73.3%, and 48.9% at 1, 5, and 10 years per Kaplan-Meier estimates. There was no difference in re-intervention-free survival between patients with MR versus MS. No risk factors for death or re-intervention were identified. Mitral valvuloplasty and replacement can be performed in infants under 1 year of age with acceptable survival and need for re-intervention.

Feasibility of real-time cine cardiac magnetic resonance imaging to predict the presence of significant retrosternal adhesions prior to redo-sternotomy.

BACKGROUND: Injury to vital structures posterior to the sternum is a complication associated with redo sternotomy in congenital cardiac surgery. The goal of our study was a novel evaluation of real-time cine cardiovascular magnetic resonance (CMR) to predict the presence of significant retrosternal adhesions of cardiac and vascular structures prior to redo sternotomy in patients with congenital heart disease. METHODS: Twenty-three patients who had prior congenital heart surgery via median sternotomy had comprehensive CMR studies prior to redo sternotomy. The real time cine (RTC) sequence that was used is an ungated balanced steady-state free precession (bSSFP) sequence using SENSitivity Encoding for acceleration with real-time reconstruction. Spontaneously breathing patients were instructed to take deep breaths during the acquisition whilst increased tidal volumes were delivered to mechanically ventilated patients. All patients underwent redo cardiac surgery subsequently and the presence and severity of retrosternal adhesions were noted at the time of the redo sternotomies. RESULTS: Median age at the time of CMR and operation were 5.5 years (range, 0.2-18.4y) and 6.1 years (range, 0.3-18.8y) respectively. There were 15 males and 8 females in the study group. Preoperative retrosternal adhesions were identified on RTC in 13 patients and confirmed in 11 (85%) at the time of surgery. In only 2 patients, no adhesions were identified on CMR but were found to have significant retrosternal adhesions at surgery; false positive rate 15% (CI 0.4-29.6%), false negative rate 20% (CI 3.7-36.4%). The total classification error of the real time cine sequence was 17% (CI 1.7-32.4%) with an overall accuracy of 83% (CI 67.7-98.4%). Standard breath-hold cine images correlated poorly with surgical findings and did not increase the diagnostic yield. CONCLUSIONS: RTC imaging can predict the presence of significant retrosternal adhesions and thus help in risk assessment prior to redo sternotomy. These findings complement the surgical planning and potentially reduce surgical complications .

Mesenchymal cell replacement corrects thymic hypoplasia in murine models of 22q11.2 deletion syndrome.

22q11.2 deletion syndrome (22q11.2DS) is the most common human chromosomal microdeletion, causing developmentally linked congenital malformations, thymic hypoplasia, hypoparathyroidism, and/or cardiac defects. Thymic hypoplasia leads to T cell lymphopenia, which most often results in mild SCID. Despite decades of research, the molecular underpinnings leading to thymic hypoplasia in 22q11.2DS remain unknown. Comparison of embryonic thymuses from mouse models of 22q11.2DS (Tbx1neo2/neo2) revealed proportions of mesenchymal, epithelial, and hematopoietic cell types similar to those of control thymuses. Yet, the small thymuses were growth restricted in fetal organ cultures. Replacement of Tbx1neo2/neo2 thymic mesenchymal cells with normal ones restored tissue growth. Comparative single-cell RNA-Seq of embryonic thymuses uncovered 17 distinct cell subsets, with transcriptome differences predominant in the 5 mesenchymal subsets from the Tbx1neo2/neo2 cell line. The transcripts affected included those for extracellular matrix proteins, consistent with the increased collagen deposition we observed in the small thymuses. Attenuating collagen cross-links with minoxidil restored thymic tissue expansion for hypoplastic lobes. In colony-forming assays, the Tbx1neo2/neo2-derived mesenchymal cells had reduced expansion potential, in contrast to the normal growth of thymic epithelial cells. These findings suggest that mesenchymal cells were causal to the small embryonic thymuses in the 22q11.2DS mouse models, which was correctable by substitution with normal mesenchyme.

Heart Failure After Cavopulmonary Connection: Conversion to Biventricular Circulatory Support.

Mechanical support of patients with superior cavopulmonary connection is challenging; multiple factors contribute to failure: elevated pulmonary vascular resistance, aortopulmonary collateral flow, venovenous collaterals, ventricular dysfunction, and atrioventricular valve regurgitation. We report 2 cases of conversion from a single ventricle circulation to biventricular mechanical support by reestablishing caval continuity. Both patients have demonstrated recovery of end-organ function and participation in rehabilitation. This method of support results in improved systemic venous pressures and pulmonary blood flow compared with systemic mechanical circulatory support with a cavopulmonary connection and transfers some of the complexity of the transplant to the ventricular assist device implant.

Use of a Modified Classic BT Shunt in a Patient With Multiple Conduit Obstructions With Positive Lupus Anticoagulant.

The use of a right ventricle-to-pulmonary artery conduit has re-emerged as a popular alternative to a systemic artery-to-pulmonary artery shunt in the Norwood procedure. Both proximal obstruction secondary to dynamic compression and distal obstruction at the anastomosis site with the pulmonary arteries are well described. In an effort to prevent complications, a technique where in the conduit is placed through the entire full thickness, or dunked, through the RV free wall has been described. We report a case of a patient with HLHS and positive lupus anticoagulant who developed recurrent conduit obstructions. The "Sano" was abandoned in favor of an autologous source of pulmonary blood flow-the modified Blalock-Taussig shunt using the "turn down" of the carotid artery.

Successful Use of Pulmonary Cryotherapy for Tracheobronchial Thrombus Extraction and Recanalization of the Tracheobronchial Tree During a Pediatric Venovenous Extracorporeal Membrane Oxygenation Run.

Impacted pediatric tracheobronchial thrombus is an uncommon diagnosis. There are no clearly proven therapeutic options for airway casts due to a similar process, plastic bronchitis. Cryotherapy, specifically cryoextraction, has shown potential as a therapeutic option in adults with tracheobronchial thrombus and cast. We describe the novel application of this method in a complex pediatric patient.

Cardio-omentopexy Reduces Cardiac Fibrosis and Heart Failure After Experimental Pressure Overload.

BACKGROUND: The pedicled greater omentum has been shown to offer benefit in ischemic heart disease for both animal models and human patients. The impact of cardio-omentopexy in a pressure overload model of left ventricular hypertrophy (LVH) is unknown. METHODS: LVH was created in rats by banding the ascending aorta after right thoracotomy (n = 23). Sham surgery was performed in 12 additional rats. Six weeks after banding, surviving LVH rats were assigned to cardio-omentopexy by left thoracotomy (LVH+Om, n = 8) or sham left thoracotomy (LVH, n = 8). Sham rats also underwent left thoracotomy for cardio-omentopexy (Sham+Om, n = 6); the remaining rats underwent sham left thoracotomy (Sham, n = 6). RESULTS: Echocardiography 10 weeks after cardio-omentopexy revealed LV end-systolic diameter, cardiomyocyte diamter, and myocardial fibrosis in the LVH group were significantly increased compared with the LVH+Om, Sham+Om, and Sham groups (p < 0.01). LV ejection fraction of the LVH group was lower than the LVH+Om group (p < 0.01). Gene expression analysis revealed significantly lower levels of sarcoendoplasmic reticulum calcium adenosine triphosphatase 2b in LVH rats than in the LVH+Om, Sham+Om, and Sham groups (p < 0.01). In contrast, collagen type 1 α 1 chain, lysyl oxidase-like protein 1, nuclear protein-1, and transforming growth factor- ß1 in the LVH group were significantly higher than in the LVH+Om cohort (p < 0.01), consistent with a reduced fibrotic phenotype after omentopexy. Lectin staining showed myocardial capillary density of the LVH group was significantly lower than all other groups (p < 0.01). CONCLUSIONS: Cardio-omentopexy reduced cardiac dilation, contractile dysfunction, cardiomyocyte hypertrophy, and myocardial fibrosis, while maintaining other molecular indicators of contractile function in this LVH model.

Pulmonary paraganglioma in a 10-year-old: a case report and review of the literature.

Paraganglioma is a rare extra-adrenal tumor of the paraganglia often found in association with sympathetic and parasympathetic nerves. The case presented is of a 10-year-old boy with hemoptysis who was found to have an obstructive bronchial mass. He underwent surgical resection and biopsy confirmed primary pulmonary paraganglioma. He was subsequently found to have an associated genetic syndrome. This is the first case report describing a primary pulmonary paraganglioma in a child.

Apelin has in vivo inotropic effects on normal and failing hearts.

BACKGROUND: Apelin has been shown ex vivo to be a potent cardiac inotrope. This study was undertaken to evaluate the in vivo effects of apelin on cardiac function in native and ischemic cardiomyopathic rat hearts using a novel combination of a perivascular flow probe and a conductance catheter. METHODS AND RESULTS: Native rats (n =32) and rats in heart failure 6 weeks after left anterior descending coronary artery ligation (n =22) underwent median sternotomy with placement of a perivascular flow probe around the ascending aorta and a pressure volume conductance catheter into the left ventricle. Compared with sham-operated rats, the ligated rats had significantly decreased baseline Pmax and max dP/dt. Continuous infusion of apelin at a rate of 0.01 microg/min for 20 minutes significantly increased Pmax and max dP/dt compared with infusion of vehicle alone in both native and failing hearts. Apelin infusion increased cardiac contractility, indicated by a significant increase in stroke volume (SV) without a change in left ventricular end diastolic volume (102+/-16% change from initial SV versus 26+/-20% for native animals, and 110+/-30% versus 26+/-11% for ligated animals), as well as an increase in preload recruitable stroke work (180+/-24 mm Hg versus 107+/-9 mm Hg for native animals). CONCLUSIONS: The present study is the first to show that apelin has positive inotropic effects in vivo in both normal rat hearts and rat hearts in failure after myocardial infarction. Apelin may have use as an acute inotropic agent in patients with ischemic heart failure.

Gene transfer of hepatocyte growth factor attenuates postinfarction heart failure.

BACKGROUND: Despite advances in surgical and percutaneous coronary revascularization, ongoing ischemia that is not amenable to standard revascularization techniques is a major cause of morbidity and mortality. Hepatocyte Growth Factor (HGF) has potent angiogenic and anti-apoptotic activities, and this study evaluated the functional and biochemical effects of HGF gene transfer in a rat model of postinfarction heart failure. METHODS AND RESULTS: Lewis rats underwent ligation of the left anterior descending coronary artery with direct intramyocardial injection of replication-deficient recombinant adenovirus encoding HGF (n=10) or empty null virus as control (n=9), and animals were analyzed after six weeks. Pressure-volume conductance catheter measurements demonstrated significantly preserved contractile function in the HGF group compared with Null control animals as measured by maximum developed LV pressure (79+/-5 versus 56+/-4 mm Hg, P<0.001) and maximum dP/dt (2890+/-326 versus 1622+/-159 mm Hg/sec, P<0.01). Significant preservation of LV geometry was associated with HGF treatment (LV Diameter HGF 13.1+/-0.54 versus Null 14.4+/-0.15 mm P<0.01; LV wall thickness 1.73+/-0.10 versus 1.28+/-0.07 mm P<0.01). Angiogenesis was significantly enhanced in HGF treated animals as measured by both Von Willebrand's Factor immunohistochemical staining and a microsphere assay. TUNEL analysis revealed a significant reduction in apoptosis in the HGF group (3.42+/-0.83% versus 8.36+/-1.16%, P<0.01), which correlated with increased Bcl-2 and Bcl-xL expression in the HGF animals. CONCLUSIONS: Hepatocyte Growth Factor gene transfer following a large myocardial infarction results in significantly preserved myocardial function and geometry, and is associated with significant angiogenesis and a reduction in apoptosis. This therapy may be useful as an adjunct or alternative to standard revascularization techniques in patients with ischemic heart failure.

Viral gene transfer of the antiapoptotic factor Bcl-2 protects against chronic postischemic heart failure.

BACKGROUND: Apoptosis secondary to acute ischemia and chronic remodeling is implicated as a mediator of heart failure. This study was designed to assess the effect of in vivo viral gene transfer of the anti-apoptotic factor Bcl-2 to block apoptosis and preserve ventricular geometry and function. METHODS AND RESULTS: In a rabbit model of regional ischemia followed by reperfusion, an experimental group treated with adeno-Bcl-2 was compared with a control group receiving empty vector adeno-null. Function was assessed by echocardiography, and sonomicrometry of the border zone was compared with the normal left ventricle (LV). Animals were killed at 6 weeks, and an additional group was killed after 3 days to see whether virus administration conferred an immediate effect. Animals that were administered Bcl-2 maintained higher ejection fractions at 2, 4, and 6 weeks compared with controls. Sonomicrocrystals demonstrated greater protection of border zone fractional shortening at 6 weeks. The Bcl-2 group had superior preservation of LV geometry with less ventricular dilatation and wall thinning. There was also reduced apoptosis compared with the controls. Finally, in the animals killed at 3 days, no functional difference was observed between the Bcl-2 and control groups. CONCLUSIONS: Gene transfer of Bcl-2 preserves LV function after ischemia despite the absence of an observed acute protective effect. The benefit at 6 weeks is postulated to result from a Bcl-2-mediated reduction in apoptosis and ventricular remodeling. Adeno-Bcl-2 administration offers a potential strategy to protect the heart from late postischemic heart failure.

Inhibition of matrix metalloproteinase activity by TIMP-1 gene transfer effectively treats ischemic cardiomyopathy.

BACKGROUND: Enhanced activity of matrix metalloproteinases (MMPs) has been associated with extracellular matrix degradation and ischemic heart failure in animal models and human patients. This study evaluated the effects of MMP inhibition by gene transfer of TIMP-1 in a rat model of ischemic cardiomyopathy. METHODS AND RESULTS: Rats underwent ligation of the left anterior descending coronary artery with direct intramyocardial injection of replication-deficient adenovirus encoding TIMP-1 (n=8) or null virus as control vector (n=8), and animals were analyzed after 6 weeks. Both systolic and diastolic cardiac function was significantly preserved in the TIMP-1 group compared with control animals (maximum left ventricular [LV] pressure: TIMP-1 70+/-10 versus control 56+/-12 mmHg, P<0.05; maximum dP/dt 2697+/-842 versus 1622+/-527 mmHg/sec, P<0.01; minimum dP/dt -2900+/-917 versus -1195+/-593, P<0.001). Ventricular geometry was significantly preserved in the TIMP-1 group (LV diameter 13.0+/-0.7 versus control 14.4+/-0.4 mm, P<0.001; border-zone wall thickness 1.59+/-0.11 versus control 1.28+/-0.19 mm, P<0.05), and this was associated with a reduction in myocardial fibrosis (2.36+/-0.87 versus control 3.89+/-1.79 microg hydroxyproline/mg tissue, P<0.05). MMP activity was reduced in the TIMP-1 animals (1.5+/-0.9 versus control 43.1+/-14.9 ng of MMP-1 activity, P<0.05). CONCLUSIONS: TIMP-1 gene transfer inhibits MMP activity and preserves cardiac function and geometry in ischemic cardiomyopathy. The reduction in myocardial fibrosis may be primarily responsible for the improved diastolic function in treated animals. TIMP-1 overexpression is a promising therapeutic target for continued investigation.

Targeted overexpression of leukemia inhibitory factor to preserve myocardium in a rat model of postinfarction heart failure.

OBJECTIVE: Myocardial infarction leads to cardiomyocyte loss. The cytokine leukemia inhibitory factor regulates the differentiation and growth of embryonic and adult heart tissue. This study examined the effects of gene transfer of leukemia inhibitory factor in infarcted rat hearts. METHODS: Lewis rats underwent ligation of the left anterior descending coronary artery and direct injection of adenovirus encoding leukemia inhibitory factor (n = 10) or null transgene as control (n = 10) into the myocardium bordering the ischemic area. A sham operation group (n = 10) underwent thoracotomy without ligation. After 6 weeks, the following parameters were evaluated: cardiac function with a pressure-volume conductance catheter, left ventricular geometry and architecture by histologic methods; myocardial fibrosis by Masson trichrome staining, apoptosis by terminal deoxynucleotidal transferase-mediated deoxyuridine triphosphate nick-end labeling assay, and cardiomyocyte size by immunofluorescence. RESULTS: Rats with overexpression of leukemia inhibitory factor had more preserved myocardium and less fibrosis in both the infarct and its border zone. The border zone in leukemia inhibitory factor-treated animals contained fewer apoptotic nuclei (1.6% +/- 0.1% vs 3.3% +/- 0.2%, P < .05) than that in control animals and demonstrated cardiomyocytes with larger cross-sectional areas (910 +/- 60 microm 2 vs 480 +/- 30 microm 2 , P < .05). Leukemia inhibitory factor-treated animals had increased left ventricular wall thickness (2.1 +/- 0.1 mm vs 1.8 +/- 0.1 mm, P < .05) and less dilation of the left ventricular cavity (237 +/- 22 microL vs 301 +/- 16 microL, P < .05). They also had improved cardiac function, as measured by maximum change in pressure over time (3950 +/- 360 mm Hg/s vs 2750 +/- 230 mm Hg/s, P < .05) and the slopes of the maximum change in pressure over time-end-diastolic volume relationship (68 +/- 5 mm Hg/[s . microL] vs 46 +/- 6 mm Hg/[s . microL], P < .05) and the preload recruitable stroke work relationship (89 +/- 10 mm Hg vs 44 +/- 4 mm Hg, P < .05). CONCLUSIONS: Myocardial gene transfer of leukemia inhibitory factor preserved cardiac tissue, geometry, and function after myocardial infarction in rats.

Ethyl pyruvate preserves cardiac function and attenuates oxidative injury after prolonged myocardial ischemia.

OBJECTIVE: Myocardial injury and dysfunction following ischemia are mediated in part by reactive oxygen species. Pyruvate, a key glycolytic intermediary, is an effective free radical scavenger but unfortunately is limited by aqueous instability. The ester derivative, ethyl pyruvate, is stable in solution and should function as an antioxidant and energy precursor. This study sought to evaluate ethyl pyruvate as a myocardial protective agent in a rat model of ischemia-reperfusion injury. METHODS: Rats underwent 30-minute ischemia and 30-minute reperfusion of the left anterior descending coronary artery territory. Immediately prior to both ischemia and reperfusion, animals received an intravenous bolus of either ethyl pyruvate (n = 26) or vehicle control (n = 26). Myocardial high-energy phosphate levels were determined by adenosine triphosphate assay, oxidative injury was measured by lipid peroxidation assay, infarct size was quantified by triphenyltetrazolium chloride staining, and cardiac function was assessed in vivo. RESULTS: Ethyl pyruvate administration significantly increased myocardial adenosine triphosphate levels compared with control (87.6 +/- 29.2 nmol/g vs 10.0 +/- 2.4 nmol/g, P =.03). In ischemic myocardium, ethyl pyruvate reduced oxidative injury compared with control (63.8 +/- 3.3 nmol/g vs 89.5 +/- 3.0 nmol/g, P <.001). Ethyl pyruvate diminished infarct size as a percentage of area at risk (25.3% +/- 1.5% vs 33.6% +/- 2.1%, P =.005). Ethyl pyruvate improved myocardial function compared with control (maximum pressure: 86.6 +/- 2.9 mm Hg vs 73.5 +/- 2.5 mm Hg, P <.001; maximum rate of pressure rise: 3518 +/- 243 mm Hg/s vs 2703 +/- 175 mm Hg/s, P =.005; maximal rate of ventricular systolic volume ejection: 3097 +/- 479 microL/s vs 2120 +/- 287 microL/s, P =.04; ejection fraction: 41.9% +/- 3.8% vs 31.4% +/- 4.1%, P =.03; cardiac output: 26.7 +/- 0.9 mL/min vs 22.7 +/- 1.3 mL/min, P =.01; and end-systolic pressure-volume relationship slope: 1.09 +/- 0.22 vs 0.59 +/- 0.2, P =.02). CONCLUSIONS: In this study of myocardial ischemia-reperfusion injury, ethyl pyruvate enhanced myocardial adenosine triphosphate levels, attenuated myocardial oxidative injury, decreased infarct size, and preserved cardiac function.