Identification of patient variables that are associated with ventricular end-diastolic pressure before the bidirectional Glenn operation.

INTRODUCTION: Systemic ventricular end-diastolic pressure is important in patients with single ventricle heart disease. Predictors of an elevated systemic ventricular end-diastolic pressure prior to bidirectional Glenn operation have been incompletely identified. METHODS: All patients who underwent bidirectional Glenn operation operation at our centre between January 2007 and March 2017 were retrospectively identified and patient variables were extracted. For patients who had undergone Fontan operation at the time of this study, post-Fontan patient variables were also extracted. RESULTS: One-hundred patients were included with a median age at pre-bidirectional Glenn operation catheterisation of 4.5 months. In total, 71 (71%) patients had a systemic right ventricle. At the pre-bidirectional Glenn operation catheterisation, the mean systemic ventricular end-diastolic pressure was higher amongst those with systemic right ventricle compared to left ventricle (9.1 mmHg ± 2.1 versus 7.7 ± 2.7 mmHg, p < 0.01). On univariate analysis, pre-bidirectional Glenn operation systemic ventricular end-diastolic pressure was positively associated with the presence of a systemic right ventricle (p < 0.01), history of recoarctation (p = 0.03), history of Norwood operation (p = 0.04), and ventricular systolic pressure (p < 0.01). On multivariate analysis, systemic ventricular end-diastolic pressure was positively associated with the presence of a systemic right ventricle (p < 0.01) and ventricular systolic pressure (p < 0.01). Amongst those who had undergone Fontan operation at the time of study (n = 49), those with a higher pre-bidirectional Glenn operation systemic ventricular end-diastolic pressure were more likely to have experienced death, transplantation, or listed for transplantation (p = 0.02) and more likely to have had heart failure symptoms (p = 0.04) at a mean time from Fontan of 5.2 years ± 1.3. CONCLUSIONS: In patients undergoing bidirectional Glenn operation operation, the volume-loaded, pre-bidirectional Glenn operation state may expose diastolic dysfunction that has prognostic value.

Successful Salvage of an Extracardiac Fontan in the Setting of Purulent Mediastinitis using Antibiotic-Impregnated Beads.

Post-cardiotomy mediastinitis is an especially serious complication after the implantation of prosthetic vascular grafts. Standard of care is irrigation, debridement, and removal of all prosthetic material present in the surgical field. The use of antibiotic impregnated beads at the site of infection has been reported in the salvage of vascular grafts in the adult population. We present the case of a 3-year-old child with hypoplastic left heart syndrome who developed mediastinitis following the Fontan operation. In a nontraditional approach, the Fontan conduit, which was surrounded by gross purulence, was successfully salvaged with the adjunctive use of vancomycin-impregnated beads.

Biatrial primary cardiac paraganglioma: a rare finding.

The majority of primary cardiac tumors are benign; of these tumors, cardiac paragangliomas are among the rarest. We report a case of biatrial cardiac paraganglioma discovered during workup for palpitations and fatigue. The tumor involved the interatrial septum, with a lobulated portion protruding through the foramen ovale into the right atrium. The tumor was successfully excised, leading to uneventful recovery.

Bedside modified Clagett procedure for empyema after pulmonary resection.

The objective of this study is to demonstrate the effectiveness and feasibility in treating empyema after pulmonary resection with a modified Clagett procedure performed at the bedside (BMCP). A retrospective review of a single surgeon's experience at a single institution was undertaken. All operative, postoperative, and outcome data were analyzed. Follow-up data were obtained from subsequent clinic charts. Five patients, including four males, were identified who underwent BMCP after pulmonary resection. The original operative procedures included two lobectomies, one pneumonectomy, one bilobectomy, and one bilateral metastastectomy. Patients were diagnosed with an empyema (positive thoracostomy tube culture, fever, and radiographic abnormality) at a mean time of 31 days from their initial procedure. Culture results disclosed Gram-positive empyemas in all patients. Three patients underwent BMCP as an outpatient, whereas the other two had BMCP during their hospitalizations. All patients are free from complications or recurrence at a mean follow up of 11.2 months. No patient required a further procedure after BMCP. The bedside modified Clagett procedure is both safe and effective. It is a valuable option in the management of postoperative empyema because it avoids additional operative procedures. This procedure is cost-effective when compared with operative management of perioperative empyema.

Adenosine A2A receptor activation reduces inflammation and preserves pulmonary function in an in vivo model of lung transplantation.

BACKGROUND: Reperfusion injury continues to significantly affect patients undergoing lung transplantation. Isolated lung models have demonstrated that adenosine A 2A receptor activation preserves function while decreasing inflammation. We hypothesized that adenosine A 2A receptor activation by ATL-146e during the initial reperfusion period preserves pulmonary function and attenuates inflammation in a porcine model of lung transplantation. METHODS: Mature pig lungs preserved with Viaspan (Barr Laboratories, Pomona, NY) underwent 6 hours of cold ischemia before transplantation and 4 hours of reperfusion. Animals were treated with (ATL group, n = 7) and without (IR group, n = 7) ATL-146e (0.05 microg kg -1 . min -1 ATL-146e administered intravenously for 3 hours). With occlusion of the opposite pulmonary artery, the animal was maintained for the final 30 minutes on the allograft alone. Recipient lung physiology was monitored before tissue evaluation of pulmonary edema (wet-to-dry weight ratio), myeloperoxidase assay, and tissue tumor necrosis factor alpha by means of enzyme-linked immunosorbent assay. RESULTS: When the ATL group was compared with the IR group, the ATL group had better partial pressure of carbon dioxide (43.8 +/- 4.1 vs 68.9 +/- 6.3 mm Hg, P < .01) and partial pressure of oxygen (272.3 +/- 132.7 vs 100.1 +/- 21.4 mm Hg, P < .01). ATL-146e-treated animals exhibited lower pulmonary artery pressures (33.6 +/- 2.1 vs 47.9 +/- 3.5 mm Hg, P < .01) and mean airway pressures (16.25 +/- 0.08 vs 16.64 +/- 0.15 mm Hg, P = .04). ATL-146e-treated lungs had lower wet-to-dry ratios (5.9 +/- 0.39 vs 7.3 +/- 0.38, P < .02), lower myeloperoxidase levels (2.9 x 10 -5 +/- 1.2 x 10 -5 vs 1.3 x 10 -4 +/- 4.0 x 10 -5 DeltaOD mg -1 . min -1 , P = .03), and a trend toward decreased lung tumor necrosis factor alpha levels (57 +/- 12 vs 96 +/- 15 pg/mL, P = .06). The ATL group demonstrated significantly less inflammation on histology. CONCLUSION: Adenosine A 2A activation during early reperfusion attenuated lung inflammation and preserved pulmonary function in this model of lung transplantation. ATL-146e and similar compounds could play a significant role in improving outcomes of pulmonary transplantation.

Another piece in the puzzle.

Pulmonary ischemia-reperfusion injury is complex and involves many cell types and mechanisms of action. Van Putte and coworkers have attempted to provide insight into and describe some of the complex components of this process. Their study describes two new components of the multifaceted process of reperfusion injury. The time-dependent course of neutrophil activation and the discovery of programmed cell death in reperfused lung tissue are two new pieces of a complex puzzle.

Improved myocardial function with the addition of pinacidil to custadiol.

BACKGROUND: This study investigates the efficacy of pinacidil, an adenosine triphosphate-sensitive potassium (KATP) channel opening agent, added to custadiol solution on myocardial protection during deep hypothermia and prolonged global ischemia on isolated rat hearts. METHODS: After 20 minutes of stabilization, 24 rats were divided into two groups. In group I (n=12), hearts were arrested with cold (4 degrees C) custadiol solution containing 50 micromol/L of pinacidil and subsequently dipped into the same solution for 120 minutes at 4 degrees C. Group I hearts were perfused with low-flow pinacidil-custadiol (PC) solution during the ischemic period. Group II (n=12) hearts, after the stabilization period, were arrested with cold custadiol solution only, then subsequently dipped and perfused with the same solution for 120 minutes at 4 degrees C. All hearts were reperfused with Krebb's-Henseleit solution at 37 degrees C for 60 minutes. Hemodynamic parameters (peak systolic pressure, end diastolic pressure, maximum rate of increase of left ventricular pressure [+dP/dt], ischemic contracture, and coronary sinus flow) were recorded at the end of the stabilization period and at 10-minute intervals during the reperfusion period. Biochemical data (creatine kinase [CK-MB] washout and troponin I [cTnI] levels) were compared between the two groups. RESULTS: There was no significant difference in any hemodynamic or biochemical parameters between the two groups during the stabilization period. The peak systolic pressure, +dP/dt, ischemic contraction amplitude, and coronary flow values were significantly higher in group I ( P<0.05) compared with group II during reperfusion. End diastolic pressures as well as CK-MB and cTnI levels were lower in the pinacidil-treated group, which is consistent with improved functional recovery during the reperfusion period. CONCLUSION: The addition of pinacidil to the preservation solution, custadiol, improves myocardial recovery after deep hypothermia and prolongs ischemia.

Tumor necrosis factor-alpha from resident lung cells is a key initiating factor in pulmonary ischemia-reperfusion injury.

OBJECTIVE: A central role of macrophages in initiating lung ischemia-reperfusion injury is emerging. Tumor necrosis factor-alpha is a proinflammatory cytokine secreted mainly by macrophages under various conditions. We hypothesized that tumor necrosis factor-alpha from resident lung cells is a key initiating factor in pulmonary ischemia-reperfusion injury. METHODS: We used an isolated, buffer-perfused lung system to explore the role of tumor necrosis factor-alpha production by resident lung cells in pulmonary ischemia-reperfusion injury. Lungs from wild-type mice and tumor necrosis factor-alpha-deficient mice were subjected to 60 minutes of ischemia followed by 60 minutes of reperfusion. Histologic injury scores and measurements of lung compliance, airway resistance, mean pulmonary artery pressure, vascular reactivity, and wet lung weight index were obtained and compared using repeated-measures analysis of variance. RESULTS: Lungs from tumor necrosis factor-alpha-deficient mice showed significantly less injury in all physiologic parameters throughout the entire 60 minutes of reperfusion compared with lungs from wild-type mice (P <.001). The most notable effects were observed in pulmonary artery pressure and airway resistance. Vascular reactivity (acute vasoconstrictive episodes per 60 minutes) was also blunted in the lungs from tumor necrosis factor-alpha-deficient mice compared with the lungs from wild-type mice (5.8 responses/hour vs 1.2 responses). Histologic injury scores and wet lung weight index were significantly reduced in lungs from tumor necrosis factor-alpha-deficient mice. CONCLUSIONS: By using the advantages of a nonblood-perfused system, we have focused our investigation on resident lung cells. Our results demonstrate that resident cell-produced tumor necrosis factor-alpha is a key initiating factor in acute lung ischemia-reperfusion injury.

Coronary artery bypass with ventricular restoration is superior to coronary artery bypass alone in patients with ischemic cardiomyopathy.

BACKGROUND: Coronary artery bypass is an acceptable therapy in patients with ischemic cardiomyopathy. However, it has been demonstrated that patients with increased left ventricular volume have a worse outcome than patients with normal ventricular volume. Our hypothesis was that ventricular restoration plus coronary artery bypass provides improved outcome compared with coronary artery bypass alone in ischemic cardiomyopathy with ventricular enlargement. METHODS: A retrospective analysis was performed of patients with ischemic cardiomyopathy (ejection fraction <30%) who underwent operation between 1998 and 2002. Patients with enlarged ventricles (end-diastolic dimension > or =6.0 cm) who underwent either coronary artery bypass alone or coronary artery bypass with ventricular restoration were compared. Preoperative and postoperative ejection fraction, morbidity, mortality, and freedom from heart failure (hospitalization secondary to heart failure) were assessed. RESULTS: Ninety-five patients were included in the study. Thirty-nine patients had coronary artery bypass alone, whereas 56 patients had ventricular restoration with coronary artery bypass. Both groups demonstrated an improved postoperative ejection fraction; however, the improvement was significantly greater in the ventricular restoration plus coronary artery bypass group (P <.01). There were no hospital deaths in either group; however, late mortality was higher in the coronary artery bypass group. Freedom from heart failure was achieved in all but 2 of the ventricular restoration plus coronary artery bypass patients (2/56, or 3.6%) versus 7 in the coronary artery bypass group (7/39, or 18%). The combined outcomes of freedom from failure and late mortality were significantly improved in the ventricular restoration plus coronary artery bypass group (P <.05). CONCLUSIONS: Ventricular restoration affords significant improvement in ejection fraction compared with coronary artery bypass alone, without added mortality. Most importantly, left ventricular restoration reduces late morbidity and mortality compared with coronary artery bypass alone in patients with large ventricles.

Transverse arch hypoplasia may predispose patients to aneurysm formation after patch repair of aortic coarctation.

BACKGROUND: Thoracic aortic aneurysm after patch repair of aortic coarctation is a potentially lethal complication. We hypothesized that transverse arch hypoplasia in association with patch repair of aortic coarctation predisposes aneurysm formation. METHODS: A retrospective analysis was performed on all patients undergoing isolated aortic coarctation repair at the University of Virginia Health Systems between 1970 and 1995. Of 244 repairs, 38 patients underwent patch repair. These 38 patients were divided into two groups. The aneurysm group (n = 15) had aortic aneurysms develop at the repair site, which required aneurysmectomy. The nonaneurysm group (n = 23) did not have any aneurysms develop. Univariate analysis and Fisher's exact text were used to identify factors that independently predict aneurysm formation. RESULTS: Univariate analysis demonstrated aortic arch hypoplasia associated with patch repair independently predicts future aneurysm formation (p < 0.01). Patients who had an aneurysm develop also had a similar incidence of bicuspid aortic valves, mild restenosis, and late hypertension compared with patients in the nonaneurysm group. CONCLUSIONS: Aneurysm formation after patch repair of aortic coarctation develops into a subgroup of patients. Aortic arch hypoplasia associated with coarctation independently predicts future aneurysm formation.

The beating heart approach is not necessary for the Dor procedure.

BACKGROUND: Ventricular reconstruction using the Dor technique has been demonstrated to improve outcome in patients with dilated left ventricles. It has been suggested that a beating heart approach improves ventricular function by allowing the surgeon to palpate that part of the ventricle to exclude. METHODS: We performed a retrospective analysis of patients who underwent an endoventricular circular patch plasty (Dor procedure) between 1998 and 2001. All patients who received ventricular restoration, with or without revascularization or valve repair, were included in the analysis. Discrete left ventricular aneurysms were excluded. Patients were divided into two groups: group 1 (n = 15) underwent ventricular reconstruction with the beating heart technique, whereas group 2 (n = 38) underwent restoration with the aorta cross-clamped. Clinical and hemodynamic data were collected from medical records and computerized databases and compared between the two groups. RESULTS: Fifty-three patients underwent endoventricular circular patch plasty. All patients had enlarged ventricles (echocardiogram demonstrating unidimensional end-diastolic diameter >/= 6.0 cm) and echocardiographic evidence of severe left ventricular dysfunction (mean ejection fraction: group 1 = 21.4%; group 2 = 23.4%). No operative mortalities occurred in either group and all patients were discharged home alive (mean postoperative hospital stay 8.3 days [6 to 22 days]). All patients had improvement in left ventricular function with mean postoperative left ventricular ejection fraction of 36.9% (25% to 52%) in group 1 versus 38.1% (31% to 50%) in group 2, p = 0.081. Ventricular arrhythmias occurred in 5 of 15 group 1 patients and in 9 of 38 group 2 patients. Two patients in the entire cohort (1 patient in group 1, and 1 patient in group 2) had at least one readmission within 12 months with evidence of heart failure. The group 1 patient went on to successful transplant 11 months later, whereas the group 2 patient died 10 months later. CONCLUSIONS: These results demonstrate that the Dor technique of ventricular restoration significantly improves left ventricular function and the beating heart approach provides no additional advantage over continuous aortic cross clamping.

Safety and efficacy of the supraclavicular approach to thoracic outlet decompression.

BACKGROUND: Thoracic outlet syndrome (TOS) is a clinical diagnosis encountered by both thoracic and vascular surgeons. The goal of surgical therapy involves relieving compression of the neurovascular structures at the superior thoracic aperture. The traditional approach to thoracic outlet decompression has been transaxillary; however more centers are moving toward a more tailored approach through a supraclavicular incision. METHODS: The medical records of 67 patients who underwent surgical decompression between 1993 and 2001 for TOS were retrospectively reviewed. Patient demographics and early outcome were assessed through clinic follow-up. RESULTS: Seventy-two thoracic outlet decompressions were performed on 67 patients with the diagnosis of TOS. Five patients underwent bilateral thoracic outlet decompression. All operations in this time period were safely accomplished through a supraclavicular approach. The syndromes associated with thoracic outlet compression were neurogenic (n = 59), venous (n = 10), and arterial (n = 3). Forty-six of 72 (63.9%) operations resulted in complete resolution of symptoms, 17 cases (23.6%) had partial resolution, and 9 patients (12.5%) had no resolution. There were no deaths and morbidity was minimal with 6 complications (8.3%). CONCLUSIONS: The supraclavicular approach is a safe and effective technique in managing all forms of thoracic outlet compression.

Beneficial effects of inhaled nitric oxide in adult cardiac surgical patients.

BACKGROUND: Pulmonary hypertension with associated right ventricular dysfunction may complicate the postoperative cardiac patient despite maximum pharmacologic and ventilatory support. The purpose of this study was to retrospectively review our experience with inhaled nitric oxide (INO) in adult postoperative cardiac patients with pulmonary hypertension. METHODS: We retrospectively reviewed the medical records of 17 adult cardiac patients treated with INO postoperatively between November 1998 and February 2000. The INO was used to manage pulmonary hypertension postoperatively in patients who had undergone coronary artery bypass graft (CABG) (n = 13), valve operation (n = 3), and combined CABG/aortic valve replacement (n = 1). Hemodynamic and respiratory measurements before INO and again 6 hours after administration were examined. Student's t test was used to analyze the data. RESULTS: Inhaled nitric oxide (20 ppm to 30 ppm) was administered for a median duration of 30.2 hours. The group, as a whole, demonstrated a significant decrease in both mean pulmonary artery pressure and right ventricular stroke work index. In addition, a significant increase in posttherapeutic cardiac index and Pao2/Fio2 ratio was observed. The vasodilatory effects of nitric oxide were specific to the pulmonary circulation as no significant change in mean arterial pressure was noted. Overall mortality was 6%. CONCLUSIONS: Inhaled nitric oxide effectively and selectively lowered right ventricular afterload and right ventricular work in critically ill adult cardiac patients with acute pulmonary hypertension.

Unrepaired tetralogy of fallot with major aortopulmonary collateral arteries in an adult patient.

Tetralogy of Fallot is characterized by a ventricular septal defect, a large, overriding aorta, subpulmonic stenosis, and right ventricular hypertrophy. These lesions can be associated with abnormal development of the pulmonary vasculature. This can include peripheral pulmonic stenosis, discontinuous pulmonary arteries, anomalous pulmonary venous return, and the development of aortopulmonary collateral vessels. Aortopulmonary collateral vessels develop to supply underperfused areas of the pulmonary bed and pose a unique and challenging problem at the time of surgical repair, which involves closure of the ventricular septal defect, relief of right ventricular outflow tract obstruction, maintenance of pulmonary valve competency when possible, and establishment of laminar pulmonary blood flow to all segments of the pulmonary bed. We describe a 36-year-old man with unrepaired tetralogy of Fallot with distinctive aortopulmonary collaterals, who underwent complete surgical repair with good outcome. Two-dimensional echocardiogram, cardiac magnetic resonance imaging, and cardiac catheterization each provided vital details allowing a stepwise approach to defining his unique anatomy for surgical correction.

Early adenosine receptor activation ameliorates spinal cord reperfusion injury.

OBJECTIVES: Adenosine receptor activation at reperfusion has been shown to ameliorate ischemia-reperfusion injury of the spinal cord, but the effects of therapy given in response to ischemic injury are unknown. We hypothesized that adenosine receptor activation with ATL-146e would produce similar protection from ischemic spinal cord injury, whether given at reperfusion or in a delayed fashion. METHODS: Twenty-two New Zealand white rabbits were divided into three groups. All three groups, including the ischemia-reperfusion group (IR, n = 8), underwent 45 min of infrarenal aortic occlusion. The early treatment group (early, n = 8) received 0.06 mug/kg/min of ATL-146e for 3 h beginning 10 min prior to reperfusion. The delayed treatment group (delayed, n = 6) received ATL-146e starting 1 h after reperfusion. After 48 h, hind limb function was graded using the Tarlov score. Finally, lumbar spinal cord neuronal cytoarchitecture was evaluated. RESULTS: Hemodynamic parameters were similar among the groups. Hind limb function at 48 h was significantly better in the early group (3.5 +/- 1.0) compared to the IR group (0.625 +/- 0.5, P < or = 0.01). There was a trend towards better hind limb function in the early group compared to the delayed group (2.4 +/- 1.1, P = 0.08). Hind limb function was similar between delayed and IR groups. Hematoxylin-eosin spinal cord sections demonstrated preservation of viable motor neurons in the early group compared to the delayed and IR groups. CONCLUSIONS: Early therapy with ATL-146e provided better protection in this study; therefore, therapy should not be delayed until there is evidence of ischemic neurological deficit. This study suggests that adenosine receptor activation is most effective as a preventive strategy at reperfusion for optimal protection in spinal cord ischemia-reperfusion injury.

A novel stentless mitral valve.

Stentless mitral valves have found little clinical utility to date due to difficulty in insertion. A new design for a stentless mitral valve, a modification of an existing aortic stentless prosthesis, is described. The new design mimics the native mitral physiology, and its insertion is easier than with existing stentless mitral valves. Commercially available stentless aortic valves were inserted into 2 pigs. The valves were modified so that the commissural posts were restrained. The valves were partially recessed into the left ventricular cavity, secured to the annulus, and anchored to the native papillary muscles. Both pigs were weaned from bypass successfully, and both valves functioned normally with trace regurgitation noted on echocardiography. This design affords the benefit of the reapproximation of native physiology. Preservation of papillary-annular continuity should allow maximal left ventricular function. Lack of a stent should allow avoidance of long-term anticoagulation.