Echocardiographic Evaluation of Postoperative Coaptation Geometry of Left AV Valve in Complete Atrioventricular Septal Defect.

Background: We sought to determine the difference in geometric parameters in the left atrioventricular valve (LAVV) postoperative complete atrioventricular septal defect (CAVSD) compared to the normal heart, and the correlation between geometric and functional parameters for detecting the mechanism of LAVV regurgitation (LAVVR) in CAVSD. Methods: LAVV geometric parameters based on complete and acceptable quality echocardiograms of 18 patients with repaired CAVSD compared with 17 normal controls. LAVVR severity was also quantified by indexed vena contracta (I-VC) (mm) and % jet area/left atrium area (% Jet/LA), and the correlation with LAVV parameters in the CAVSD group was investigated. Results: In the CAVSD group, the posterior closing angle (Pc) was nearly the same as the anterior closing angle (Ac), yet in the normal heart, the Pc angle was double the Ac angle. The anterior opening angle (Ao) and posterior-to-anterior leaflet diameter ratio (a/p) in the CAVSD group was also significantly smaller. The CAVSD group also had a shorter indexed coaptation length (I-CL) and indexed tenting height (I-TH). Displacement length (ΔD) differed completely between the CAVSD and Normal groups, and also showed a strong positive correlation to the functional parameters of LAVVR (% Jet/LA: r = .70, P = .02; I-VC: r = .60, P = .02). Conclusions: The parameters in this study were applicable to CAVSD AV valve coaptation characteristics. We introduced 2 novel measures that may provide important insights into the differences in geometry and performance of the LAVV in repaired CAVSD as compared to normal hearts.

Superior restoration of left ventricular performance after prolonged single-dose del Nido cardioplegia in conjunction with terminal warm blood cardioplegic reperfusion.

OBJECTIVES: An incomplete restoration of left ventricular contractility after del Nido cardioplegia was noted in our recent study. This study tested the hypothesis that terminal warm blood cardioplegia promotes a prompt restoration of left ventricular performance after a prolonged single-dose del Nido cardioplegia. METHODS: Fourteen piglets were subjected to 120 minutes of arrest by del Nido cardioplegia without terminal warm blood cardioplegia (del Nido cardioplegia group; n = 7) or with terminal warm blood cardioplegia before reperfusion (terminal warm blood cardioplegia group; n = 7). The other 7 piglets underwent total cardiopulmonary bypass without ischemia/reperfusion for 150 minutes (control group). Left ventricular function was assessed by percent recovery of end-systolic elastance as the contractility and percent end-diastolic pressure-volume relationship as the compliance using a conductance catheter. Troponin T and the mitochondrial score were also measured. RESULTS: Depressed percent recovery of end-systolic elastance was sustained in the del Nido cardioplegia group, and a prompt restoration of end-systolic elastance was achieved using terminal warm blood cardioplegia (57.9 ± 17.8 vs 94.7 ± 13.1, P < .028). Percent end-diastolic pressure-volume relationship at the early phase was better in the terminal warm blood cardioplegia compared with the del Nido group (88.5 ± 24.0 vs 101.4 ± 16.8, P = .050). Troponin T was higher in the terminal warm blood cardioplegia compared with the control group (0.80% ± 0.21% and 1.49% ± 0.31%, respectively, P = .002). The mitochondrial score was equivalent in all groups. Spontaneous restoration to sinus rhythm was more frequent in the terminal warm blood cardioplegia group than in the del Nido cardioplegia group (6/7 vs 1/7, P < .028). CONCLUSIONS: The supplementary use of terminal warm blood cardioplegia achieved prolongation of the safe ischemic time up to 120 minutes for a single-dose application.

Evaluation of Ductal Tissue in Coarctation of the Aorta Using X-Ray Phase-Contrast Tomography.

We assessed the histological accuracy of X-ray phase-contrast tomography (XPCT) and investigated three-dimensional (3D) ductal tissue distribution in coarctation of the aorta (CoA) specimens. We used nine CoA samples, including the aortic isthmus, ductus arteriosus (DA), and their confluences. 3D images were obtained using XPCT. After scanning, the samples were histologically evaluated using elastica van Gieson (EVG) staining and transcription factor AP-2 beta (TFAP2B) immunostaining. XPCT sectional images clearly depicted ductal tissue distribution as low-density areas. In comparison with EVG staining, the mass density of the aortic wall positively correlated with elastic fiber formation (R = 0.69, P < 0.001). TFAP2B expression was consistent with low-density area including intimal thickness on XPCT images. On 3D imaging, the distances from the DA insertion to the distal terminal of the ductal media and to the intima on the ductal side were 1.63 ± 0.22 mm and 2.70 ± 0.55 mm, respectively. In the short-axis view, the posterior extension of the ductal tissue into the aortic lumen was 79 ± 18% of the diameter of the descending aorta. In three specimens, the aortic wall was entirely occupied by ductal tissue. The ductal intima spread more distally and laterally than the ductal media. The contrast resolution of XPCT images was comparable to that of histological assessment. Based on the 3D images, we conclude that complete resection of intimal thickness, including the opposite side of the DA insertion, is required to eliminate residual ductal tissue and to prevent postoperative re-coarctation.

Modified Del Nido Cardioplegia and Its Evaluation in a Piglet Model.

Del Nido cardioplegia (DN) is not available worldwide as the required solution is made from a commercial base (PlasmaLyte) that is not approved in all countries. We report our own modified DN solution and confirm its safety and effectiveness. Fourteen piglets were subjected to 90 minutes of global ischemia on cardiopulmonary bypass induced by original DN (n = 7) or NS (normal saline)-based DN (n = 7). Our DN solution begins with a base of NS (800 mL) and distilled water (200 mL), to which are added 15 mL KCl (2 mEq/mL), 17 mL NaHCO3 (1 mEq/mL), 10 mL MgSO4 (0.2 g/mL), 13 mL lidocaine 1%, and 13 mL mannitol 25%. LV function recovery was assessed in end-systolic elastance (EES) as systolic function and end-diastolic pressure-volume relationship (EDPVR) as diastolic function using a conductance catheter. Creatine kinase-MB (CK-MB) and mitochondrial score were also measured. Left ventricular (LV) contractility after ischemia (%EES ± SD) was not significantly different between the group induced by original DN (89.3 ± 20.6%) and the group induced by NS-based DN (99.3 ± 18.4%). LV compliance (%EDPVR ± SD) was likewise not significantly different between these groups (102.7 ± 28.2% vs 94.4 ± 22.8%, PL vs NS, respectively). CK-MB was equivalent between the groups. Mitochondrial scores were not significantly different between the groups, and this difference did not cause severe damage. NS-based DN preserves LV function recovery after prolonged global ischemia as effectively and as safely as original DN does. NS-based modified DN can be substituted for original DN.

Reassessment of the Location of the Conduction System in Atrioventricular Septal Defect Using Phase-Contrast Computed Tomography.

The location of the atrioventricular conduction axis in the setting of atrioventricular septal defect has previously been shown by histology and intraoperative recordings. We have now reassessed the arrangement using phase-contrast computed tomography, aiming to provide precise measurements so as to optimize future surgical repairs. We used the system based on an X-ray Talbot grating interferometer using the beamline BL20B2 in a SPring-8 synchrotron radiation facility available in Japan. We analyzed 18 specimens. The atrioventricular node was found within a nodal triangle 1.7 mm from the coronary sinus, with 95% confidence intervals from 1.45 to 2.0 millimeters. The depth of the node from the right atrial endocardium was 1.0 mm, with 95% confidence intervals from 0.73 to 1.34 mm. The overall length of the scooped-out ventricular septum was 30.8 mm, with 95% confidence intervals from 27.5 to 34.1 millimeters. The length from the inferior atrioventricular junction to the take-off of the right bundle branch was 12.8 mm, with 95% confidence intervals from 11.12 to 14.38 mm, giving a ratio of 0.43 for the extent of the axis along the inferior septum, with 95% confidence intervals of 0.38-0.48. The length of the non-branching bundle was 6.6 mm, with 95% confidence intervals from 5.57 to 7.7 mm. The proportion of septum occupied by the non-branching bundle was 0.22, with 95% confidence intervals from 0.18 to 0.26. Our findings confirm previous histological studies, extending them by providing precise measurements to guide placement of sutures during surgical repair.

Effect of Long-term Administration of Prostaglandin E1 on Morphologic Changes in Ductus Arteriosus.

BACKGROUND: To improve survival of patients with hypoplastic left heart syndrome, combination therapy with bilateral pulmonary artery banding and prostaglandin E1 (PGE1)-mediated ductal patency was developed as an alternative for high-risk neonates in Japan. However, the effect of long-term PGE1 administration on ductus arteriosus remains unclear. Synchrotron radiation-based X-ray phase-contrast tomography (XPCT) enables clear visualization of soft tissues at an approximate spatial resolution of 12.5 µm. We aimed to investigate morphologic changes in ductus arteriosus after long-term PGE1 infusion using XPCT. METHODS: Seventeen ductus arteriosus tissue samples from patients with hypoplastic left heart syndrome were obtained during the Norwood procedure. The median duration of lipo-prostaglandin E1 (lipo-PGE1) administration was 48 days (range, 3 to 123). Structural analysis of ductus arteriosus was performed and compared with conventional histologic analysis. RESULTS: The XPCT was successfully applied to quantitative measurements of ductal media. Significant correlation was found between the duration of lipo-PGE1 infusion and mass density of ductal media (R = 0.723, P = .001). The duration of lipo-PGE1 administration was positively correlated with elastic fiber staining (R = 0.799, P < .001) and negatively correlated with smooth muscle formation (R = -0.83, P < .001). No significant increase in intimal cushion formation was found after long-term lipo-PGE1 administration. Expression of ductus arteriosus dominant PGE2-receptor EP4 almost disappeared in specimens when lipo-PGE1 was administered over 3 days. CONCLUSIONS: Disorganized elastogenesis and little intimal cushion formation after long-term lipo-PGE1 administration suggest that ductus arteriosus remodeled to the elastic artery phenotype. Because EP4 was downregulated and ductus arteriosus exhibited elastic characteristics, the dosage of lipo-PGE1 might be decreased after a definite administration period.

Visualization and quantification of the atrioventricular conduction axis in hearts with ventricular septal defect using phase contrast computed tomography.

OBJECTIVE: To visualize and quantify the atrioventricular conduction axis in the setting of ventricular septal defect using phase contrast computed tomography. METHODS: We used the SPring-8 synchrotron radiation facility in Hyogo prefecture in Japan, processing and reconstructing the data with 3-dimensional software. RESULTS: We studied 8 hearts obtained from patients known to have had ventricular septal defects, aged from 6 to 150 days, with a median of 24.5 days. None of the individuals, however, had undergone corrective surgery. The penetrating bundle was found at a median of 1.43 mm from the septal crest, with a range of 0.99 to 1.54 mm. The distance to the nonbranching bundle to the right ventricular endocardium was 1.10 mm, with a range from 0.49 to 2.49 mm, to the origin of the left bundle branch was 2.46 mm, with a range from 1.7 to 3.18 mm, and to the origin of the right bundle branch was 2.34 mm, with a range from 0.50 to 2.59 mm. The median distance from the edge of the caudal limb of the septomarginal trabeculation to the right bundle branch was 1.04 mm, with a range from 0.81 to 1.16 mm. CONCLUSIONS: We were able to show the precise location of the axis, with our findings suggesting that longitudinal sutures placed along the posteroinferior rim should be effective in avoiding iatrogenic injury, but sutures should not be placed in the valley between the limbs of the septomarginal trabeculation.

Excellent Restoration of Left Ventricular Compliance After Prolonged Del Nido Single-Dose Cardioplegia in an In Vivo Piglet Model.

Del Nido cardioplegia (DN) is used in congenital heart surgery and recently in adults, a single dose has been administered. However, the tolerable ischemic time has not been established. The objective is to evaluate the left ventricular (LV) function recovery and accompanying biochemical and histologic markers to clarify the tolerable ischemic time in an in vivo cardiopulmonary bypass (CPB) piglet model. Twenty-one piglets were subjected to either 90 minutes (with or without topical cooling; TC) or 120 minutes (with TC) of global ischemia induced by single-dose DN, while the other 7 served as the control group (CPB only). The CPB temperature was established with a perfusion temperature of 30°C. The LV function recovery was assessed by the percent change in end-systolic elastance (Ees) and the end-diastolic pressure-volume relationship (EDPVR). Creatine kinase-MB (CK-MB) levels and the mitochondrial score were also assessed. LV contractility assessed by %Ees after 90 and 120 minutes of ischemia (89.3 ± 20.6% and 57.9 ± 17.8%) was lower compared with the control group (122.6 ± 35.8%, P = 0.001). Conversely, LV compliance assessed by %EDPVR was preserved in both groups (102.7 ± 28.2% and 88.5 ± 24.0%), which was comparable to the control group (105.8 ± 36.9%, P = 0.531). There was no change in LV contractility after 90 minutes of ischemia with or without TC (89.3 ± 20.6% or 84.8 ± 16.2%, P = 0.657), whereas LV compliance was lower but not statistically different without TC (102.7 ± 28.2% vs 78.0 ± 38.9%). CK-MB and the mitochondrial score were equivalent between all groups. The proposed single-dose ischemic time for redosing is 90 minutes using TC.

[A New-born Case of Total Conus Defect and Single Coronary Artery with Situs Inversus Totalis Suspected Kartagener Syndrome].

We report a new-born case of total conus defect type ventricular septal defect (VSD) and single coronary artery with situs inversus totalis, suspected Kartagener syndrome clinically. After the birth, as the patient had suffered from respiratory distress due to high pulmonary blood flow through the large defect, surgery was planned at age of 14-days after birth. Under median sternotomy and cardiac arrest, patch closure of VSD was performed as ordinary fashion. In spite of the situs inversus totalis and single coronary artery arose from right coronary sinus, operator could have completed all of surgical procedure at the right side of patient as usual. No remarkable respiratory complication was seen postoperatively and she was discharged from hospital 18th day in a good condition.

A Devised Option of Neonatal Palliation for Compromised Tetralogy of Fallot with Absent Pulmonary Valve Syndrome.

Neonatal primary repair of tetralogy of Fallot (TOF) with absent pulmonary valve (APV) syndrome is associated with high mortality rates. Our plan involves a staged repair that avoids one-stage intracardiac repair (ICR), with a first palliation that closes the main pulmonary orifice using an expanded polytetrafluoroethylene (ePTFE) patch, pulmonary arterioplication, and an adjustable Blalock-Taussig (BT) shunt. This strategy was used for a neonatal case with TOF/APV syndrome with hypoplastic left ventricle (LV). There was evidence of subsequent progressive increase in the LV size, and bronchial compression was relieved and an ICR was performed successfully at 9 months of age.

Synergistic effects of remote perconditioning with terminal blood cardioplegia in an in vivo piglet model.

OBJECTIVES: This study tested the hypothesis that remote perconditioning offers effective and synergistic cardioprotection to terminal warm blood cardioplegia for prompt ventricular recovery after prolonged cardioplegic arrest in an in vivo piglet model. METHODS: Twenty-four piglets were subjected to 120 min of single-dose cardioplegic arrest and were divided into 4 groups according to the mode of reperfusion: control (simple aortic unclamp), remote perconditioning, terminal warm blood cardioplegia or remote perconditioning + terminal warm blood cardioplegia; remote perconditioning (4 cycles of 5-min ischaemia-reperfusion of the lower limb) was applied prior to aortic unclamping. Left ventricular systolic and diastolic functions were assessed by pressure-volume loop analysis at baseline and after 60 min of reperfusion. Biochemical injury was evaluated by plasma troponin T level. RESULTS: The control group showed decreased end-systolic elastance, preload recruitable stroke work and inverse of end-diastolic pressure-volume relationship of 51.3 ± 14.0%, 46.1 ± 22.5% and 34.8 ± 14.9%, respectively. Percentage recovery of end-systolic elastance and preload recruitable stroke work were significantly better with terminal warm blood cardioplegia (with or without remote perconditioning) (end-systolic elastance: 95% confidence interval, 38.6-84.1; preload recruitable stroke work: 95% confidence interval, 0.4-54.3). Percentage recovery of inverse of end-diastolic pressure-volume relationship was significantly better in the remote perconditioning groups (with or without terminal warm blood cardioplegia) (95% confidence interval, 1.6-41.6). No synergistic effects of remote perconditioning and terminal warm blood cardioplegia on troponin T release were noted. CONCLUSIONS: Remote perconditioning offers promising synergistic cardioprotection to terminal warm blood cardioplegia, implicating potential clinical benefit by contributing to prompt left ventricular functional recovery during paediatric open-heart surgery.

Intact Imaging of Human Heart Structure Using X-ray Phase-Contrast Tomography.

Structural examination of human heart specimens at the microscopic level is a prerequisite for understanding congenital heart diseases. It is desirable not to destroy or alter the properties of such specimens because of their scarcity. However, many of the currently available imaging techniques either destroy the specimen through sectioning or alter the chemical and mechanical properties of the specimen through staining and contrast agent injection. As a result, subsequent studies may not be possible. X-ray phase-contrast tomography is an imaging modality for biological soft tissues that does not destroy or alter the properties of the specimen. The feasibility of X-ray phase-contrast tomography for the structural examination of heart specimens was tested using infantile and fetal heart specimens without congenital diseases. X-ray phase-contrast tomography was carried out at the SPring-8 synchrotron radiation facility using the Talbot grating interferometer at the bending magnet beamline BL20B2 to visualize the structure of five non-pretreated whole heart specimens obtained by autopsy. High-resolution, three-dimensional images were obtained for all specimens. The images clearly showed the myocardial structure, coronary vessels, and conduction bundle. X-ray phase-contrast tomography allows high-resolution, three-dimensional imaging of human heart specimens. Intact imaging using X-ray phase-contrast tomography can contribute to further structural investigation of heart specimens with congenital heart diseases.

Three Dimensional Visualization of Human Cardiac Conduction Tissue in Whole Heart Specimens by High-Resolution Phase-Contrast CT Imaging Using Synchrotron Radiation.

BACKGROUND: The feasibility of synchrotron radiation-based phase-contrast computed tomography (PCCT) for visualization of the atrioventricular (AV) conduction axis in human whole heart specimens was tested using four postmortem structurally normal newborn hearts obtained at autopsy. METHODS: A PCCT imaging system at the beamline BL20B2 in a SPring-8 synchrotron radiation facility was used. The PCCT imaging of the conduction system was performed with "virtual" slicing of the three-dimensional reconstructed images. For histological verification, specimens were cut into planes similar to the PCCT images, then cut into 5-µm serial sections and stained with Masson's trichrome. RESULTS: In PCCT images of all four of the whole hearts of newborns, the AV conduction axis was distinguished as a low-density structure, which was serially traceable from the compact node to the penetrating bundle within the central fibrous body, and to the branching bundle into the left and right bundle branches. This was verified by histological serial sectioning. CONCLUSION: This is the first demonstration that visualization of the AV conduction axis within human whole heart specimens is feasible with PCCT.

Variability of Pulmonary Regurgitation in Proportion to Pulmonary Vascular Resistance in a Porcine Model of Total Resection of the Pulmonary Valve: Implications for Early- and Long-Term Postoperative Management of Right Ventricular Outflow Tract Reconstruction With Resulting Pulmonary Valve Incompetence.

INTRODUCTION: Pulmonary regurgitation (PR) is a major concern after right ventricular (RV) outflow tract surgery. We assessed the impact of physiological changes in pulmonary vasculature on hemodynamic severity of PR and RV function and their potential clinical implications for postoperative management using a porcine model with severe PR. MATERIALS AND METHODS: Eight porcine models of acute PR were established by means of resection of pulmonary valve on cardiopulmonary bypass. After separation from bypass and stabilization, blood flow in the main pulmonary artery was measured by a pulsed Doppler flowmeter, and RV systolic function was assessed on the basis of RV segment shortening (RVSS), which was analyzed by sonomicrometry. In the acute PR model, we verified the impact of pulmonary vascular resistance (Rp) on pulmonary regurgitant fraction (PRF) and RV function. Pulmonary vascular resistance was changed by manipulating the level of PaCo 2 and by inhalation of nitric oxide (NO). RESULTS: After bypass, the mean PRF was 40% ± 5%, and there was a deterioration of RV function. Under each ventilation condition (high CO2, low CO2, and NO 20 ppm), Rp was 836 ± 207 dyne × s × cm(-5), 499 ± 125 dyne × s × cm(-5), and 340 ± 102 dyne × s × cm(-5), respectively, and PRF was 60% ± 10%, 37% ± 5%, and 24% ± 4%, respectively, under each condition. They also showed a positive correlation in all animals. Cardiac output and RVSS were decreased by hypercapnia, while they were significantly improved after NO inhalation. CONCLUSIONS: This study indicates that low Rp after right ventricular outflow tract reconstruction (RVOTR) resulting in acute PR is advantageous in reducing the severity of PR and RV volume load. These findings may have clinical implications for early and long-term postoperative management of patients subjected to RVOTR with resulting pulmonary valve incompetence.

Inflammatory response to hyperoxemic and normoxemic cardiopulmonary bypass in acyanotic pediatric patients.

BACKGROUND: Hyperoxemic management during cardiopulmonary bypass (CPB) is still common, and there is no consensus about physiologic oxygen tension strategy (normoxemic management) during pediatric CPB. In this study, we compared the postoperative conditions and measures of inflammatory response among patients with acyanotic congenital heart disease subjected to either hyperoxemic or normoxemic management strategy during CPB. METHODS: We studied 22 patients with a ventricular septal defect and pulmonary artery hypertension. The patients were divided into two groups. Group I (n=9) received normoxemic management (PaO2=100-150 mm Hg) and group II (n=13) received hyperoxemic management (PaO2=200-300 mm Hg) during CPB. There was no difference between groups with regard to age, body weight, duration of CPB, and aorta clamping time or preoperative pulmonary hypertension (pulmonary pressure/systemic pressure [Pp/Ps]). In each group, the blood samples to measure the cytokine levels were collected before and after the CPB. RESULTS: Although we observed no statistically significant differences in postoperative intubation time, alveolar-arterial oxygen difference, creatine kinase MB level, and pulmonary hypertension (Pp/Ps) between group I (10.7±13.4 hours, 197±132 mm Hg, 148±58.6 IU/L, 42.8%±22.1%, respectively) and group II (27.8±36.5 hours, 227±150 mm Hg, 151±72.6 IU/L, 50.4%±16.0%, respectively), levels of median interleukin 6 and tumor necrosis factor α were lower in group I (129.8 and 17.0 pg/mL, respectively) than that in group II (487.8 and 22.5 pg/mL, respectively). CONCLUSION: During the CPB in acyanotic pediatric patients, normoxemic management can minimize the systemic inflammatory response syndrome associated with CPB. We can apply this physiologic oxygen tension strategy to surgical advantage during heart surgeries in acyanotic pediatric patients.

Distal aortic arch aneurysm associated with persistent fifth aortic arch.

Persistent fifth aortic arch (PFAA) associated with interruption of the fourth aortic arch is a rare malformation, usually requiring surgical intervention in childhood. A 51-year-old woman developed a distal aortic arch aneurysm associated with PFAA after patch aortoplasty for coarctation of the aorta at the age of 18. To our knowledge, this is the first reported case of a distal aortic arch aneurysm associated with PFAA. Residual tissues of the ductus and PFAA, which is not a definitive aortic arch, and the implanted synthetic patch may have been related to the development of the aneurysm. Graft interposition between the proximal border of PFAA and the descending aorta was performed because severe adhesions impeded the application of the fourth aortic arch as a proximal anastomotic site of the graft. Accurate diagnosis and sufficient understanding of PFAA allow an appropriate surgical treatment in childhood with a good result over the long term.

Surgical reoxygenation injury of the myocardium in cyanotic patients: clinical relevance and therapeutic strategies by normoxic management during cardiopulmonary bypass.

Cyanotic hearts are associated with depleted endogenous antioxidants (glutathione peroxidase, superoxide dismutase, and catalase), and thereby is more susceptible to myocardial ischemia/reperfusion injury during open heart surgery compared with acyanotic ones. Clinically, when surgery is performed on cyanotic infants, cardiopulmonary bypass (CPB) is usually initiated at high PaO(2), without consideration of possible cytotoxic effects of hyperoxia. The concept of "surgical reoxygenation injury of cyanotic myocardium" was proposed, wherein unintended abrupt reoxygenation of cyanotic myocardium at the onset of routine CPB causes oxygen-mediated injury, which may render the reoxygenated myocardium more susceptible to subsequent surgical ischemia/reperfusion injury and accentuates post-CPB myocardial dysfunction. The experimental studies using acute and chronic hypoxia models confirmed the role of reoxygenation injury mediated by reactive oxygen species in the pathogenesis of post-CPB myocardial dysfunction and addressed the importance of controlling PaO(2) at the onset of CPB. The clinical relevance of this injury was shown by subsequent clinical studies, which demonstrated depleted antioxidant reserve capacity and troponin release during the initial reoxygenation on hyperoxic CPB prior to cardioplegic arrest. Furthermore recent randomized clinical trials verified that hyperoxic CPB provokes biochemical multi-organ damage including myocardium, lung, liver, and brain after open heart surgery in cyanotic patients, which can be successfully reduce by normoxic CPB management (i.e., reducing PaO(2) at onset of CPB, gradual reoxygenation and controlled reoxygenation protocol). Based on these experimental and clinical studies, avoidance of using hyperoxic PaO(2) on routine CPB is strongly recommended in the cyanotic patients.

Reversal of oxidant-mediated biochemical injury and prompt functional recovery after prolonged single-dose crystalloid cardioplegic arrest in the infantile piglet heart by terminal warm-blood cardioplegia supplemented with phosphodiesterase III inhibitor.

PURPOSE: The benefit of terminal blood cardioplegia (TWBCP) is insufficient after prolonged ischemia associated with inevitable oxidant-mediated injury by this modality alone. We tested the effects of TWBCP supplemented with high-dose olprinone, which is a phosphodiesterase III inhibitor, a clinically available compound with the potential to reduce oxidant stress and calcium overload. We evaluated the effects with respect to avoiding oxidant-mediated myocardial reperfusion injury and prompt functional recovery after prolonged single-dose crystalloid cardioplegic arrest in a infantile piglet cardiopulmonary bypass (CPB) model. METHODS: Fifteen piglets were subjected to 90 min of cardioplegic arrest on CPB, followed by 30 min of reperfusion. In group I, uncontrolled reperfusion was applied without receiving TWBCP; in group II, TWBCP was given; in group III, TWBCP was supplemented with olprinone (3 µg/ml). Myocardial performance was evaluated before and after CPB by a left ventricular (LV) function curve and pressure-volume loop analyses. Biochemical injury was determined by measurements of troponin-T and lipid peroxide (LPO) in coronary sinus blood. RESULTS: Group III showed significant LV performance recovery (group I, 26.5% ± 5.1%; group II, 42.9% ± 10.8%; group III, 81.9% ± 24.5%, P < 0.01 vs. groups I and II), associated with significant reduction of troponin-T and LPO at the reperfusion phase. No piglets in group III needed electrical cardioversion. CONCLUSION: We concluded that TWBCP with olprinone reduces myocardial reperfusion injury by reducing oxidant-mediated lipid peroxidation, and it accelerates prompt and persistent LV functional recovery with suppression of reperfusion arrhythmia.