Fumikazu Nomura

Evaluation of prostacyclin analogue OP-41483 as an adjunct to crystalloid cardioplegia in infants and children

A chemically stable prostacyclin analogue (PGI2-A, carbacyclin, OP-41483) was evaluated as an adjunct to potassium cardioplegia in infants (n = 13) and children (n = 32), in whom the current potassium cardioplegia may be limited in its effects. PGI2-A was added in a dose of 300 micrograms/L to the potassium cardioplegic solution. Postoperatively, peak levels of the myocardial-specific isoenzyme of creatine kinase (MB-CK) were compared for the PGI2 group and a control group (n = 65). In patients 1 year of age or older (n = 32 and 49 for the PGI2 and control groups, respectively), the MB-CK level was significantly lower in the PGI2 group only when compared between the subgroups with an aortic cross-clamp time of 120 minutes or more (n = 9 and 10; MB-CK level, 35.2 +/- 15.6 vs 68.3 +/- 32.4 IU/L;p less than 0.05). In patients less than 1 year of age, in whom aortic cross-clamp times were generally less than 120 minutes, the MB-CK level was also lower in the PGI2-A group than in the control group (n = 13 and 16; MB-CK level, 33.6 +/- 14.3 vs 61.6 +/- 36.3 IU/L;p less than 0.05). Infants less than 6 months of age (n = 18) underwent ultrastructural assessment of left ventricular myocardial biopsy specimens, and the PGI2-A group showed better results in mitochondrial and intracellular edema scores. This clinical trial showed beneficial effects of PGI2-A used with crystalloid potassium cardioplegia in infants and children.

Response of right ventricular systolic function to exercise stress: Effects of pulmonary vascular resistance on right ventricular systolic function

To elucidate factors influencing responses of right ventricular systolic function to exercise stress, we evaluated the right ventricular ejection fraction and peak ejection rate with two different loading conditions, atrial septal defect and mitral stenosis, at rest and during exercise by means of gated equilibrium blood pool radionuclide ventriculography. In both atrial septal defect and mitral stenosis, strong correlations between changes in the right ventricular ejection fraction with exercise and pulmonary vascular resistance at rest (r = −0.97, p < 0.001; r = −0.86, p < 0.0005: respectively) were found. Significant correlations between changes in the right ventricular peak ejection rate with exercise and pulmonary vascular resistance at rest (r = −0.85, p < 0.05; r = −0.75, p < 0.01: respectively) were found in atrial septal defect and mitral stenosis. Both the right ventricular ejection fraction and peak ejection rate were lower during exercise than at rest when pulmonary vascular resistance at rest was more than 200 dynes·sec·cm−5·m2 in both atrial septal defect and mitral stenosis. In conclusion, right ventricular systolic function responding to exercise stress was influenced by the pulmonary vascular resistance in both atrial septal defect and mitral stenosis.

Application of Ultra Short Acting Beta Blockade (Esmolol) in Pediatric Open Heart Surgery: A Trial in Total Anomalous Pulmonary Venous Return

Abstract Background: In the repair of total anomalous pulmonary venous return (TAPVR) under cardiopulmonary bypass, esmolol, ultra short acting beta blocker, was applied to obtain low heart rate and weak ventricular contraction under mild hypothermic cardiopulmonary bypass. Methods: Five infants aged from 14 to 158 days with an average of 70 days, underwent a primary or palliative repair of TAPVR. The type of anomalous return was supracardiac type (2), infracardiac (2), and intracardiac (1). A primary repair was done in three for isolated TAPVR with bypass time of 65 to 76 minutes, and a palliative repair for two with complex anomalies with bypass time of 64 and 87 minutes. Results: There was one operative death from cerebral bleeding in an infant with complex TAPVR who underwent simultaneous pulmonary banding. Conclusion: This strategy seems to be applicable in pediatric cardiac surgery when aortic cross‐clamping is better to be avoided and the surgery is mainly limited to the atrial level.

Assessment of Prostacyclin and Thromboxane A2 Release during Reperfusion after Global Ischemia Induced by Crystalloid Cardioplegia – Comparison between Warm and Cold Ischemia

The metabolites of prostacyclin (PGI2) and thromboxane A2 (TxA2), 6-keto-PGF1 alpha and thromboxane B2 (TxB2), were investigated during reperfusion (RP) following warm (37 degrees C, 60 min, n = 9) or cold (15 degrees C, 120 min, n = 11) ischemia induced by cold (4 degrees C) or normothermic (30 degrees C) K+ cardioplegia (CP) in isolated canine hearts subjected to global ischemia and RP. 6-Keto-PGF1 alpha flux was significantly higher (p less than 0.025) in the warm group at 1, 5, and 10 min of RP (4,202 +/- 1,412, 2,475 +/- 1,875, and 1,255 +/- 633 pg/g.min, mean +/- SD) compared to those in the cold group (1,504 +/- 1,245, 434 +/- 641, and 370 +/- 329 pg/g.min). TxB2 flux was small in amount compared to 6-keto-PGF1 alpha in both groups. Regarding the coronary hemodynamics, the cold group alone showed statistically significant relationships of coronary sinus blood flow to TxB2 level and TxB2/6-keto-PGF1 alpha ratio in coronary sinus blood. Also, coronary vascular resistance showed linear relations to these two parameters of the metabolites. In a supplementary experiment only with cold ischemia for 180 min, 6-keto-PGF1 alpha was released at each coronary flush-out by CP and the incremental amount showed a gradual increase during ischemia. These results indicated that significant production and release of PGI2 occurred during ischemia and RP following CP arrest and these related to the degree of myocardial damage while the response of TxA2 seemed less significant. The role of PGI2 release during RP following cardioplegic arrest was discussed.

Direct anastomosis of pulmonary artery-to-right ventricular outflow for correction of tetralogy of fallot with pulmonary atresia

A case of tetralogy of Fallot with well-developed infundibulum and pulmonary atresia was successfully repaired with direct anastomosis to reconstruct the pulmonary arterial trunk without using an extracardiac conduit. This technique may give the maximum chance for growth of the new pulmonary trunk and vasculature.