[A case report of right ventricular pseudoaneurysm after extracardiac valved conduit surgery].
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Biomedical subjects
Publications and source records attributed to F Okamoto.
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This study tests the hypothesis that aspartate enrichment of glutamate-blood cardioplegia improves metabolic and functional recovery after ischemic and reperfusion damage. Ischemic and reperfusion damage were produced in 15 dogs by 45 minutes of aortic clamping at 37 degrees C and 5 minutes of blood reperfusion, before 2 more hours of aortic clamping (simulated operation). Six received multidose blood cardioplegia at 4 degrees C. In nine others, the cardioplegic solution was infused at 37 degrees C for the first 5 minutes, followed by multidose infusions at 4 degrees C. Four received 26 mmol glutamate-enriched cardioplegic solution. In five, the glutamate (13 mmol) cardioplegic solution was enriched with aspartate (13 mmol). Oxygen uptake and ventricular function (stroke work index, left atrial pressure) were measured. These data suggest aspartate enrichment produced the highest oxygen uptake (32 +/- 4 versus 17 +/- 2 ml/100 gm for glutamate and 7 +/- 1 ml/100 gm for 4 degrees C blood cardioplegia). Complete functional recovery occurred in aspartate/glutamate-treated hearts (stroke work index 90% +/- 4%, left atrial pressure 12 +/- 2 mm Hg), whereas recovery was incomplete with both glutamate alone (stroke work index 66% +/- 14%, left atrial pressure 20 +/- 3 mm Hg) and 4 degrees C blood cardioplegia at low cardiac outputs. Eight of 10 hearts not receiving aspartate failed at high cardiac outputs. Aspartate enrichment of glutamate-blood cardioplegia improves recovery after severe ischemic/reperfusion damage by improving oxidative metabolism during cardioplegic infusion and during postischemic work.
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Cold blood cardioplegic techniques are limited in their ability to protect energy-depleted hearts during aortic clamping. This study extends our previous observations on the benefits of amino acid (L-glutamate) enrichment of blood cardioplegic solutions as well as the added metabolic benefits of normothermic induction of cardioplegic arrest to increase the rate of repair of energy-depleted hearts. The results demonstrate that L-glutamate enrichment of blood cardioplegic solutions significantly improves metabolic recovery (greater oxygen consumption, better anaerobic metabolism) and ventricular performance. Normothermic induction of glutamate-enriched cardioplegia allowed complete recovery of myocardial metabolism and function compared to cold blood cardioplegic technique and may be used as a form of "active resuscitation" of energy-depleted hearts.
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In order to perform intracardiac repair safely during aortic cross clamping, we designed this study to evaluate the protective effect of coenzyme Q10 (CoQ10) on hypertrophied ischemic myocardium from the aspect of energy metabolism. Six to nine months preceding the study, aortic bandings were carried out on 14 puppies to produce left ventricular hypertrophy (LVH). These dogs with LVH were then subjected to total cardiopulmonary bypass and were evenly divided into control and CoQ10-treated groups (10 mg/kg of intravenous administration plus 1 mg/kg per hr of intracoronary injection). Myocardial ischemia was induced by aortic cross clamping for 2 hr under moderate systemic hypothermia. The results indicated that the administration of CoQ10 had a protective effect on hypertrophied ischemic myocardium, since depletion of high-energy phosphate (HEP) was uniformly prevented, and accumulation of lactate was simultaneously decreased during the 2 hr of aortic cross clamping. On the other hand, there were marked exhaustion of HEP and rapid increase in lactate following the 2 hr of ischemia in the control group, these being much more predominant in the subendocardial layer.
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Factors affecting the surgical results of total anomalous pulmonary venous drainage were evaluated in 17 patients in an attempt to establish an appropriate plan of management. The mortality rate correlated with age, size of interatrial communication, arterial oxygen saturation and left heart volume but not with pulmonary to systemic systolic pressure ratio, vascular resistance ratio and right ventricular volume. In cases where the symptoms appeared early in life, left heart volume was small and clinical features were severe. Four children with a left ventricular end-diastolic volume of less than 65% of normal died of low cardiac output syndrome. In those with an unusually small left heart, enlargement of the left atrium and/or delayed ligation of the anomalous vertical vein were considered more favorable. Left atrial and ventricular volumes were restored to normal after the surgery.
This study tests the hypothesis that warm induction of cardioplegia prior to prolonged maintenance by multidose infusions of cold blood cardioplegic solution would increase the tolerance of energy-depleted hearts to subsequent aortic clamping. Eighty percent depletion of subendocardial adenosine triphosphate (ATP) was produced in 30 dogs by 45 minutes of normothermic ischemia. This was followed either by unmodified blood reperfusion or 2 additional hours of aortic clamping with multidose cold blood cardioplegia. We compared a brief (5 minute) period of 37 degrees C cardioplegic induction to standard 4 degrees C blood cardioplegic induction to determine if warm induction would enhance metabolic and functional recovery. Warm cardioplegic induction resulted in more oxygen consumption than cold induction (16.9 versus 8.1 cc/100 gm), and lower levels of glucose-6-phosphate (G6P), suggesting better aerobic metabolism (0.97 versus 1.87 microM/gm wet weight). Prompt repletion of creatine phosphate (CP) occurred with warm and cold cardioplegic induction, although ATP levels levels remained low. Hearts undergoing ischemia and unmodified reperfusion consumed insufficient oxygen to meet basal metabolic needs during reperfusion (7 cc/100 gm below requirement) and recovered only 33% +/- 5% of control left ventricular performance. Better function occurred with cold cardioplegic induction (63% +/- 5%), and almost complete recovery (85% +/- 5%) occurred when warm induction of cardioplegia was used. We conclude that warm induction followed by prolonged cold multidose blood cardioplegic arrest enhances aerobic metabolism, results in normal left ventricular performance, and improves tolerance of aortic clamping in energy-depleted hearts.
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In a total of 107 cases with transposition of the great arteries (TGA-s), 20 died preoperatively and 76 underwent surgical treatment: 11 palliative and 65 primary corrective surgeries, with hospital mortality 36.4% and 46.2% respectively. Of 31 survivors after Mustard operation, tricuspid regurgitant murmur and ECG abnormalities were recognized at 26.7% and 33.3% respectively in simple TGA, and 62.5% and 37.5% respectively in complicated TGA during an average follow-up of 4 years. Angiocardiogram, performed more than 2 years postoperatively, revealed decreased ejection fraction (EF) with compensatory increase of right ventricular end-diastolic volume (RVEDV): EF 0.43 +/- 0.04, RVEDV 168 +/- 41% of normal in simple TGA and 0.36 +/- 0.12, 173 +/- 55% in complicated TGA. In 3 long-term survivors of arterial switch operation (Stansel, Kaye), no serious complications were observed, and ejection fraction and echocardiographic findings of systemic ventricle showed an earlier normalizing than in Mustard operation: EF 0.65 or more when no VSD leakage and pre-ejection period (PEP/ejection time (ET) 0.35 +/- 0.05 after switch operation, 0.45 +/- 0.05 in simple TGA and 0.47 +/- 0.07 in complicated TGA after Mustard operation. From these long-term postoperative evaluations, our policy at present is to prefer arterial switch operation to Mustard operation in corrective surgery for TGA.
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