The objective of this study was to investigate the edema suppresive effect of single-dose crystalloid cardioplegia against immature myocardium. 50 puppies (3-21-day-old) were separated into 4 groups by the method of myocardial preservation, group A: preservation at 30°C, group B: topical cooling used only, group C: topical cooling with cardioplegia (St. Thomas Hospital solution: 4°C, pH 7.8, 350 mOsm/l), group D: topical cooling with oxygenated cardioplegia, and gravimetric water content of myocardium (%) was measured at control, 5, 30, 60, 90, 120, 150, and 180 min after aortic clamp. All hearts had elevated myocardial water content with linear change pattern, although which in groups A and B was consecutively increased while which in groups C and D was increased immediately after aortic clamp followed by slow increase thereafter. Increase of myocardial water content from 5 min after aortic clamp in group B at 90 min was significantly higher (p<0.01) than those in groups C and D, at 180 min that in group A was higher than that in group C and that in group B was higher than those in groups C and D (p<0.05, p<0.01, p<0.01, respectively). This study has shown that evolution of myocardial edema was suppressed by the administration of cardioplegia, while myocardial water content was seemingly higher because coronary vascular dilatation resulted in increase of intravascular water. We could not find the effect of the topical cooling only or oxygenated cardioplegia.

Spinal cord injury is a dreaded and serious complication of operative procedures on the descending aorta. To avoid this serious complication, 53 patients underwent somatosensory evoked potential (SEP) monitoring during operations on the aorta which required cross-clamping of the descending aorta. 38 patients whose SEPs were kept normal during and after operations did not develop spinal cord injury. Among the 14 patients who developed both abnormal decrease in amplitude and elongation of peak latency, 13 lost their SEPs during aortic cross-clamping. Peripheral nerve ischemia seemed to be the cause of those abnormalities in 8 to whom cross-clamping was given to the abdominal aorta. Inadequate perfusion of the distal aorta was suspected in 6 to whom cross-clamping was given to the descending thoracic aorta. In these cases, however, SEP monitoring was not specific in differentiating spinal cord ischemia from peripheral nerve ischemia. Spinal cord injury was noted in only one of the 6 patients. The remaining one patient developed complete loss of SEP and spinal cord injury on the first postoperative day despite the well preserved SEP during the operation. Since this patient underwent flow reversal and thromboexclusion method for the dissecting aneurysm, gradual thrombotic occlusion of the important radicular arteries draining to spinal cord might have resulted delayed appearance of the spinal cord injury. In conclusion, SEP monitoring is the reliable method to detect the spinal cord ischemia which might be developed during cross-clamping of the descending aorta. However, this method bears limitation in its clinical application due to the following reasons. First, intraoperative SEP monitoring cannot predict delayed occurence of spinal cord injury. Secondly, this method cannot detect the qualitative extent of ischemia of spinal cord and the safe range of the cross-clamp time.

The authors experienced a case of fatal cerebellar, and brainstem infarction accompanying clamping of the left subclavian artery during operation for thoracic aortic aneurysm. Autopsy of this case revealed that right vertebral artery became markedly hypoplastic distal to the posteroinferior cere bellar artery, and left vertebral and basilar arteries were occluded by thrombus formation. These findings indicate that clamping of the dominant left subclavian artery is responsible for severe vertebrobasilar ischemia producing the fatal brain infarction. Since the occurrence of this devastating complication, we have performed pancerebral angiography and balloon occlusion test of the left subclavian artery in patients who might undergo proximal clamping of the aortic arch between the left carotid artery and the left subclavian artery during operations for thoracic aortic aneurysm. Selective perfusion of the left subclavian artery is then planned for those with abnormal vertebrobasilar communications producing neurological signs.

Left ventricular hypertrophy in patients with aortic valve disease has long been recognized as a significant risk factor for aortic valve replacement. Higher operative mortality in such patients has been attributed to poor myocardial preservation. In these patients improvement of left ventricular subendocardial blood flow during reperfusion seems to be mandatory to avoid subendocardial injury. Therefore, we attempted to increase subendocardial blood flow during reperfusion by terminal warm blood cardioplegia (TWBCP) followed by controlled aortic root reperfusion (CARR) in patients requiring isolated aortic valve replacement. The patients with TWBCP and CARR had a tendency towards severe left ventricular hypertrophy and more advanced NYHA function class compared to those with hypothermic cardioplegia alone. Nevertheless, the patients with TWBCP and CARR showed significantly better recovery of left ventricular function, i.e., spontaneous recovery of beating and higher cardiac index as well as left ventricular stroke work index, despite significantly less catecholamine support. These resuls suggest that TWBCP followed by CARR may offer significant benefits over unmodified reperfusion during aortic valve replacement for patients with severe left ventricular hypertrophy.

Three-channeled aortic dissection of the ascending aorta is rare. A 38-year-old man was given a diagnosis of DeBakey type I aortic dissection with three-channel at the ascending aorta on a chest CT scan. Right axillar and left femoral artery and two-stage right atrial cannulas were used to institute cardiopulmonary bypass. Hemiarch replacement was performed. The open proximal anastomosis technique was used under deep hypothermic circulatory arrest and selective cerebral perfusion. This three-channeled aortic dissection was thought to be produced by DeBakey type II dissection first followed by a retrograde dissection of DeBakey type III b. Since obstruction of the brachiocephalic artery due to the expansion of the pseudolumen was found during rewarming, reconstruction of the brachiocephalic artery was necessary. The present case was treated successfully by right axillary artery perfusion and subsequent reconstruction of the brachiocephalic artery.

Subclavian arterial aneurysms are relatively rare compared to aortic aneurysms. The common causes of subclavian arterial aneurysms are arteriosclerosis, non-specific inflammation, thoracic outlet syndrome, and trauma. A case of a subclavian arterial aneurysm is reported. The patient was a 57-year-old woman. She had no previous history of hypertension, infection and trauma. She underwent complete resection of the aneurysm and reconstruction of right subclavian artery. Exploration of the aneurysmal wall revealed circumferential ridge which caused stenosis of the right subclavian artery at the orifice of the aneurysm. It has been suggested that a subclavian arterial aneurysm developed as a result of abnormal development of the embryologic right fourth and distal sixth aortic arches.

Sixteen patients with congenitally corrected transposition of the great arteries (CTGA) underwent operative closure of ventricular septal defects (VSD). Ages of the patients ranged from 10 months to 25 years. Three different approaches were employed to access to the defect: through right ventriculotomy 3, through left ventriculotomy 5, and de Leval's maneuver 8. Here, right or left ventricle refers to its anatomic morphology. Early postoperative death occurred in a patient who concomitantly underwent extracardiac couduit repair between left ventricle and pulmonary trunk. Late death occourred in 5 (left ventriculotomy in 1 and righ ventriculotomy in 4), among whom 2 expired suddenly of unknown cause (one in each of the right and left ventriculotomy), and 1 expired of pneumonia. Two other deaths were related to their reoperations for replacement of the incompetent left atrioventricular (AV) valve. Another patient who had been repaired by de Leval's maneuver also underwent replacement of the left AV valve and survived. Two patients who had undergone left ventriculotomy developed com-plete heart block leading to implantation of permanent pacemaker. Postoperative complete heart block was temporarily noted in a patient who had been repaired by de Leval's maneuver but returned to sinus rhythm on the 10th postoperative day. Late postoperative function of the systemic ventricle was assessed in 8 by gated radionuclide ventriculography. Calculated ejection fractions in each of the methods were the followings. Left ventriculotomy: 0.38, 0.47. Right ventriculotomy: 0.13. de Leval's maneuver: 0.29, 0.54, 0.66, 0.47, 0.36. These results draw us to the following conclusions that either ventriculotomy holds its drawbacks, that is, left ventriculotomy is apt to develop complete heart block and right ventriculotomy can predispose incompetent left AV valve ultimately leading to the fatal congestive heart failure. de Leval's maneuver, however, is rare to be complicated by the above morbidity and is considered to be the best operative method currently available.

It is commonly believed that prosthetic valve implantation in actively infected patients is to be avoided. After normalization of C-reactive protein and white blood cell counts, and sterilization of blood cultures by treatment with antibiotics, we performed valvular surgery. We performed mitral valve repair in cases where the mitral valve lesion did not involve the annulus. From July 1992 to November 1996, 13 patients (mean age, 50 years) were treated surgically for infective endocarditis (IE) at Kansai Medical University. Twelve of the patients had native valve endocarditis (NVE), and 1 had prosthetic valve endocarditis (PVE). In 6 patients, the causative organisms were determined. These included: α-Streptococcus in 4 patients, Enterococcus in 1, and methicillin-resistant Staphylococcus aureus (MRSA) in 1. The affected valves were as follows: aortic valve alone in 4 patients, mitral valve alone in 6, aortic and mitral valves in 2, and a prosthetic aortic valve in 1. The PVE was due to a MRSA infection which occurred 9 months after aortic valve replacement. All patients were treated preoperatively for heart failure and the infection. The surgical procedures performed were: aortic valve replacement in 4 patients, mitral valve replacement in 3, mitral repair in 3, double valve replacement in 2, and re-aortic valve replacement in 1. There were no deaths or recurrences of IE in hospital or during follow-up to date. In all of the mitral valve repair cases, the mitral regurgitation on follow-up echocardiograms was grade I. Our results show that surgical treatment of IE after management of preoperative conditions can be successful. Furthermore, despite the absence of laboratory findings indicative of ongoing inflammation or infection, pathologic examination revealed active inflammatory reactions and organisms in 4 cases. In 1 patient, MRSA was culthued from an annular abscess that was resected intraoperatively. We suggest that cessation of antibiotic therapy be regarded with caution and suggest that the infected site must be resected surgically.