Aortic arch replacement with proximal first technique.

BACKGROUND: Deep hypothermic circulatory arrest (DHCA) without retrograde cerebral perfusion (RCP) has a strict time limit. We modified a surgical technique for anastomosis to shorten the period of DHCA and unilateral cerebral perfusion (UCP). METHODS: Between March 1993 and August 2001, retrospective analysis was done on 23 consecutive patients, who underwent aortic arch replacement with branches. The patients were divided into two groups: DHCA group and UCP group. The DHCA group, in which DHCA alone and without additional cerebral perfusion was performed, comprised of nine patients. Proximal aortic anastomosis was performed first during systemic cooling; then both the brachiocephalic artery and left carotid artery were reconstructed with the branches of the artificial graft during circulatory arrest; thereafter, cerebral and coronary perfusions were resumed. The UCP group, in which DHCA was not used but right hemisphere perfusion during deep hypothermia was performed when the origin of brachiocephalic artery was safely clamped, consisted of 14 patients. RESULTS: Mean time of DHCA was 18.8+/-4.2 minutes and that of right hemisphere perfusion time was 11.0+/-3.8 minutes, respectively. Twenty-one patients survived the surgery (91.3%), and two (8.7%) died during hospitalization. Transient cerebral complication occurred in four patients in the DHCA group and all recovered. Logistic regression analysis revealed that DHCA was the only parameter to significantly influence temporary neurological dysfunction. There was no other significant difference between the two groups. CONCLUSION: With our modified and simple surgical technique for aortic arch repair, we were able to successfully shorten the DHCA time and right hemisphere perfusion time. However, because DHCA was the only parameter to significantly influence temporary neurological dysfunction, some form of continuous cerebral perfusion at deep hypothermia may be a safer method to preserve cerebral function.     

Left thoracotomy approach in reoperative off-pump coronary revascularization

Objective: Reoperative coronary bypass grafting is at high risk. Particularly in redo cases where the patent graft is running near the midline of the sternum, the graft may be exposed to injury by a median sternotomy and subsequent dissection. Whereas, off-pump bypass grafting from the left axillary artery or descending thoracic artery by a left thoracotomy approach is safe for preventing graft damage.Methods: From March 1998 to February 2002, we performed off-pump coronary artery bypass grafting by a left thoracotomy approach in 9 patients. The left axillary artery was used as the inflow vessel in 4 cases, and the descending thoracic, aorta in 5.Results: The radial artery was anastomosed proximally to the axillary artery in 4 cases and the descending thoracic aorta in one case. The saphenous vein graft was anastomosed, proximally to the descending thoracic aorta in 4 cases. Transdiaphragmatic minimally invasive bypass grafting for the right coronary artery was simultaneously performed in 3 cases. Postoperative cardiac events were ventricular arrhythmia in 6 cases and supraventricular arrhythmia in 3 cases. There was no damage to the patent grafts. Postoperative coronary angiography performed, in 8 cases revealed all the grafts to be patent without stenosis. Cardiac symptoms were not found after the operation in any of the cases.Conclusions: These procedures can prevent the injury to patent grafts caused by a median sternotomy, and will be one of the useful strategies for reoperative off-pump coronary artery bypass grafting.     

Outcomes in patients with interrupted aortic arch and associated anomalies: a 20-year experience.

OBJECTIVE: The surgical results for the repair of interrupted aortic arch (IAA) have evolved in recent years. We report our results for staged repair of this complex congenital malformation. METHODS: Sixty-five patients (mean age, 16.9+/-41.7 days) were diagnosed with IAA and referred for surgical therapy. The surgical management strategy at our institution between 1982 and 2005 has been one-stage complete repair (n=13) or staged repair (n=52) in selected patients. Non-complex patients (group I, n=51) had a ventricular septal defect (87%), aortopulmonary window (8%), and left ventricular outflow tract obstruction (27%). Group II (n=14) were patients with Taussig-Bing double outlet right ventricle (n=6) or truncus arteriosus (n=8). Method of staged repair of IAA was to transect and turn down the left carotid artery and anastomosis it to the descending aorta (n=41) or graft interposition (n=2) combined with a pulmonary artery (PA) banding followed in a few months by delayed ventricular septal defect (VSD) closure and PA de-banding. RESULTS: There were 5 early and 10 late deaths. The actuarial survival including early mortality was 92% at 1 year, 81% at 5 years, and 76% at 10 and 15 years. There was an 81% 15-year survival for children in group I compared with a 54% for children in group II (p<0.001). Risk factors for increased mortality by univariate analysis were as follows: (1) primary aortic anastomosis (p=0.03), (2) presence of complex anomalies (p=0.05), and (3) initial IAA repair performed before 1994 (p=0.05). Actuarial freedom from any type of aortic reoperation or intervention was 86% at 1 year, 69% at 5 years, and 60% at 10 and 15 years. Univariate and multivariate analyses identified no tested variables as risk factors for reoperation. The majority (86%) was in New York Heart Association (NYHA) class I, and 14% remained in NYHA class II. During the postoperative course there were no neurologic deficits, seizures, and growth disturbances in any patient. CONCLUSION: Staged repair of IAA using a left carotid artery turn down can be safely applied in IAA patients with and without other intracardiac anomalies with good results. Use of the left carotid artery for arch reconstruction did not result in any detectable neurological events or growth disturbances later in life. Associated anomalies played an important role in outcomes. The long-term probability for reoperation and/or reintervention remains high regardless of operative technique.     

Experimental focal cerebral ischemia produced by embolization with silicone cylinder in normotensive (NTR) and spontaneously hypertensive rats (SHR): comparison of neurological and pathological findings

A focal cerebral ischemic model was produced by occlusion of the intracranial main cerebral artery with a silicone cylinder in normotensive (NTR) and spontaneously hypertensive rats (SHR). Main cerebral artery could be successfully occluded in approximately 90%. The most frequent embolized site was the distal part of the internal cerebral artery (ICb) and less frequently the horizontal segment of the anterior cerebral artery (Al). Mortality rate of NTR with ICb occlusion (NTR-ICb) was 43% at 72 hours after embolization and that of SHR with ICb occlusion (SHR-ICb) was 67% at 24 hours after embolization. NTR-ICb showed neurological signs (i.e. circling movement, hemiparesis, poor response to pain stimuli) and histologically, showed infarction in the deep cerebral structures (i.e. thalamus, hypothalamus, hippocampus, and internal capsule) accompanied with mild disruption of blood-brain barrier (BBB). SHR-ICb showed more serious neurological signs and more severe cerebral infarction in the deep cerebral structures with severe disruption of BBB. In SHR-ICb, ischemic cerebral edema was more prominent which may deteriorate symptoms and pathological findings compared to NTR-ICb. This embolization model is proposed to be useful for studying the pathophysiology of focal cerebral ischemia, especially, early ischemic edema.     

A case of unruptured anterior temporal artery aneurysm showing pupil-sparing oculomotor palsy

The authors report a case of unruptured anterior temporal artery aneurysm showing pupil-sparing oculomotor palsy. The patient was a 55-year-old male with the complaints of left blepharoptosis and diplopia. He had a history of tuberculous meningitis 9 years previously, and since then he suffered from paraparesis of lower extremities and bladder and bowel disturbance. Neurological examination on admission revealed left blepharoptosis and disturbance of medial and vertical movement of the left eye ball, but the pupils were isocoric with normal light reaction. Carotid angiography demonstrated that the left internal carotid artery was tortuous toward the medial side in the C2 portion, and the saccular aneurysm was present in the anterior temporal artery 3 mm distal from the middle cerebral artery. At operation it was revealed that the aneurysm which had a diameter of 17 mm located in the proximal portion of the anterior temporal artery, and compressed the dorsal aspect of the oculomotor nerve. A month after operation the left oculomotor palsy disappeared. There had been no report of the case of unruptured middle cerebral artery aneurysm causing oculomotor palsy. Pupil-sparing oculomotor palsy is characteristic of diabetic oculomotor palsy, and rare cases showing pupil-sparing oculomotor palsy are caused almost by aneurysms of the internal carotid-posterior communicating artery junction. Anatomical study revealed that the parasympathetic fibers which go to the pupil constrictor muscle were in the dorsomedial aspect of the oculomotor nerve in the subarachnoid portion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Light microscopy of GTP-binding protein (Go) immunoreactivity within the retina of different vertebrates

To examine species differences in the distribution pattern of guanosine triphosphate (GTP)-binding protein (Go) within the vertebrate retina, paraffin-embedded retinae from a number of vertebrate species, including the goldfish, frog, turtle, chicken, monkey, and human, were immunohistochemically stained with affinity-purified antibody against the alpha-subunit of Go. Go-immunoreactive products were found to be located in the neuropil, but not in the cell bodies of neurons, in the retina of all these species. However, some species differences were observed. In the frog, monkey and human, the inner plexiform layer (IPL) was homogeneously stained with this antibody, but in the goldfish, turtle and chicken, the IPL was heterogeneously stained. In the frog, chicken, turtle and human, the outer plexiform layer (OPL) was densely stained with this antibody, but in the goldfish and monkey, the OPL was rather faintly immunoreactive to the antibody. In the goldfish, monkey and human, the outer nuclear layer (ONL) was not immunoreactive to the Go-antibody, whereas in the frog, turtle and chicken, the ONL was immunoreactive to it. The implications of these species differences in Go localization in the vertebrate retina are discussed.     

在免眼中进行经瞳孔阈值下温热疗法的组织学效应和蛋白表达

目的：研究阈值下经瞳孔温热疗法（TTT）对视网膜组织学的效应。方法：对正常视网膜色素的兔眼进行TTT，通过1个810nm激光二极管产生直径为1．2mm能量为50mW的光斑，持续时间为15、30和60秒。4周后进行荧光血管造影并摘除眼球，通过电子显微镜和免疫组化染色来检查。     

An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia

Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immuno-reactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.     

Case of dermatomyositis complicated with massive pleural effusion that preceded the myopathy]

A 36-year-old man was admitted to a hospital with complaints of fever, polyarthralgia and dyspnea. Erythema was observed on his face, extensor surface of the fingers and extremities, and a chest X-ray revealed massive bilateral pleural effusion. He had no sign of myopathy at this point. Pleural fluid was proved to be exudative and contained extremely high levels of hyaluronic acid. He was also complicated with interstitial pneumonitis and was given a pulse therapy with methyl prednisolone followed by daily administration of 55 mg prednisolone (PSL). Twenty days after the commencement of the therapy, pleural effusion decreased but muscle weakness gradually appeared, accompanied by elevation of myogenic enzymes. Myogenic changes on electromyogram, and irregularity of the muscle fibers with slight inflammatory cell infiltrates in a biopsy specimen were demonstrated. He was transferred to our hospital, and a diagnosis of dermatomyositis was made. Later, pleural effusion waxed and waned depending on the dosage of PSL, but no other causative disorder was demonstrated by extensive examinations. This case indicates that the pleuritis could be one of the vasculitic manifestations of dermatomyositis.     

Histopathological study on the effects of aging in myocardium of hypertrophied hearts

To clarify the effects of aging in myocardium of hypertrophied hearts, 555 autopsied hearts were studied histopathologically. Degrees of myocyte hypertrophy, disarrangement and fibrosis and lipofuscin deposits were estimated light-microscopically in tissue specimens taken from the anterior wall of the left ventricle. Myocyte hypertrophy was assigned to one of four classes from 0 to 3+ according to size. Other findings were estimated using the conventional three classes. All cases were divided according to heart weight, into the following groups: severe hypertrophy (Group I; more than 450 g for males and 400 g for females), mild hypertrophy (Group II; 450 greater than HW greater than 350 g for males and 400 greater than HW greater than 300 g for females) and no hypertrophy (Group III: less than 350 g for males and 300 g for females). Lipofuscin deposits increased with aging, but in Group I the increase was delayed in comparison to that in other groups. As a rule, myocyte size in the outer layer was equal to or smaller than that in the inner layer (outer-layer-selective atrophy). This was particularly true in pressure-overloaded hypertrophy and less so in volume-overloaded hypertrophy. Myocyte disarrangement was observed in the inner and median layers in the oldest group. Peri-vascular fibrosis became thick with aging, and perimysial fibrosis increased with age. The fibrotic process was accelerated in hypertrophied myocardium. As to the mode of hypertrophy, aging appears to result in a kind of myocardial asymmetry of layer-selective atrophy.(ABSTRACT TRUNCATED AT 250 WORDS)