Chronic localized hypotension and resetting of carotid sinus baroreceptors. Electrophysiological and histological studies in the dog.

Resetting of carotid sinus (CS) baroreceptors to chronically elevated systemic pressure in hypertension has been demonstrated. The effects of chronic system hypotension on CS baroreceptor afferents has not been elucidated, however. The purpose of the present study was to determine the electrophysiological and histological characteristics of CS baroreceptors exposed to chronic hypotension. Chronic unilateral hypotension was produced by anastomosis of the common carotid artery to the external jugular vein. CS nerve activity and histology of the normotensive sinus (mean CS pressure +/- SD = 96 +/- 10.9 torr) were compared to those of the hypotensive sinus (mean CF pressure 50 +/- 14.2 torr) 44-49 days after anastomosis in nine mongrel dogs. An isolated CS pouch preparation was used to produce standard pressure changes. Threshold pressure for hypotensive sinuses (15.5 +/- 5.19 torr) was significantly less (P less than 0.05) than for normotensive sinuses (40.6 +/- 9.73 torr). Saturation pressure was also significantly less in the hypotensive sinus (P less than 0.05). There were no significant differences between slopes of the stimulus-response curve or in architecture of intima or media of the two sides. Thus, the stimulus-response curve was shifted to the left in chronic CS hypotension, and this effect could not be related to a change in CS light microscopic histology.

Abdominal aortic aneurysm and retroperitoneal fibrosis. Ultrasonographic diagnosis and treatment.

Until changes of ureteric or vascular compromise are noted, retroperitoneal fibrosis usually goes unnoticed. When symptomatic retroperitoneal fibrosis has been associated with abdominal aortic aneurysm, ureteral involvement has uniformly been present. Three cases demonstrate a new ultrasonographic picture that can aid in early identification of retroperitoneal fibrosis before complications are manifest. In patients with abdominal aortic aneurysms, routine sonography may identify unsuspected retroperitoneal fibrosis, a factor that may be important in preoperative planning for safe surgical intervention.

Pathologic findings in the aortocoronary vein grafts. A scanning electron microscope study.

Examination of totally or partially obstructed human aortocoronary vein grafts, obtained at different time intervals after the bypass operation, has shown that the initial occlusive process is due to thrombosis and may appear a few hours or days after surgery. The cellular phase of intimal proliferation affecting most of the grafts becomes apparent about 4 weeks after the operation. After 1 year the intimal hyperplasia acquires a cell-poor, fibrotic character; the graft usually remains patent. About one-half of the vein grafts obtained 3 or more years after the operation show complicated atherosclerotic lesions. These findings indicate that most of the vein grafts undergo extensive structural changes and some may show similar degenerative lesions as they develop in the coronary arteries.

The spectrum of pathologic changes in aortocoronary saphenous vein grafts.

Aortocoronary vein grafts removed at autopsy of 182 patients who died up to 5 years after the bypass operation were examined by light and electron microscopy. During the first month after surgery, graft occlusion was due to thrombi, some of them recent, some organized and recanalized. Intimal proliferation of the graft first appeared 4 weeks after the bypass surgery; several cases of total occlusion of the lumen by this process were seen within 6 months of the operation. A change in the morphological features of the intimal thickening from cellular to fibrotic and hylain-like was observed in several grafts implanted for more than 1 year. Typical atherosclerosis developed in vein grafts in three of the six patients surviving the operation for more than 3 years.

Late lesions in aorta-coronary artery vein grafts.

Aorta-coronary artery vein grafts, obtained from 2 patients 37 and 59 months after an aorta-coronary bypass operation, showed extensive mural changes characterized by degenerative tissue lesions, loss of normal morphological features of the intima, and extracellular accumulation of lipids. Both patients had increased plasma triglyceride levels.

Pathological changes in surgically removed aortocoronary vein grafts.

Pathological changes in aortocoronary vein grafts were investigated in 17 patients who had a second revascularization procedure 1 to 53 1/2 months after their initial operation. Subendothelial proliferation was present in all grafts and had resulted in total occlusion of 7. With increasing duration of implantation the proliferative lesions tended to show hyalinization and to affect the media. Advanced atherosclerosis had developed in 2 grafts.

Atherosclerosis of the internal mammary artery.

To better evaluate the incidence of atherosclerosis in the internal mammary artery (IMA), 215 IMA segments from routine postmortem examinations were evaluated microscopically. Significant atherosclerotic narrowing was seen in 9 patients (4.2%). No patient had more than a 50% reduction in lumen diameter. The degree of incipient atherosclerosis correlated well with age, hypertension, diabetes, and peripheral vascular disease.

Scanning electron microscope study of human veins and aorta-coronary artery vein grafts.

Scanning electron microscope study of two vein grafts which were removed after 50 months of implantation as aorta-coronary artery vein grafts showed considerable subendothelial thickening, which consisted of relatively cell-poor fibrous layer. In one of the grafts the endothelial surface was intact; the second graft showed focal loss of endothelial cells. Sections of two fresh human veins, studied prior to their insertion as aorta-coronary artery vein grafts, have shown that they retained an intact endothelial layer. A third fresh vein, however, showed focal damage with missing endothelial cells and adherent fibrin.

Surgery for congenital heart disease in the adult.

A total of 205 adults with a variety of congenital heart lesions underwent operation for total correction of their defects. Operative and long-term mortality were 3 and 4 percent, respectively. There has been only one operative death in the past five years (85 patients). While most defects were repaired with good hemodynamic and symptomatic improvement, the three lesions associated with the worst results were cyanotic tetralogy of Fallot, severe pulmonic stenosis complicated by atrial septal defect, and ostium primum atrial septal defect. Myocardial failure due to end-stage myocardial fibrosis was the major cause of operative mortality. Myocardial fibrosis and irreversible pulmonary changes seemed to be the two factors limiting operative correctio