The contribution of inducible nitric oxide and cytomegalovirus to the stability of complex carotid plaque.

BACKGROUND: Although the association between inflammation and atherosclerosis is well established, the biologic events that trigger the local inflammatory response within plaque are not fully understood. Cytotoxic free radicals and infectious agents, both of which are associated with an inflammatory response, have previously been implicated in the initiation and progression of atherosclerosis. In this study, we analyzed carotid plaque for evidence of oxidative vascular injury by determining the presence and distribution of inducible nitric oxide synthase (iNOS) expression and nitrotyrosine formation and for evidence of infection with cytomegalovirus. METHODS: Carotid plaque from 51 patients who underwent endarterectomy for either primary (n = 37) or recurrent (n = 14) stenosis were examined histologically (hematoxylin-eosin staining and Masson's trichrome staining) and with immunohistochemistry with specific antibodies to alpha-smooth muscle actin, macrophages (CD68), T-lymphocytes (CD3), and T-cell activation (human leukocyte antigen-DR). Twenty-eight specimens from patients with primary (n = 15) and recurrent (n = 13) stenosis were examined for the presence of iNOS and nitrotyrosine with immunohistochemistry and in situ hybridization (iNOS). Twenty-three additional specimens (22 primary, and 1 recurrent) were analyzed with antibodies to p53, cytomegalovirus, and the polymerase chain reaction (cytomegalovirus, n = 8). RESULTS: Primary atherosclerotic lesions were either complex heterogenous cellular plaques (n = 29) or relatively acellular fibrous plaques (n = 8). Ten of 14 recurrent plaques were either complex or fibrous lesions, and the remaining four were typical of myointimal thickening. CD68-positive staining cells were detected in all specimens regardless of their structural morphology. CD3-positive cells were interspersed between macrophages in all heterogeneous cellular plaques and only infrequently noted in fibrous plaques. iNOS and nitrotyrosine immunoreactivity were detected in macrophages and smooth muscle cells in all complex and fibrous plaques and in two of four myointimal plaques. The presence of iNOS and nitrotyrosine in plaque correlated with the existence of symptoms in 80% of primary and 62% of recurrent lesions. Cytomegalovirus was detected in only two of 23 carotid specimens (9%). CONCLUSION: The association between ischemic cerebrovascular symptoms and iNOS and nitrotyrosine immunoreactivity in complex primary and recurrent carotid plaque and the infrequent occurrence of cytomegalovirus in primary carotid lesions suggests that ongoing free radical oxidative damage rather than viral infection may contribute to plaque instability in patients with complex and fibrous carotid plaques.

RAD53, DUN1 and PDS1 define two parallel G2/M checkpoint pathways in budding yeast.

Eukaryotic checkpoint genes regulate multiple cellular responses to DNA damage. In this report, we examine the roles of budding yeast genes involved in G2/M arrest and tolerance to UV exposure. A current model posits three gene classes: those encoding proteins acting on damaged DNA (e.g. RAD9 and RAD24), those transducing a signal (MEC1, RAD53 and DUN1) or those participating more directly in arrest (PDS1). Here, we define important features of the pathways subserved by those genes. MEC1, which we find is required for both establishment and maintenance of G2/M arrest, mediates this arrest through two parallel pathways. One pathway requires RAD53 and DUN1 (the 'RAD53 pathway'); the other pathway requires PDS1. Each pathway independently contributes approximately 50% to G2/M arrest, effects demonstrable after cdc13-induced damage or a double-stranded break inflicted by the HO endonuclease. Similarly, both pathways contribute independently to tolerance of UV irradiation. How the parallel pathways might interact ultimately to achieve arrest is not yet understood, but we do provide evidence that neither the RAD53 nor the PDS1 pathway appears to maintain arrest by inhibiting adaptation. Instead, we think it likely that both pathways contribute to establishing and maintaining arrest.

Vitamin E levels in human atherosclerotic plaque: the influence of risk factors.

Recent studies suggest that vitamin E may be an important preventative factor in the development and progression of atherosclerosis. In order to more clearly define the role of vitamin E in atherosclerosis, we measured vitamin E, conjugated diens, and lipid flurochromes, as well as cholesterol, triglycerides and phospholipid in arterial and venous tissue of 83 patients. Serum cholesterol and triglyceride levels were significantly higher (P < 0.05) in patients with aortic occlusive (AIOD) and aneurysmal (AAA) disease than in control organ donors (OD). Tissue cholesterol concentrations were significantly elevated in AAA tissue when compared to OD and tissue from patients with peripheral occlusive disease (POD). Tissue from patients with AIOD contained greater concentrations of phospholipid (PL) than were measured in patients with POD and in OD. Vitamin E concentrations were highest in POD tissue and approximately 3.0, 2.0, and 1.6 fold greater than OD, AIOD and AAA tissue respectively. Diene conjugates and lipid flurochromes, measures of early and intermediate products of lipid peroxidation, were markedly elevated in all diseased arterial tissue compared to controls. There were no significant differences in tissue or serum lipid levels between saphenous vein (SVBG) and diseased vein grafts (DVG). However, conjugated diene concentrations were elevated in DVG compared to SVBG. Vitamin E levels were significantly elevated in diseased arterial and venous tissue (AIOD, AAA, POD, DVG) removed from patients with diabetes (P = 0.013) and hypertension (P = 0.049) compared to those without these risk factors. Diabetes was the only risk factor associated with significantly increased (P = 0.005) levels of vitamin E when only data from atherosclerotic arterial tissue (AAA, POD, AIOD) were analyzed. These preliminary data provide additional evidence of altered vitamin E metabolism and free radical processes in the tissues of patients with various manifestations of atherosclerosis.

Incidence and histologic characteristics of blebs in patients with abdominal aortic aneurysms.

PURPOSE: Aortic blebs-focal outpouchings within aortic aneurysms-may contribute to their eventual rupture. In this study we determine the incidence of aortic blebs and describe their microscopic features. METHODS: Computed tomographic scans of the abdominal aorta were obtained in 188 patients with aortic diameters measuring > or = 3 cm and were independently evaluated by a radiologist. The number and location of blebs were recorded, and each was measured with calipers. Sixteen blebs, with an adjacent uninvolved aneurysmal segment of aorta, and tissue from two patients with ruptured aneurysms were examined by light microscopy and immunohistochemical analysis. Specimens from six blebs and five aneurysms were examined for alpha 1 (I) procollagen messenger RNA by in situ hybridization. RESULTS: Twenty blebs, ranging in size from 5 to 30 mm (mean, 12 +/- 7 mm), were detected in 11% (20 of 188) of computed tomographic scans. Blebs were observed in 10% (11 of 111) of patients with aortic diameters between 3.0 and 4.9 cm, 10% (6 of 61) of patients with aneurysms between 5.0 and 6.9 cm, and 19% (3 of 16) of patients with aortic diameters > or = 7 cm. Histologically, the major difference between the aneurysmal aortic wall and blebs was found in the media. In aneurysmal aortas, the media consisted of multiple layers of fragmented elastic lamellae, whereas the number of elastic tissue elements along the circumference of the blebs progressively decreased; only a few isolated fragments of elastic tissue were present at the apices. Histologic evidence of rupture was evident in two specimens. A chronic inflammatory cell infiltrate composed of T and B lymphocytes, plasma cells, and macrophages, common to both the aneurysmal and the blebs, was most prominent in the adventitia of aneurysmal tissue, but involved both the media and adventitia of the blebs. In situ hybridization demonstrated the presence of alpha 1 (I) procollagen messenger RNA in four of the five aneurysm segments that were evaluated, compared with only one of six blebs. CONCLUSIONS: Blebs were discovered in aneurysms of all sizes; their frequency appeared to be unrelated to aneurysm size. The presence of inflammatory cell infiltrates and absence of alpha 1 (I) procollagen messenger RNA in five of six blebs suggest that a local imbalance of matrix degradation and repair plays a role in the cause of these lesions. Attenuation of the aortic wall accompanying the formation of blebs may predispose these sites to rupture.

Long-term results of cardiac transplantation in patients older than sixty years. UTAH Cardiac Transplant Program.

Advanced age has traditionally been a contraindication to cardiac transplantation. We have, however, offered cardiac transplantation to patients older than 60 years with end-stage heart failure if they were otherwise acceptable candidates. From 1985 to 1994, 527 patients underwent cardiac transplantation. Among these patients, 101 were older than 60 years at transplantation. The mean follow-up of this group is 6 years. Patients older than 60 years had significantly fewer rejection episodes per patient than those who were younger than 60 years at transplantation (1.9 +/- 1.3 vs 2.6 +/- 1.8, p = 0.009). No difference in the number of infectious complications per patient was detected between the two groups. Both short-term and long-term survival after transplantation were significantly lower for patients who were older than 60 years at transplantation than for younger patients (p < 0.05). The 6-year actuarial survival after transplantation for patients older than 60 years was 54% compared with 72% for patients younger than 60 years at transplantation (p < 0.05). Patients older than 60 years at transplantation were more likely to die of infectious complications or malignant disease after transplantation (p < 0.05). We believe caution is warranted in offering cardiac transplantation to patients older than 60 years. This group of patients should be carefully observed for the development of potentially life-threatening infectious complications or new malignant tumors after transplantation.

Abdominal wall hernias in patients with abdominal aortic aneurysmal versus aortoiliac occlusive disease.

BACKGROUND: This study was undertaken to determine the incidence of ventral incisional hernias (VIHs) and inguinal hernias (IHs) in patients with abdominal aortic aneurysmal (AAA) versus those with aortoiliac occlusive disease (AIOD). PATIENTS AND METHODS: The medical records of 193 patients (128 with AAA and 65 with AIOD) who had undergone elective aortic reconstruction were reviewed to determine the number and location of abdominal wall hernias (AWHs). RESULTS: Forty-one AWHs (28 IHs and 13 VIHs) were detected in patients with AAA compared to 13 (11 IHs and 2 VIHs) in patients with AIOD. There was a significantly greater incidence of VIHs in patients with AAA versus patients with AIOD (10% versus 3%, P < 0.05) and recurrent AWHs (28% versus 19%, P < 0.01), but not of IHs (22% versus 17%). CONCLUSION: Patients with AAA have a higher incidence of VIHs and recurrent AWHs--without a corresponding increase in patient-related risk factors--than patients without aneurysm, suggesting that as yet unidentified etiologic factors may contribute to the development of AWHs in these patients.

Cellular origin and rate of endothelial cell coverage of PTFE grafts.

To determine the origin, cell type present, and rate of endothelial cell coverage of PTFE grafts, 5-cm segments of 4-mm-diameter, 60-microns PTFE grafts were implanted end-to-end bilaterally in the carotid arteries of greyhound dogs. An external jugular vein wrap was applied to the outer surface of one of the PTFE grafts; the contralateral PTFE graft, which was unwrapped, served as its control. Two dogs each were sacrificed at 3, 5, 7, 14, 21, 28, and 35 days postimplantation. Anastomotic endothelial ingrowth was analyzed using scanning electron microscopy. Microvessel ingrowth was documented in longitudinal H&E sections. Cell identity was established by immunohistochemistry with factor VIII antibody, Ulex europaes, leukocyte common antigen, and antibodies to alpha-actin, desmin, vimentin, and basic fibroblast growth factor. All grafts were patent at the time of harvest. Endothelial cell migration from the native artery adjacent to the anastomosis commenced at 7 days, extended to 5 mm beyond the proximal and distal anastomoses by 14 days and to 1.0 cm by 35 days. Endothelialization of the mid-portion of the wrapped grafts occurred via microvessel ingrowth, a process which began at 7 days. Microvessels reached the luminal surface by 28 days and an endothelial cell monolayer was established by 35 days. Wrapping the external surface of the graft with vein increased the rate of graft healing. Basic fibroblast growth factor was detectable by immunohistochemistry at the vein wrap-graft interface in the first 14 days.

The effects of improved hemodynamics on aortic dimensions in patients undergoing heart transplantation.

PURPOSE: Retrospective studies have demonstrated an accelerated growth rate of abdominal aortic aneurysms in heart transplant patients. This prospective study was undertaken to define the relationship between cardiac hemodynamics and posttransplant aortic dilation. METHODS: Sixty-eight patients undergoing heart (n = 60) or heart-lung (n = 8) transplantation were prospectively evaluated with abdominal ultrasonography before transplantation and annually after transplantation. Risk factors implicated in aneurysm growth, including age, indication for transplantation, immunosuppression, posttransplantation hypertension, and abdominal aortic dimension before transplantation were recorded. All patients underwent annual coronary artery catheterization and multiple gated acquisition scanning. RESULTS: Thirty-seven patients (54%) had no change in aortic diameter after transplantation (pretransplantation and posttransplantation diameter = 1.8 +/- 0.3 cm), over a mean follow-up period of 28 +/- 14 months. In the remaining 31 (46%) patients, aortic diameter increased by 0.5 +/- 0.6 cm over 31 +/- 15 months (p < 0.05). Four (6%) of these 31 patients had abdominal aortic aneurysms (mean aortic diameter = 5.0 +/- 0.8 cm). The mean increase in aortic diameter among these 4 patients was 1.8 +/- 0.2 cm (annual rate of growth = 0.96 +/- 0.3 cm/year). Patients experiencing an increase in aortic dimension after transplantation had significantly lower (p < 0.005) pretransplantation ejection fractions (17.1% +/- 10.5% vs 28.6% +/- 18.1%) and, as a consequence, significantly greater (p < 0.05) increases in their ejection fractions after transplantation compared with patients with stable aortic dimensions (42.7% +/- 12.6% vs 31.8% +/- 18.0%). CONCLUSIONS: Of 68 heart transplant patients prospectively evaluated, aortic diameter increased in 31 (46%); new aneurysms developed in four of these patients. Greater incremental increases in cardiac ejection fraction were significant correlates with aortic enlargement.

Factors influencing the safety of colostomy closure in the elderly.

Although colostomy closure is a commonly performed surgical procedure, there remains concern that the attendant risks may be misjudged, especially in the elderly. The purpose of this study was to evaluate the safety of performing colostomy closure and to define the factors that may influence morbidity and mortality in patients over the age of 70. Three hundred seven patients (178 males, 129 females) underwent colostomy closure over a 5-year period. The mean age was 52 years and 84 (27%) of the patients were 70 years or older. The indications for colostomy included diverticulitis, 115 (38%); malignancy, 47 (15%); perforation 35 (11%); trauma, 34 (11%); congenital anomalies, 26 (8%); obstruction, 13 (4%); bleeding, 6 (2%); colovesical fistulae, 6 (2%); polyps, 2 (0.7%); and miscellaneous, 23 (8%). An end colostomy was performed in 193 (63%) patients and a transverse loop colostomy in the remaining 114 (37%). There were no deaths. Complications occurred in 27 (9%) patients: 17 were directly related to colostomy closure (8 wound infections, 3 intraabdominal abscesses, 3 small bowel obstructions, 2 anastomotic strictures, and 1 anastomotic leak) while 10 were nonsurgical. Risk factors statistically associated with increased morbidity included age > 70 years (13% versus 5%), end versus loop colostomy (10% versus 2%), an operative time > 2 hr, and estimated blood loss > or = 500 ml (P < 0.05). ASA classification was only predicative of postoperative complications in patients over 70 years of age. We conclude that although colostomy closure can be performed without mortality, the increased morbidity associated with this procedure in patients 70 years or older necessitates careful preoperative assessment.

Suramin, a protein kinase C inhibitor, impairs hepatic regeneration.

Previously we have shown that partial hepatectomy (PH) or exposure of the liver to the mitogen prolactin induces activation of hepatic protein kinase C (PKC). Here, we used suramin, an antitrypanosomal and chemotherapeutic drug which inhibits that enzyme, as a probe of PKC signal transduction in the regenerative response after PH in the rat. Suramin was administered i.p. in nonhepatotoxic doses of 20 to 160 mg/kg 14 days prior to PH. Three measures of hepatic DNA synthesis or cell division, thymidine kinase activity, [3H]thymidine incorporation, and mitotic index were inhibited in a dose-dependent fashion. Baseline PKC activity, in both the cytosolic and particulate fractions, was unchanged by suramin. After PH, PKC activation, signalled by an increase in activity in the particulate fraction, was observed in control rats at 30 and 60 min. However, rats which had previously received suramin demonstrated dose-dependent inhibition of PKC activation. Suramin is known to also disrupt the binding of certain growth factors to their receptors. But if inhibition of PKC activation were conferred by interference with growth factor-receptor binding by suramin, then the generation of diacylglycerol, the second messenger for PKC activation, should likewise be impaired. However, we observed that the diacylglycerol mass generated at 15, 30, and 45 min after PH was not altered by suramin pretreatment. We conclude that the diminution in DNA synthesis after PH by suramin is likely the consequence of direct inhibition of PKC, suggesting that PKC activation is an important, perhaps obligatory, signal transduction event in liver regeneration.

The hepatotoxicities of endotoxin and ethanol comparisons in vitro using the precision-cut rat liver slice model.

Using the precision-cut rat liver slice model, the in vitro toxicities of endotoxin and ethanol, independently and in combination, were evaluated. Hepatotoxicity was assessed by two measures: the leakage of LDH from slice to medium and the ability of slices to reduce a tetrazolium compound, MTT. Ethanol, in concentrations of 1% and greater, exhibited a time and dose dependent hepatotoxicity; MTT reductive capacity was more profoundly affected than LDH leakage. Endotoxin (0.1 to 100 micrograms/ml), however, had only a modest effect on MTT reduction and did not perturb LDH leakage. When combined in vitro, the toxicities of 2% ethanol and various concentrations of endotoxin were additive. Slices prepared from the livers of rats injected ip with endotoxin one day previously sustained considerably more injury (compared to normal rat liver slices) upon subsequent in vitro exposure to either endotoxin or ethanol. Prior in vivo exposure to ethanol, however, did not affect the subsequent in vitro toxicity of endotoxin. Thus, while endotoxin exhibits only subtle toxic effects upon liver slices in vitro, exposure to endotoxin in vivo renders the liver more susceptible to subsequent direct injury by endotoxin or ethanol.

Putative vascular endothelial cell chemotactic factors: comparison in a standardized migration assay.

While a number of chemoattractants of vascular endothelial cells have now been identified in vitro, differences in methodology preclude comparisons of substances evaluated in different assays. Here, we report a standardized chemotactic assay in which the migration of calf pulmonary artery endothelial cells in a 48-well microchemotaxis chamber was determined. Nonstimulated (control) migration was remarkably constant (mean +/- SD, 96 +/- 14) from plate to plate, thus allowing the indexing of relative migration of stimulated cells to that of nonstimulated cells in the control wells of that plate. Based on the relative migrations observed in response to each of the substances evaluated, those proving to be stimulatory of migration were placed in rank order by potency. The growth factors epidermal growth factor, transforming growth factor-alpha, and basic fibroblast growth factor (followed by pentosan polysulfate, plasmin, fibronectin, fibrinogen, granulocyte-macrophage colony stimulating factor heparin, adenosine, and MgSO4) were the most potent. Only the platelet factors platelet-derived growth factor-BB and platelet activating factor proved inhibitory of migration. Combining fibrinogen with other chemoattractants produced either stimulation or inhibition in comparison to the migration observed with fibrinogen alone, suggesting that more than one signal transduction mechanism was, in all likelihood, invoked by the various agents. This assay will allow the rapid screening and rank ordering of additional putative chemoattractants, will facilitate the study of the biochemical mechanisms involved in endothelial cell migration, and will permit the evaluation of pharmacologic agents capable of modulating stimulated or unstimulated migration.

Hepatic ischemia, caused by celiac axis compression, complicating pancreaticoduodenectomy.

OBJECTIVE: In the course of pancreaticoduodenectomy, profound hepatic ischemia developed in two patients (one with ampullary carcinoma, the other with chronic pancreatitis). This article addresses the diagnosis and correction of the celiac axis compression responsible in this complication. SUMMARY BACKGROUND DATA: Since hepatic ischemia appeared immediately after division of the gastroduodenal--pancreaticoduodenal arcade, which provides mesenteric to celiac collateral circulation, celiac axis narrowing or occlusion was suspected. Previous reports have indicated that celiac axis disease may be present in about 10% of such patients. METHODS: Doppler flow studies, and in the second patient, intraoperative angiography were performed. The celiac axis was exposed and mobilized in both. RESULTS: Initially, no flow could be detected in the celiac axis. Dense fibrous tissue was found encasing it. Division of the entrapping tissue restored flow to the upper abdominal viscera. CONCLUSIONS: The anatomic deformation of the celiac axis predisposing to this complication is detectable on the lateral projection of a preoperative celiac angiogram. If, however, an angiogram has not been done, an initial test occlusion of the gastroduodenal artery before its division permits anticipation of the complication, correction of the celiac impingement, and hence, avoidance of hepatic ischemia.

Effect of surgical manipulation of polytetrafluoroethylene grafts on microstructural properties and healing characteristics.

The effects on graft healing of alterations in the microstructure of polytetrafluoroethylene (PTFE) grafts induced by surgical instruments have not been fully elucidated. This study evaluates changes in the structural and physical properties of PTFE grafts resulting from the intentional application of commonly used surgical instruments and the influence of these changes on cellular ingrowth. The extent of cellular ingrowth into intact (10, 30, and 60 microns unreinforced and 30 microns reinforced [R]) and structurally compromised PTFE grafts (30 reinforced and 60 microns nonreinforced) implanted subcutaneously in Sprague-Dawley (n = 14) rats was evaluated at 7 and 21 days. The thrombogenicity of 10-, 30-, 60-, and 80-microns intact graft segments was determined gravimetrically after suspension in the internal jugular vein of dogs for 90 minutes. Cellular ingrowth consisting of fibroblasts, macrophages, and microvessels was directly related to porosity and was most extensive in 60-microns uncompromised graft segments, being 7-, 17-, and 20-fold greater than was observed in 60- and 30R-microns compromised grafts and undamaged 10-microns grafts, respectively. There was a direct relationship between porosity and thrombogenicity of intact graft segments suspended in the jugular vein. The amount of thrombus adherent to 80-microns graft segments was eightfold greater compared with 10-microns grafts. Manipulation of PTFE with surgical instruments significantly impairs healing and may be a possible etiologic factor in the poor long-term performance of these grafts.

Peripheral vascular disease in heart transplant recipients.

The improved longevity of heart transplant recipients demands heightened awareness of the long-term complications of the procedure. Between 1979 and 1990, 232 patients received 241 heart transplants at our institution. Accelerated coronary atherosclerosis occurred in 45 (19%) of the 232 patients, typically appearing within 2 years of transplantation, whereas peripheral vascular disease (PVD) appeared in 23 (10%) of the 232 patients, usually within 3 years of transplantation. In the patients with PVD, 13 had occlusive disease, nine had aneurysms, and one patient suffered a vertebral artery dissection. Accelerated coronary atherosclerosis afflicted 12 (52%) of the 23 patients affected by PVD (p < 0.05) and preceded the development of PVD in all 12. Logistic regression analysis revealed risk factors predictive of the development of PVD after transplantation to be a pretransplant history of ischemic cardiomyopathy and posttransplant hypertension and hypertriglyceridemia (p < 0.05), with the presence of more than one risk factor increasing the probability of development of PVD. Those patients thus identified as at risk should be closely monitored for the development of PVD. Aggressive medical management of hypertension and hyperlipidemia in this subpopulation may forestall or prevent the development of peripheral vascular disease after heart transplantation.

Identification of prolactin receptors in hepatic nuclei.

Prolactin is a trophic hormone which may act directly at the hepatocyte nucleus. In this study, specific prolactin binding sites were sought in purified rat liver nuclei. Saturable and specific, high affinity 125I-prolactin binding sites were demonstrated to be on or within the nucleus. Prolactin binding was competitively inhibited by rat and ovine prolactins but not by rat growth hormone. Using immunogold electron microscopy, we detected prolactin receptors throughout the nucleus, in association with heterochromatin. Furthermore, endogenous immunoreactive prolactin was demonstrated to be within hepatic nuclei. We conclude that rat liver nuclei possess prolactin binding sites which likely participate in hormone-directed growth processes.

Influence of spousal opinions on residency selection.

Fourth-year medical students face the difficult task of choosing a residency consistent with their career goals. Our study investigates the input of the spouse on the residency selection. From July 1, 1988, to July 1, 1990, questionnaires were sent to all 69 spouses of fourth-year medical students at the University of Arizona Medical Center. Fifty-six were returned for a response rate of 81%. Of the 16 women and 40 men who responded (mean age: 27 years), 55 (98%) spouse stated that there had been family discussions on the choice of a residency program, and 41 (73%) respondents thought that they had significant input. When asked to rank the items that most influenced their support for a particular training program, career goals of the medical student (68%) and lifestyle (21%) were most important, whereas prestige, earning capacity, and program length were ranked lowest. Specific concerns expressed by spouses on the selection of a surgical residency included time commitment as the most commonly cited (79%), followed by fatigue (48%). A statistically significant correlation existed between those spouses actively discouraging the choice of general surgery and those objecting to the time commitment during residency (p less than 0.05). We conclude that spouses have significant preferences regarding the choice of a training program following medical school. Career goals and lifestyle appear to be the most important factors; however, despite concern about the time commitment, the majority of spouses are supportive of the selection of a surgical residency.

Improved sterile technique diminishes the incidence of positive line cultures in cardiovascular patients.

In order to determine the incidence of positive line cultures, especially as affected by differing protocols for line insertion, cultures were obtained from lines in residence for up to 4 days from cardiac patients (who received Cefuroxime) and vascular patients (who received Cefazolin) as prophylaxis perioperatively. Positive cultures were obtained from 95 (19%) of 496 lines in cardiac patients and 83 (31%) of 261 lines in vascular patients. There was a linear relationship between duration of line residence and the incidence of positive line cultures, increasing from 14% on Day 1 to 33% on Day 4. The use of full sterile technique at the time of insertion halved the incidence of subsequent positive line cultures. Four of the 403 (1%) patients each had a single episode of postoperative line sepsis. Another four patients developed wound infections with the same organisms as cultured from their lines. One patient has had a vascular graft infection with the same organism cultured as was isolated from a Swan-Ganz line 1 year previously. These data suggest that monitoring lines should be inserted using full sterile technique and removed as soon as the patient is hemodynamically stable.