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Background: The aim of this study was to investigate the impact of transfusion of blood products on intermediate outcome after coronary artery bypass surgery.Patients: Complete data on perioperative blood transfusion in patients undergoing coronary artery bypass surgery were available from 2001 patients who were operated at our institution.Results: Transfusion of any blood product (relative risk = 1.678, 95% confidence interval = 1.087–2.590) was an independent predictor of all-cause mortality. The additive effect of each blood product on all-cause mortality (relative risk = 1.401, 95% confidence interval = 1.203–1.630) and cardiac mortality (relative risk = 1.553, 95% confidence interval = 1.273–1.895) was evident when the sum of each blood product was included in the regression models. However, when single blood products were included in the regression model, transfusion of fresh frozen plasma/Octaplas®was the only blood product associated with increased risk of all-cause mortality (relative risk = 1.692, 95% confidence interval = 1.222–2.344) and cardiac mortality (relative risk = 2.125, 95% confidence interval = 1.414–3.194). The effect of blood product transfusion was particularly evident during the first three postoperative months. Since follow-up was truncated at 3 months, transfusion of any blood product was a significant predictor of all-cause mortality (relative risk = 2.998, 95% confidence interval = 1.053–0.537). Analysis of patients who survived or had at least 3 months of potential follow-up showed that transfusion of any blood product was not associated with a significantly increased risk of intermediate all-cause mortality (relative risk = 1.430, 95% confidence interval = 0.880–2.323).Conclusions: Transfusion of any blood product is associated with a significant risk of all-cause and cardiac mortality after coronary artery bypass surgery. Such a risk seems to be limited to the early postoperative period and diminishes later on. Among blood products, perioperative use of fresh frozen plasma or Octaplas seems to be the main determinant of mortality.

Objective: the extent of the processing of type III procollagen to type III collagen was determined in nine human abdominal aortic aneurysms (AAA), and compared with ten samples of aortoiliac occlusive disease (AOD).Methods: the aminoterminal propeptide (PIIINP) and telopeptide (IIINTP) of type III procollagen and collagen, respectively, were immunologically measured in the soluble and insoluble fractions of the extracellular matrix. The assay for PIIINP in the insoluble matrix was further validated. Results: the insoluble matrices of AAAs contained at least 12 times more incompletely processed type III pN-collagen than AOD specimens (0.74% and 0.061%, respectively). Also, the soluble extracts of AAAs tended to contain more non-processed type III pN-collagen than free, properly cleaved aminoterminal propeptide. Conclusions: the larger amount of type III pN-collagen suggests an alteration in the metabolism of type III collagen in AAAs. This may partially explain the decreased tensile strength of the aortic tissue.

Objective: To evaluate the impact of duplex ultrasonography on the treatment plan of patients with uncomplicated primary varicose veins.Methods: Forty-nine consecutive patients (62 legs) with primary uncomplicated varicose veins were examined clinically and with hand-held Doppler (HHD) and duplex ultrasonography in an outpatient clinic on the same day. The plans for subsequent treatment were recorded separately after the two ultrasound examinations.Results: The accuracy of the HHD examination was 0.71 in the saphenofemoral junction (SFJ) and long saphenous vein (LSV trunk). In fifty-six limbs (90%) duplex scanning did not affect the surgical treatment of the patients.Conclusions: Most operations on primary varicose veins can be performed on the basis of clinical and HHD examinations by an experienced surgeon. Duplex ultrasonography can be used selectively in the patients with suspected saphenopopliteal junction (SPJ) reflux or equivocal HHD findings.

Beside neurological morbidity, mortality is a relevant end-point of experimental porcine model of hypothermic circulatory arrest (HCA) and this study was conducted to identify the determinants for postoperative death.

Objective:This study was an attempt to determine risk factors for rupture and to improve management of patients with type B aortic dissection who survive the acute phase without operation. Methods: We studied 50 patients by means of serial computer-generated 3-dimensional computed tomographic scans. All patients who did not undergo operative treatment before the completion of at least 2 computed tomographic scans a minimum of 3 months apart after an acute type B dissection were included in the study. The median duration of follow-up was 40 months (range 0.9-112 months). Only 1 patient died of causes unrelated to the aneurysm during follow-up. Nine patients had fatal rupture (18%); 10 patients underwent elective aneurysm resection because of rapid expansion or development of symptoms, and 31 patients remained alive without operation or rupture. Possible risk factors for rupture in patients in the rupture, operative, and event-free groups were compared, as were dimensional data from first follow-up and last computed tomographic scans. Results: Older age, chronic obstructive pulmonary disease, and elevated mean blood pressures were unequivocally associated with rupture (rupture versus event-free survival, P < .05), and pain was marginally significantly associated. Analysis of dimensional factors contributing to rupture was complicated by the fact that patients who underwent elective operation had significantly larger aneurysms and faster expansion rates than did either of the other groups, leaving comparisons of aneurysmal diameter between groups with and without rupture showing only marginal statistical significance. The last median descending aortic diameter before rupture in the rupture group was 5.4 cm (range 3.2-6.7 cm). Conclusions: In an environment in which patients with large and rapidly expanding aneurysms are usually referred for surgical treatment, older patients with chronic type B dissections, especially if they have uncontrolled hypertension and a history of chronic obstructive pulmonary disease, are significantly more likely to have rupture than are younger, normotensive patients without lung disease. Neither the presence of a persistently patent false lumen nor a large abdominal aortic diameter appears to increase the risk of rupture. Overall, our nondimensional data strikingly resemble the natural history of patients with nondissecting aneurysms, suggesting that calculations derived from data on chronic descending thoracic and thoracoabdominal aneurysms would provide an overly conservative individual estimate of rupture risk for patients with chronic type B dissection, who tend toward earlier rupture of smaller aneurysms. A more aggressive surgical approach toward treatment of patients with chronic type B dissection seems warranted. (J Thorac Cardiovasc Surg 1999;117:776-86)

Background: Seroepidemiologic studies have indicated an association between chronic Chlamydia pneumoniae infection and coronary heart disease. The organism, which is a common respiratory pathogen, has been demonstrated in atherosclerotic lesions of the aorta and coronary arteries. Abdominal aortic aneurysms are frequently associated with atherosclerosis, and inflammation may actually be an important factor in aneurysmal dilatation. Hence it could be assumed that C. pneumoniae may play a role in maintaining an inflammation and triggering the development of aortic aneurysms. Methods and Results: Specimens from abdominal aortic aneurysm were examined for the presence of C. pneumoniae by immunohistochemical analysis, the polymerase chain reaction amplifying omp1 gene, transmission electron microscopy, and culture methods with histologically atherosclerosis-negative human aortic tissues used as a control group. Chlamydial lipopolysaccharide and C. pneumoniae specific antigens were found by immunohistochemistry in 12 and 8 of 12 aneurysm specimens, respectively, and C. pneumoniae DNA could be demonstrated in 6 of 6 aneurysm specimens studied. Furthermore electron microscopy revealed the presence of Chlamydia-like elementary bodies in three of four aneurysm specimens tested. None of the control samples gave positive reaction in the polymerase chain reaction, and C. pneumoniae antigens were not detected in any of them. Conclusions: C. pneumoniae is frequently found in the vessel wall of abdominal aortic aneurysm. The potential etiopathogenetic role of C. pneumoniae in the development of these aneurysms remains to be studied. (J Vasc Surg 1997;25:499-505.)

Purpose: The pathogenesis of abdominal aortic aneurysm (AAA) involves many factors; elastin degradation is believed to lead to initial dilation, whereas changes in the collagen structure predispose the aneurysm to rupture. The major collagens in the aortic wall are types I and III. We set out here to determine whether changes in serum propeptide of type III procollagen (PIIINP), a biologically relevant marker of type III collagen turnover, could be associated with the characteristics of AAA. Methods: The aminoterminal PIIINP and the carboxyterminal propeptide of type I collagen were measured by radioimmunoassay in 87 patients with AAA and 90 control subjects with aortodistal arteriosclerosis. The samples were taken from the peripheral blood and from the abdominal aorta at the levels of the diaphragm and the common iliac artery. Results: Mean PIIINP concentrations were higher in patients with AAA than in control subjects (3.47 @mg/L vs 2.73 @mg/L, p < 0.0001), correlating positively with aneurysm diameter in the former (r = 0.27, p = 0.04) and with the maximum thickness of the intraluminal thrombus (r = 0.39, p = 0.003). The gradient in PIIINP between the upper and lower end of the abdominal aorta was significant in the AAA group ( -0.30 @mg/L, range -0.20 to -0.50 vs -0.10 @mg/L, range -0.20 to 0.30, p = 0.002). Conclusions: These studies indicate that the turnover of type III collagen is increased in patients with AAA. (J VASC SURG 1995;22:155-60.)

Acidification of bile is one of the factors that prevents calcium precipitation and thereby gallstone formation. Carbonic anhydrase II (CA II) has previously been shown to be one of the key factors in the human alimentary tract that regulates the acid-base balance. We demonstrated CA II expression in the human gallbladder epithelium using immunohistochemical techniques, elucidated the CA II content of the epithelium by digital image analysis of the immunohistochemically stained enzyme in samples from 16 patients undergoing cholecystectomy, and correlated the results with the calcium content of the gallstones. Nine patients had symptomatic gallstone disease and seven an acalculous, histologically normal gallbladder. The patients were classified into two groups on the basis of the calcium content of their gallstones: no gallstones or gallstones containing no calcium (Group 1) and gallstones with 2-87% calcium by weight (Group 2). The immunohistochemical techniques showed distinct epithelial CA II-positive staining in most of the gallbladder samples, but digital image analysis revealed distinct variations in staining intensity among them. The median staining intensity index was significantly higher in Group 1 (0.4463) than in Group 2 (0.2376; p = 0.0262). The results suggest that CA II is abundantly expressed in the normal gallbladder epithelium and that decreased expression may be associated with the formation of calcified gallstones. These findings are relevant to the pathogenesis of gallstone disease.

Objectives:: To investigate (i) elastin degradation and the possible association between proteolysis and inflammation in abdominal aortic aneurysm disease (AAA), and (ii) the presence of cytomegalovirus (CMV) infection in the walls of AAA. Materials:: Specimens from 12 infrarenal AAAs, eight aortas with occlusive disease (AOD) and two normal aortas were studied by conventional light microscopy, immunohistochemistry using a monoclonal anti-elastin antibody BA-4 and anti-CMV antibody and transmission electron microscopy (TEM). Main results:: In AAA the decrease in elastin immunoreactivity and the presence of elastin degradation was associated with increased mononuclear inflammatory cell infiltrates (p=0.004 and p=0.00002, respectively). The CMV immunostainings of the normal aortic wall and all the AAA and AOD samples were negative, nor could any CMV particles be demonstrated by TEM. Conclusions:: The chronic inflammation and degradation of elastin in AAA suggests a possible immune-mediated mechanism. The inflammation may be induced by the chemotactic properties of elastin-derived peptides.

Purpose: This study was performed to test whether tenascin, a large oligomeric glycoprotein of the extracellular matrix, is present in AAA disease and whether it could play a pathophysiologic role in the development of this disease. Methods: Tenascin immunoreactivity was investigated from samples of the aneurysmal walls of 17 patients with AAAs, and the results were compared with the results of those of six patients with aortoiliac occlusive disease (AOD) and one normal control patient. To study the source of tenascin mRNA synthesis, some tissue samples were also examined with a tenascin RNA probe by in situ hybridization. Results: The difference in immunoreactivity between the AODs and AAAs was especially prominent in the adventitial layer, where the specimens from AAAs displayed strong diffuse and reticular immunostaining. In AAAs the immunostaining was clearly associated with the degree of mononuclear inflammatory cell infiltrate and with the neovascularization of the adventitial layer. Conclusion: Tenascin expression is evident in AAA disease and is distinctly associated with mononuclear inflammatory cells. The adhesive properties of tenascin may offer a relevant explanation for the mechanism by which monocytes transmigrate into the aortic wall. The definitive role of tenascin in AAA process may be more complex, however, and will necessitate further investigation. (J Vasc Surg 1997;26:670-5.)

Purpose: We evaluate here whether serial changes in the concentration of the aminoterminal propeptide of type III procollagen (PIIINP) in serum bear any relationship to the rate of abdominal aortic aneurysm (AAA) expansion and whether serum PIIINP has any predictive value with respect to the rupture event. Methods: One hundred thirty-nine patients with asymptomatic AAAs were followed-up at intervals of 6 to 12 months by means of a clinical examination, B-mode ultrasound scan, and serum markers of collagen metabolism. Similar laboratory samples were also obtained from 18 patients who had a rupture of the AAA as their primary symptom soon after onset. Results: The primary correlation between serum PIIINP and AAA diameter was 0.22 (p = 0.01), and that between serum PIIINP and the thickness of the thrombus was 0.49 (p = 0.001). Toward the end of the follow-up, however, the correlation increased to 0.55 (p = 0.002) for serum PIIINP and diameter, but remained at 0.42 (p = 0.02) for serum PIIINP and the thickness of the thrombus. Serum PIIINP values were very high among the 18 patients who had ruptured AAAs. Conclusions: Acceleration of AAA growth is reflected in serum PIIINP, and a marked elevation of serum PIIINP during follow-up of a patient with an AAA may predict an approaching rupture event. (J Vasc Surg 1997;25:909-15.)

One hundred and ninety-five patients operated on for adenocarcinoma of the gastric cardia during the years 1961–90 were analysed and the present data indicate that the more enthusiastic attitude adopted towards resective surgery led to a significant increase in operative explorations performed and in resectability rate, from 50% (44/88) and 35% (28/88) during the years 1961–75 to 84% (90/107) and 56% (60/107) during the years 1976–90, respectively. The difference between radical resections, 54% (15/28) and 67% (34/60), remained non-significant. The overall postoperative mortality and morbidity after resective surgery were 14% and 35% and these rates did not rise with time. The anastomotic leakage rate was 15%. Anastomotic leakage was, in fact, not only the most common postoperative complication but also the most common cause of death. Overall cumulative survivals at 1, 3 and 5 years were 47%, 11% and 5%. Comparison of the cumulative survival rates between the 15-year periods indicated that there were no differences in overall survival or in survival after resective surgery. We regard these results disappointing, because over half of the patients died in 1 year and because the long-term survival remained dismal.

Objective: We assessed the impact on histologic and behavioral outcome of an interval of retrograde cerebral perfusion after arterial embolization, comparing retrograde cerebral perfusion with and without inferior vena caval occlusion with continued antegrade perfusion. Methods: Sixty Yorkshire pigs (27 to 30 kg) were randomly assigned to the following groups: antegrade cerebral perfusion control; antegrade cerebral perfusion after embolization; retrograde cerebral perfusion control; retrograde cerebral perfusion after embolization; retrograde cerebral perfusion with inferior vena cava occlusion, retrograde cerebral perfusion with inferior vena cava occlusion control, and retrograde cerebral perfusion with inferior vena cava occlusion after embolization. After cooling to 20^o C, a bolus of 200 mg of polystyrene microspheres 250 to 750 (@mm diameter (or saline solution) was injected into the isolated aortic arch. After 5 minutes of antegrade cerebral perfusion, 25 minutes of antegrade cerebral perfusion, retrograde cerebral perfusion, or retrograde cerebral perfusion with inferior vena cava occlusion was instituted. After the operation, all animals underwent daily assessment of neurologic status until the time of death on day 7. Results: Aortic arch return, cerebral vascular resistance, and oxygen extraction data during retrograde cerebral perfusion showed differences, suggesting that more effective flow occurs during retrograde cerebral perfusion with inferior vena cava occlusion, which also resulted in more pronounced fluid sequestration. Microsphere recovery from the brain revealed significantly fewer emboli after retrograde cerebral perfusion with inferior vena cava occlusion. Behavioral scores showed full recovery in all but one control animal (after retrograde cerebral perfusion with inferior vena cava occlusion) by day 7 but were considerably lower after embolization, with no significant differences between groups. The extent of histopathologic injury was not significantly different among embolized groups. Although no histopathologic lesions were present in either the antegrade cerebral perfusion control group or the retrograde cerebral perfusion control group, mild significant ischemic damage occurred after retrograde cerebral perfusion with inferior vena cava occlusion even in control animals. Conclusions: Although effective washout of particulate emboli from the brain can be achieved with retrograde cerebral perfusion with inferior vena cava occlusion, no advantage of retrograde cerebral perfusion with inferior vena cava occlusion after embolization is seen from behavioral scores, electro- encephalographic recovery, or histopathologic examination; retrograde cerebral perfusion with inferior vena cava occlusion results in greater fluid sequestration and mild histopathologic injury even in control animals. Retrograde cerebral perfusion with inferior vena cava occlusion shows clear promise in the management of embolization, but further refinements must be sought to address its still worrisome potential for harm.(J Thorac Cardiovasc Surg 1998;115:1142-59) J Thorac Cardiovasc Surg 1998;115:1142-59