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Biomedical subjects

S Thelin

Publications and source records attributed to S Thelin.

At least 19 recordsLinked to original sources
PubMed1999

Quality of life in survivors of thoracic aortic surgery.

BACKGROUND: The results of surgical repair of thoracic aortic lesions are improving. Still, mortality and morbidity are considerable. Outcomes need to be studied in greater detail. We studied quality of life in survivors of thoracic aortic surgery, which has not been reported before. METHODS: During a 5-year period, 115 patients underwent thoracic aortic repair. All mid- to long-term survivors (n = 81; median follow-up time, 26 months) received the Short Form-36 (SF-36) health questionnaire plus specific questions related to surgery. Five patients were lost to follow-up. RESULTS: Scores for the eight dimensions of SF-36 (range, 0 to 100, 100 reflecting best function) were compared with a normal population. The mean deficits from the norm were bodily pain, 0.1 (95% confidence interval, -3.4 to 3.6) points below norm; mental health, 8.3 (5.7 to 10.9); vitality, 9.5 (6.7 to 12.3); social functioning, 10.1 (6.9 to 13.3); general health, 11.1 (8.5 to 13.7); physical functioning, 16.6 (13.4 to 19.8); role emotional, 20.6 (15.3 to 25.9); and role physical, 30.2 (24.7 to 35.7). Subgroup scores for acute versus elective cases, ascendens versus arch versus descendens procedures, and major complication versus no major complication were not significantly different. Sixty-six percent (50 of 76) stated a general health perception improvement. In 82% (62 of 76), the quality of life improved or was preserved. Ninety-one percent (69 of 76) considered the operation successful. CONCLUSIONS: Considering the seriousness of the conditions, quality-of-life scores after thoracic aortic surgery were acceptable, although lower than in a normal population, except for bodily pain. Postoperative quality of life justifies thoracic aortic surgical repair.

Aortic Dissection↗
PubMed1999

Surgical repair of type B aortic dissection complicated by early postoperative lung vein and artery thrombosis.

A 24-year old man with Marfan syndrome previously operated for abdominal aortic aneurysm and type A dissection sustained a type B dissection. He underwent graft replacement of the descending and upper abdominal aorta, complicated by infarction of the left upper lobe and lobectomy was carried out. The postoperative course was uneventful. The mechanism for this rare complication is discussed.

Adult↗
PubMed1998

Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: an experimental study.

BACKGROUND: Respiratory failure secondary to cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors previously found that the increase in intrapulmonary shunt was well correlated with the amount of atelectasis. They tested the hypothesis that post-CPB atelectasis can be prevented by a vital capacity maneuver (VCM) performed before termination of the bypass. METHODS: Eighteen pigs received standard hypothermic CPB (no ventilation during bypass). The VCM was performed in two groups and consisted of inflating the lungs during 15 s to 40 cmH2O at the end of the bypass. In one group, the inspired oxygen fraction (FIO2) was then increased to 1.0. In the second group, the FIO2 was left at 0.4. In the third group, no VCM was performed (control group). Ventilation-perfusion distribution was measured with the inert gas technique and atelectasis by computed tomographic scanning. RESULTS: Intrapulmonary shunt increased after bypass in the control group (from 4.9 +/- 4% to 20.8 +/- 11.7%; P < 0.05) and was also increased in the vital capacity group ventilated with 100% oxygen (from 2.2 +/- 1.3% to 6.9 +/- 2.9%; P < 0.01) but was unaffected in the vital capacity group ventilated with 40% oxygen. The control pigs showed extensive atelectasis (21.3 +/- 15.8% of total lung area), which was significantly larger (P < 0.01) than the proportion of atelectasis found in the two vital capacity groups (5.7 +/- 5.7% for the vital capacity group ventilated with 100% oxygen and 2.3 +/- 2.1% for the vital capacity group ventilated with 40% oxygen. CONCLUSION: In this pig model, postcardiopulmonary bypass atelectasis was effectively prevented by a VCM.

Animals↗
PubMed1997

The macrophage migration inhibitory factor MIF is a phenylpyruvate tautomerase.

A macrophage migration inhibitory factor (MIF), originally described as a product of activated lymphocytes, has been defined as a 12 kDa protein, expressed in a wide variety of tissues. Here MIF is identified as a phenylpyruvate tautomerase (EC 5.3.2.1) having p-hydroxyphenylpyruvate and phenylpyruvate as its natural substrates. The definition of MIF as an enzyme may yield insight into the mechanism of action of this proinflammatory and immunomodulating cytokine.

Amino Acids↗
PubMed1997

Variable FHIT transcripts in non-neoplastic tissues.

We used nested reverse transcriptase PCR to investigate the expression of the FHIT gene, a presumptive tumor suppressor gene located in chromosomal band 3p 14.2, in non-neoplastic samples. Multiple transcripts of the FHIT gene were found in peripheral blood lymphocytes, skeletal muscle, and liver of healthy individuals, as well as in a cell line derived from isynovial tissue. The data indicate that variable splicing of the FHIT transcript, leading to deletions of exons and thus anomalous or absent FHIT protein production, occurs frequently in non-neoplastic tissues. Hence, the finding of multiple nonfunctional FHIT transcripts is not tumor-specific and cannot be used as a genetic marker of neoplasia.

Acid Anhydride Hydrolases↗
PubMed1997

Monocyte tissue factor expression, cell activation, and thrombin formation during cardiopulmonary bypass: a clinical study.

OBJECTIVES: Cardiopulmonary bypass is associated with extensive thrombin generation and cell activation. Our main hypothesis in this study was that the expression of tissue factor on circulating monocytes contributes to the formation of thrombin. METHODS: Markers of activation of the coagulation cascade and cell activation were measured in 26 patients undergoing elective heart operations randomized to the use of heparin-coated (Duraflo II, n = 13) or standard cardiopulmonary bypass circuits (n = 13). RESULTS: Thrombin generation, measured as the thrombin-antithrombin complex, increased considerably during cardiopulmonary bypass with peak levels 3 hours afterward and with remaining elevation 20 hours later. Despite increased monocyte and granulocyte activation and increased levels of monocyte chemotactic protein-1, which upregulates monocyte tissue factor expression in vitro, monocyte tissue factor expression was not increased at the end of cardiopulmonary bypass. Furthermore, at this time the monocytes were less sensitive to in vitro stimulation by endotoxin. These results might be explained by simultaneous enhanced levels of interleukin-10, which effectively downregulates monocyte tissue factor expression in vitro. Twenty hours after cardiopulmonary bypass was discontinued, the tissue factor expression on freshly isolated monocytes and on monocytes stimulated by endotoxin was significantly increased compared with preoperative levels. At this time increased activation markers of granulocytes, monocytes, and lymphocytes were also recorded. None of the measured parameters was found to be different between the groups. CONCLUSIONS: The tissue factor expression on circulating monocytes is upregulated the day after heart operations. The clinical relevance and the regulatory mechanism behind the enhanced expression, however, are not fully elucidated.

Aged↗
PubMed1997

Effects of heparin-coating of cardiopulmonary bypass circuits on leukocytes during simulated extracorporeal circulation.

Heparin-coated circuits used during extracorporeal circulation reduce many postoperative complications occurring after heart surgery. Such complications are partly related to leukocyte activation with subsequent release of active substances, e.g. oxygen free radicals, myeloperoxidase and lactoferrin. This experiment was performed to elucidate a possible influence of heparin-coating on leukocytes. A 2-h-long simulated extracorporeal circulation was performed on two groups of five extracorporeal circulation circuits, primed with heparinized, fresh whole human blood and Ringer's solution. Heparin-coated circuits (HC group) were compared with uncoated circuits (NC group). Oxygen free radical production was estimated by determination of malonyldialdehyde in plasma and erythrocyte suspension. Granulocyte activation was measured in terms of myeloperoxidase and lactoferrin release. Time-related changes in leukocyte subset counts were analysed. Heparin-coating diminished myeloperoxidase and lactoferrin release. There were significant inter-group differences after 90 and 120 min of extracorporeal circulation for myeloperoxidase (101 (12) microg/l and 107(12) microg/l in the HC group versus 154(20) microg/l and 174(23) microg/l in the NC group), and after 120 min of extracorporeal circulation for lactoferrin (78(5) microg/l in the HC group versus 212(49) microg/l in the NC group). No significant changes of MDA concentration were observed in plasma or erythrocytes; however, a tendency towards lower MDA levels was seen after 90 and 120 min of extracorporeal circulation in the NC group. Neutrophil, monocyte and eosinophil numbers decreased significantly in the NC group but were unchanged in the HC group, as were lymphocyte counts. Heparin-coated extracorporeal circulation circuits significantly reduce granulocyte activation and better preserve the number of circulating neutrophils, eosinophils and monocytes, but do not change oxygen free radical production during simulated extracorporeal circulation.

Anticoagulants↗
PubMed1997

Duraflo II coating of cardiopulmonary bypass circuits reduces complement activation, but does not affect the release of granulocyte enzymes : a European multicentre study.

OBJECTIVE: This study was carried out to: (a) compare complement and granulocyte activation during cardiac operations in patients operated with cardiopulmonary bypass coated with heparin by the Duraflo II method, with activation in patients operated with uncoated circuits; and (b) relate complement, and granulocyte activation to selected adverse effects. METHODS: In a multicentre study among Rikshospitalet, Ullevaal Hospital in Norway and Uppsala University Hospital in Sweden, plasma concentrations of the complement activation products C4b/iC4b/C4c (C4bc), C3b/iC3b/C3c (C3bc), the terminal SC5b-9 complement complex (TCC), and the granulocyte proteins myeloperoxidase and lactoferrin were assessed in two groups of patients undergoing aortocoronary bypass. Seventy-six patients underwent surgery operated with circuits coated by the Duraflo II heparin coating and 75 uncoated circuits. The same amount of systemic heparin was administered to all patients. RESULTS: In both groups a significant increase in C4bc was first seen by the end of operation, from 86.7 +/- 12.5 to 273.0 +/- 277.4 nM in controls and from 86.9 +/- 18.5 to 320.2 +/- 190.5 nM in the control group, confirming previous documentation that the classical pathway is not activated during CPB, but as a consequence of protamin administration. The formation of C4bc did not differ significantly between the two groups. In the uncoated group the C3bc concentration increased from 124.0 +/- 15.3 to a maximum of 1176.1 +/- 64.7 nM (P < 0.01) and in the coated group it increased from 129.8 +/- 16.1 to a maximum of 1019.4 +/- 54.9 nM (P < 0.01) during CPB. Summary values but not peak values differed significantly between the groups. In the uncoated group the TCC concentration increased from 0.52 +/- 0.03 to a maximum value of 8.09 +/- 0.57 AU/ml (P < 0.01) while in the coated group the TCC concentration increased from a baseline of 0.53 +/- 0.03 to a peak value of 5.2 +/- 0.24 AU/ml (P <0.01). The difference between the peak values was statistically significant (P = 0.00002). In both groups a significant increase in myeloperoxidase and lactoferrin release was observed by the end of operation. There was no difference in myeloperoxidase or lactoferrin release between the two groups. TCC levels were compared to the occurrence of perioperative infarction, development of lung or renal failure, postoperative bleeding, time on ventilator and days in hospital. Three patients developed perioperative infarction; the peak levels of TCC were significantly higher in these patients than in the 148 patients that did not develop infarction. The reduction in TCC formation in the heparin-coated group was not associated with differences in any of the other clinical parameters. Few adverse effects occurred in the study. The peak values of C3bc were higher in the patients needing inotropic support that in those who did not, the relevance of this finding remains uncertain. CONCLUSION: It is concluded that the Duraflo II heparin coating reduces complement activation, particularly TCC formation, during CPB, but not the release of specific neutrophil granule enzymes. No certain correlation was established between complement and granulocyte activation and clinical outcome.

Aged↗
PubMed1997

Biocompatibility reflected by haemostasis variables during cardiopulmonary bypass using heparin-coated circuits.

Cardiopulmonary bypass (CPB) is associated with haemostatic disturbances and signs of acute inflammatory response, most likely related to poor biocompatibility of the artificial surfaces. Some haemostatic variables are known as markers of acute-phase reaction, blood cell trauma, and endothelial damage. The aim of the study was to evaluate the effect of heparin-coating of artificial surfaces on those variables of hemostasis. 14 patients operated on with elective coronary artery revascularization were randomized into two groups. In group H (n = 7), heparin-coated CPB circuits and in control group C (n = 7), noncoated CPB sets were used. Patients in group C received normal heparinization, e.g. bolus 300 IU/kg and additional doses to maintain activated coagulation time (ACT) over 400 sec during CPB. In group H, a bolus heparin dose was reduced by 25% (to 225 IU/kg) in order to compensate for the amount of heparin immobilized on circuit surfaces and the corresponding ACT limit was 300 sec. There were significant increases of the von Willebrand factor (vWf), plasminogen activator inhibitor-1 (PAI) and tissue-plasminogen activator (tPA) starting at CPB end and rising to about twice the baseline levels postoperatively. This reaction was less evident in group H, as indicated by significantly lower levels of tPA compared to group C at CPB end (135% +/- 9 in group H versus 241% +/- 15 in group C, p < 0.0005) and at two hours postoperatively. The rates of tPA and vWF increase were lower in group H, also indicating reduced endothelial damage in this group. Marginally significant, a higher value of PAI was found in the C group early after CPB onset. Group H showed significantly lower concentrations of circulating complex between elastase and alpha 1-antitrypsin at CPB end and postoperatively, implicating a reduced granulocyte activation (60 min after protaminization 41 micrograms/L +/- 5 in group H versus 256 micrograms/L +/- 55 in group C, p < 0.05). It was concluded that the heparin-coated CPB circuits demonstrated improved biocompatibility which may be related to less disturbed haemostasis.

Anticoagulants↗
PubMed1997

Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study.

BACKGROUND: Respiratory failure after cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors tested the hypothesis that atelectasis is an important factor responsible for the increase in intrapulmonary shunt after CPB. METHODS: Six pigs received standard CPB (bypass group). Six other pigs had the same surgery but without CPB (sternotomy group). Another six pigs were anesthetized for the same duration but without any surgery (control group). The ventilation-perfusion distribution was measured with the inert gases technique, extravascular lung water was quantified by the double-indicator distribution technique, and atelectasis was analyzed by computed tomography. RESULTS: Intrapulmonary shunt increased markedly after bypass but was unchanged over time in the control group (17.9 +/- 6.2% vs. 3.5 +/- 1.2%; P < 0.0001). Shunt also increased in the sternotomy group (10 +/- 2.6%; P < 0.01 compared with baseline) but was significantly lower than in the bypass group (P < 0.01). Extravascular lung water was not significantly altered in any group. The pigs in the bypass group showed extensive atelectasis (32.3 +/- 28.7%), which was significantly larger than in the two other groups. The pigs in the sternotomy group showed less atelectasis (4.1 +/- 1.9%) but still more (P < 0.05) than the controls (1.1 +/- 1.6%). There was good correlation between shunt and atelectasis when all data were pooled (R2 = 0.67; P < 0.0001). CONCLUSIONS: Atelectasis is produced to a much larger extent after CPB than after anesthesia alone or with sternotomy and it explains most of the marked post-CPB increase in shunt and hypoxemia. Surgery per se contributes to a lesser extent to postoperative atelectasis and gas exchange impairment.

Animals↗
PubMed1997

High incidence of Chlamydia pneumoniae in sclerotic heart valves of patients undergoing aortic valve replacement.

Chlamydia pneumoniae has previously been demonstrated in the atherosclerotic lesions of various arteries, including the coronary arteries, and has been proposed to play a role in the pathogenesis of atherosclerosis. A prospective study of the incidence of C. pneumoniae in the sclerotic valves of patients undergoing aortic valve replacement because of aortic stenosis and in the aortic valves of cases dying of non-cardiac reasons and undergoing forensic autopsy was undertaken. The results were correlated to serological markers of past (IgG) or persistent (IgA) C. pneumoniae infection. C. pneumoniae, as determined by the polymerase chain reaction (PCR), was detected in the aortic valve in 19/39 (49%) patients and in 1/11 (9%) autopsy controls (p = 0.018) and confirmed by electron microscopy in one patient. There was no significant difference in the incidence rate of IgG or IgA antibody positivity between PCR-positive and PCR-negative cardiac patients. These results extend the hypothesis of a pathogenic role of C. pneumoniae in atherosclerosis to include also aortic valve sclerosis.

Adult↗
PubMed1997

Haemostasis at low heparin dosage during cardiopulmonary bypass with heparin-coated circuits in pigs.

Cardiopulmonary bypass (CPB) causes activation of cascade systems. Although heparin coating of CPB circuits improves biocompatibility, the effects on coagulation remain controversial. Theoretically, heparin coating should permit the reduction of systemic anticoagulation during CPB. We investigated influences on haemostatic variables in animal CPB, comparing heparin-coated circuits and reduced systemic heparinization (group HC) with uncoated circuits and full heparinization (group C). Twenty pigs underwent 2-h CPB. Seven (HC, n = 4; C, n = 3) were weaned from CPB and studied for up to 4 h. Total administered heparin was 470 +/- 6 IU/kg (mean +/- SEM) in group C and 100 +/- 0 IU/kg in group HC. Protamine dosage was significantly reduced in group HC. In group C, levels of prothrombin complex, factor VIII and adhesive platelets were reduced significantly during CPB, and postoperatively there were significantly lower values of prothrombin complex, fibrinogen, antithrombin III, factor VIII and adhesive platelets but a significantly increased concentration of von Willebrand factor and cumulative bleeding after 4 h. In conclusion, heparin-coated CPB circuits combined with lowered heparin dosage reduced coagulation factor consumption and preserved platelet function, possibly contributing to improved postoperative haemostasis.

Animals↗
PubMed1997

Haemostasis at low heparin dosage during cardiopulmonary bypass with heparin-coated circuits in pigs.

Cardiopulmonary bypass (CPB) causes activation of cascade systems. Although heparin coating of CPB circuits improves biocompatibility, the effects on coagulation remain controversial. Theoretically, heparin coating should permit the reduction of systemic anticoagulation during CPB. We investigated influences on haemostatic variables in animal CPB, comparing heparin-coated circuits and reduced systemic heparinization (group HC) with uncoated circuits and full heparinization (group C). Twenty pigs underwent 2-h CPB. Seven (HC, n = 4; C, n = 3) were weaned from CPB and studied for up to 4 h. Total administered heparin was 470 +/- 6 IU/kg (mean +/- SEM) in group C and 100 +/- 0 IU/kg in group HC. Protamine dosage was significantly reduced in group HC. In group C, levels of prothrombin complex, factor VIII and adhesive platelets were reduced significantly during CPB, and postoperatively there were significantly lower values of prothrombin complex, fibrinogen antithrombin III, factor VIII and adhesive platelets but a significantly increased concentration of von Willebrand factor and cumulative bleeding after 4 h. In conclusion, heparin-coated CPB circuits combined with lowered heparin dosage reduced coagulation factor consumption and preserved platelet function, possibly contributing to improved postoperative haemostasis.

Animals↗
PubMed1996

The FHIT and PTPRG genes are deleted in benign proliferative breast disease associated with familial breast cancer and cytogenetic rearrangements of chromosome band 3p14.

We have used nested reverse transcription-PCR (RT-PCR) and PCR on genomic DNA to search for aberrations in the FHIT and PTPRG genes, both located in chromosomal band 3p14.2, in specimens from cytogenetically analyzed benign breast lesions (three samples with atypical hyperplasia and one with fibroadenosis) from two women belonging to breast cancer families. The transcription analysis showed that the FHIT gene was either not expressed or that its expression was dramatically reduced to a level not detectable by nested RT-PCR in the samples with atypical hyperplasia. Genomic analysis of exons 3 and 5 of FHIT and exon 12 of PTPRG provided evidence that these DNA segments were homozygously deleted in the majority of the cells. These data are in line with the histopathological features and cytogenetic findings in the three samples; none contained normal parenchyma, and all had chromosomal aberrations involving band 3p14. RT-PCR analysis of the fibroadenosis specimen, which had a normal karyotype, detected the expected 856-bp fragment as well as an additional alternative transcript variant of FHIT with 1014 bp. The additional 158-bp sequence, which may add 38 amino acids to the NH2-terminal part of the previously described FHIT protein, was inserted between exons 4 and 5 and seems to be a new exon located in intron 4 of FHIT.

Acid Anhydride Hydrolases↗