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ASAIO J. 2004 Jul-Aug;50(4):369-72. PMEA coating of pump circuit and oxygenator may attenuate the early systemic inflammatory response in cardiopulmonary bypass surgery. Ueyama K, Nishimura K, Nishina T, Nakamura T, Ikeda T, Komeda M. Department of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, Shogoin, Sakyo-Ku, Kyoto, Japan. We investigated the effects of coating a cardiopulmonary bypass (CPB) circuit and oxygenator with poly-2-methoxy-ethyl acrylate (PMEA) on the systemic inflammatory response during and after CPB. Thirty patients undergoing elective cardiac surgery were randomized into three groups (each group n = 10): noncoated (group N), heparin coated (group H), and PMEA coated circuit and oxygenator (group X). Bradykinin (BK), complement 3 activation (C3a) and interleukin-6 (IL-6) levels were measured as early phase indicators of inflammatory response, as were maximum C reactive proteins (CRP) and white blood cell (WBC) levels. The alveolar-arterial oxygen gradient (A-a DO2) was measured as a parameter of respiratory function. IL-6 levels after CPB were significantly higher in group N than in groups H and X (p < 0.05). Serum BK and C3a levels showed similar patterns in all groups. A-a DO2 was lower at the end of and 3 hours after CPB in groups H and X than in group N (p < 0.05). Maximum CRP levels were lower in group X than in groups N (p < 0.05). This prospective study suggests that PMEA coated CPB may improve respiratory function and decrease systemic inflammatory response after cardiac surgery, possibly because this circuit is as biocompatible as heparin coated CPB circuit. |
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Masui. 2004 Jul;53(7):744-52. [Effects of perfusion pressure on cerebral blood flow and oxygenation during normothermic cardiopulmonary bypass] Hamada H, Nakagawa I, Uesugi F, Kubo T, Hiramatsu T, Kai T, Hidaka S, Hamaguchi K. Department of Anesthesiology and Critical Care, Division of Clinical Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima 734-8551. BACKGROUND: Central nervous system dysfunction after cardiopulmonary bypass (CPB) is an important cause of morbidity and mortality after cardiac surgery. Perfusion pressure (PP) during CPB could be one of the important determinants of cerebral blood flow (CBF). The objective of the present study was to determine the effect of PP on CBF and cerebral oxgenation during normothermic CPB. METHODS: Twelve adult patients undergoing coronary artery bypass graft surgery were randomly assigned to one of two groups based on PP (High and Low group). Patients in High group received phenylephrine immediately after the onset of CPB to maintain PP between 60 and 80 mmHg. Oxyhemoglobin (O2Hb), deoxyhemoglobin (HHb), tissue oxygenation index (TOI), and oxidized cytochrome aa3 (CtOx) were measured by near-infrared spectroscopy, and internal jugular venous bulb blood oxygen saturation (SjvO2) was measured simultaneously. S-100 beta protein concentrations were also measured before and after CPB. RESULTS: SjvO2 in High group increased significantly during CPB. CtOx in Low group decreased significantly during CPB, whereas TOI was unchanged. Although S-100 beta increased significantly at the end of CPB, there was no difference between the groups. CONCLUSIONS: These results suggest that maintaining high PP is benefical for CBF during normothermic CPB. |
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J Am Coll Cardiol. 2004 Jul 21;44(2):276-86. Cardiac protection during acute myocardial infarction: where do we stand in 2004? Kloner RA, Rezkalla SH. Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, USA. rkloner@goodsam.org Despite better outcomes with early coronary artery reperfusion for the treatment of acute ST-elevation myocardial infarction (MI), morbidity and mortality from acute myocardial infarction (AMI) remain significant, the incidence of congestive heart failure continues to increase, and there is a need to provide better cardioprotection (therapy that reduces the amount of necrosis that may be coupled with better clinical outcome) in the setting of AMI. Since the introduction of the concept of cardiac protection over a quarter of a century ago, various interventions have been investigated to reduce myocardial infarct size. Intravenous beta-blockers administered in the early hours of infarction were clearly shown to be of benefit. Intravenous adenosine appeared promising for anterior wall AMIs, as did cariporide in some studies. Glucose-insulin-potassium infusion was beneficial in certain subgroups of patients, particularly diabetics. A variety of other medications were studied with negative or marginal results. The best strategy to limit infarct size is early reperfusion with percutaneous coronary stenting or thrombolytic therapy. Stenting is superior and should be adopted whenever there is a qualified laboratory available. Available resources should focus on decreasing time from onset of symptoms to start of reperfusion and maintaining vessel patency. Future studies powered to better assess clinical outcome are needed for adjunctive therapy with adenosine, K(ATP) channel openers, Na(+)/H(+) exchange inhibitors, and hypothermia. |
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Chest. 2004 Jul;126(1):135-41. Cytokine response to pulmonary thromboendarterectomy. Langer F, Schramm R, Bauer M, Tscholl D, Kunihara T, Schafers HJ. Department of Thoracic and Cardiovascular Surgery, University Hospitals Homburg, Germany. BACKGROUND: Pulmonary thromboendarterectomy (PTE) is an effective but challenging treatment for chronic thromboembolic pulmonary hypertension (CTEPH). PTE is associated with marked hemodynamic instability in the perioperative course, suggesting the involvement of circulating mediators. The aim of this study was to characterize the expression of proinflammatory and anti-inflammatory cytokines in patients undergoing PTE. METHODS: Fourteen patients with CTEPH (mean [+/- SD] pulmonary vascular resistance, 1,056 +/- 399 dyne.s.cm(-5)) underwent PTE using cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA). Peripheral arterial blood samples were drawn prior to patients undergoing sternotomy, during CPB, before and after DHCA, and 0, 8, 16, 24, and 48 h after surgery. An enzyme-linked-immunosorbent assay was used to analyze the plasma levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-10. Seven patients undergoing aortic arch replacement (ARCH) in DHCA served as a control group. RESULTS: Prior to and during PTE, the CTEPH patients exhibited elevated TNF-alpha levels, which decreased within the first 24 postoperative hours (p = 0.02). There was no TNF-alpha release among patients in the ARCH group. IL-6 levels were similar in both groups throughout the perioperative course. A profound anti-inflammatory response was observed in the PTE group, which was reflected by elevated IL-10 levels prior to surgery and a marked peak level immediately after surgery. A positive correlation was found between maximum vasopressor support and peak levels of IL-6 (r = 0.82) in the PTE patients. CONCLUSION: Heart failure due to CTEPH appears to generate a pronounced inflammatory response with the release of proinflammatory and anti-inflammatory cytokines. PTE results in the rapid normalization of preoperatively elevated TNF-alpha levels. IL-6-mediated systemic inflammatory cascades may be involved in the regulation of peripheral vascular tone after PTE. |
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J Card Surg. 2004 Jul-Aug;19(4):338-42. Minimized mortality and neurological complications in surgery for chronic arch aneurysm: axillary artery cannulation, selective cerebral perfusion, and replacement of the ascending and total arch aorta. Shimazaki Y, Watanabe T, Takahashi T, Minowa T, Inui K, Uchida T, Koshika M, Takeda F. Second Department of Surgery, Yamagata University School of Medicine, Yamagata, Japan. OBJECTIVE: Cerebral complication is still a major concern in surgery for arteriosclerotic aortic arch disease. For preventing this complication, axillary artery cannulation, selective cerebral perfusion, and replacement of the ascending and arch aorta were applied to thoracic aortic aneurysm involving aortic arch. METHOD: From May 1999 to July 2002, consecutive 39 patients with true aneurysm (29 patients) or chronic aortic dissection (10 patients) involving aortic arch underwent replacement of the ascending and arch aorta with an elephant trunk under hypothermic cardiopulmonary bypass through the axillary artery cannulation and selective cerebral perfusion. The brain was continuously perfused without any intermission through the axillary artery. Concomitant operation included coronary artery bypass grafting (CABG) in two patients, aortic valve replacement (AVR) in one, Bentall operation in two, mitral valve replacement (MVR) in one, and aortic valve sparing operation in one. Patient age at operation was 40-84 (72 + 9) years and 24 of them were older than 70 years of age. RESULTS: There was one operative death (2.5%) due to bleeding from the left lung, and one hospital death due to respiratory failure. Postoperative permanent neurological dysfunction was found in one patient (2.5%). Two patients presented temporary neurological dysfunction (5%). Thirty-six of the 39 patients were discharged from hospital on foot. CONCLUSION: Continuous perfusion through the axillary artery with selective cerebral perfusion and replacement of the ascending and arch aorta may minimize cerebral complication leading to satisfactory results in patients with chronic aortic aneurysm involving aortic arch. |
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Cytokine. 2004 Jul 21-Aug 7;27(2-3):81-9. Methylprednisolone favourably alters plasma and urinary cytokine homeostasis and subclinical renal injury at cardiac surgery. McBride WT, Allen S, Gormley SM, Young IS, McClean E, MacGowan SW, Elliott P, McMurray TJ, Armstrong MA. Department of Anaesthetics and Intensive Care Medicine, The Queen's University of Belfast, Belfast, Northern Ireland, Ireland. williamthomasmcb@aol.com Whilst elevated urinary transforming growth factor beta-1 (TGFbeta) is associated with chronic renal dysfunction its role in acute peri-operative renal dysfunction is unknown. In contrast, peri-operative increases in urinary IL-1 receptor antagonist (IL-1ra) and TNF soluble receptor-2 (TNFsr-2) mirror pro-inflammatory activity in the nephron and correlate with renal complications. Steroids modulate some plasma cytokines (decreasing TNFalpha, IL-8, IL-6 and increasing IL-10), whereas ability to reduce plasma and urinary TNFsr-2 and IL-1ra and peri-operative renal injury is unknown. Patients undergoing coronary artery bypass grafting with cardiopulmonary bypass (CPB) were randomised to receive methylprednisolone (n = 18) or placebo (n = 17) before induction of anaesthesia. Plasma and urinary pro- and anti-inflammatory cytokine balance was determined along with subclinical proximal tubular injury and dysfunction, measured by urinary N-acetyl-beta-d-glucosaminidase (NAG)/creatinine and alpha-1-microglobulin/creatinine ratios, respectively. In the control group compared with baseline, plasma IL-8, TNFalpha, IL-10, IL-1ra and TNFsr-2 were significantly elevated along with urinary IL-1ra, TNFsr-2 and TGFbeta1. Urinary NAG/creatinine and alpha-1-microglobulin/creatinine ratios rose from completion of revascularisation until 6 h with recovery at 24 h with a further rise in NAG/creatinine ratio at 48 h. Compared to placebo, the methylprednisolone group showed significantly reduced plasma IL-8, TNFalpha, IL-1ra and TNFsr-2 whereas plasma IL-10 increased. Compared to placebo, the methylprednisolone group demonstrated significantly reduced urinary NAG/creatinine ratio, TNFsr-2 and TGFbeta1 at 24 h whereas urinary alpha-1-microglobulin/creatinine ratios increased. CONCLUSIONS: Methylprednisolone administration during cardiac surgery significantly reduces plasma and urinary TNFsr-2 and IL-1ra, urinary TGFbeta1 and subclinical renal injury but not dysfunction. Copyright 2004 Elsevier Ltd. |
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Med Sci Monit. 2004 Jul;10(7):CR294-9. Epub 2004 Jun 29. Comparison of pulsatile and non-pulsatile cardiopulmonary bypass in patients with chronic obstructive pulmonary disease. Tarcan O, Ozatik MA, Kale A, Akgul A, Kocakulak M, Balci M, Undar A, Kucukaksu DS, Sener E, Tasdemir O. Turkiye Yuksek Ihtisas Hospital Cardiovascular Surgery Clinic, Ankara, Turkey. onurcantarcan@hotmail.com BACKGROUND: Patients with chronic obstructive pulmonary disease have an increased risk of mortality and morbidity after open-heart surgery. This is mostly due to a dysfunction of the pulmonary system during and after non-pulsatile cardiopulmonary bypass. The purpose of this study was to compare the pulsatile and non-pulsatile blood flows during cardiopulmonary bypass in patients with chronic obstructive pulmonary disease. MATERIAL/METHODS: This is a prospective study. Ten patients with chronic obstructive pulmonary disease had open-heart surgery with pulsatile flow, and another 9 patients with non-pulsatile flow. We compared clinical, hemodynamic, biochemical and hematological parameters and arterial and venous blood gases before initiating cardiopulmonary bypass, at aortic cross-clamping and de-clamping, and 1 and 24 hours postoperative. RESULTS: In the pulsatile flow group, systemic vascular resistance at the time of aortic cross clamping (p=0.041), pulmonary vascular resistance 1 hour postoperative (p=0.05), and the percentage of neutrophils 1 hour postoperative (p=0.034) were significantly lower than those of the non-pulsatile group. Though white blood cell count was significantly high in the pulsatile group 1 hour postoperative, absolute neutrophil count was significantly low (p=0.034). The postoperative mechanical ventilation period was significantly shorter in the pulsatile flow group (p=0.016). CONCLUSIONS: Pulsatile blood flow during cardiopulmonary bypass has a favorable influence on patients with chronic obstructive pulmonary disease, who have high risk in open-heart surgery. |
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J Thorac Cardiovasc Surg. 2004 Jul;128(1):109-16. Inhaled prostacyclin reduces cardiopulmonary bypass-induced pulmonary endothelial dysfunction via increased cyclic adenosine monophosphate levels. Fortier S, DeMaria RG, Lamarche Y, Malo O, Denault A, Desjardins F, Carrier M, Perrault LP. Research Center and Department of Surgery, Montreal Heart Institute, Montreal, Quebec, Canada. OBJECTIVE: Cardiopulmonary bypass triggers a systemic inflammatory response that alters pulmonary endothelial function, which can contribute to pulmonary hypertension. This study was designed to demonstrate that inhaled prostacyclin, a selective pulmonary vasodilator prostaglandin, prevents pulmonary arterial endothelial dysfunction induced by cardiopulmonary bypass. METHODS: Three groups of Landrace swine were compared: control without cardiopulmonary bypass (control group); 90 minutes of normothermic cardiopulmonary bypass (bypass group); 90 minutes of cardiopulmonary bypass and treated with prostacyclin during cardiopulmonary bypass (continuous nebulization with continuous positive airway pressure until the end of the cardiopulmonary bypass; prostacyclin group). After 60 minutes of reperfusion, swine were put to death and pulmonary arteries harvested. After contraction to phenylephrine, endothelium-dependent relaxation to bradykinin and acetylcholine was studied in standard organ chamber experiments. The pulmonary artery intravascular cyclic adenosine monophosphate content was compared between the 3 groups (post-cardiopulmonary bypass). RESULTS: There was a statistically significant improvement of the endothelium-dependent relaxation to bradykinin in the prostacyclin group when compared with the bypass group (P <.05). There was no statistically significant difference for endothelium-dependent relaxation to acetylcholine (P >.05) between the prostacyclin and the bypass groups. There was a statistically significant decrease in the cyclic adenosine monophosphate content and a statistically significant increase of the mean pulmonary artery pressure in the bypass group only (P <.05). CONCLUSION: Prophylactic use of inhaled prostacyclin has a favorable impact on the pulmonary endothelial dysfunction induced by cardiopulmonary bypass associated with preservation of pulmonary intravascular cyclic adenosine monophosphate content and the pulmonary vascular tone. |
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Ann Thorac Surg. 2004 Jul;78(1):181-7. Outcome analysis of major cardiac operations in low weight neonates. Bove T, Francois K, De Groote K, Suys B, De Wolf D, Verhaaren H, Matthys D, Moerman A, Poelaert J, Vanhaesebroeck P, Van Nooten G. Department of Cardiac Surgery, University Hospital of Gent, Gent, Belgium. BACKGROUND: From June 1995 to January 2003, 49 consecutive neonates of less than 2,500 g underwent early surgery for congenital heart disease. A retrospective analysis was performed to evaluate the early to medium term outcome. METHODS: Major cardiac surgery for congenital heart defects included a complete correction in 31 patients (group I) and a palliative procedure in 18 patients (group II). Mean age at operation was 15.2 days (1 day-90 days) and mean weight was 2,190 g (1,300 g-2,500 g). Twenty-four children (49%) were born prematurely. All neonates were critically ill and 47% were already ventilated preoperatively. Heart defects included mainly ventricular septal defect (10), tetralogy of Fallot complexes (8), aortic coarctation (8), transposition complexes (7), single ventricle anomalies (4), pulmonary atresia with intact septum (4), interrupted aortic arch (3), totally anomalous pulmonary venous return (3), and common atrioventricular septal defect (2). RESULTS: Overall surgical mortality was 18%: 4 neonates died after definitive repair and 5 after palliation; representing, respectively, 13% and 28% of each group. Postoperative morbidity occurred in half of the patients (53%). Age, weight, prematurity, type of first surgical procedure, and use of cardiopulmonary bypass did not influence the early outcome. After a mean follow-up of 2.82 years (2 months to 6 years), survival was 87% in the correction group and 54% in the palliation group. All children were in NYHA class I-II. Freedom from reintervention at 18 months was 68% after correction versus 8% after palliation. CONCLUSIONS: Cardiac surgery for congenital malformations in critically ill, low weight neonates can be achieved with acceptable mortality, at the cost of an increased morbidity. Early outcome seems independent of age, weight, prematurity, use of extracorporeal perfusion, and type of first intervention. Moreover, primary correction appears to result in an early survival benefit, remaining constant over time. |
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Thromb Haemost. 2004 Jul;92(1):124-31. Formation of tissue factor-bearing leukocytes during and after cardiopulmonary bypass. Shibamiya A, Tabuchi N, Chung J, Sunamori M, Koyama T. Graduate School of Health Sciences, Tokyo Medical and Dental University, Tokyo, Japan. During cardiopulmonary bypass (CPB), the extrinsic coagulation system initiated by tissue factor (TF) is a major procoagulant stimulus. TF is present in surgical wounds and could be expressed on activated monocytes. However, recent studies have suggested that collagen stimulation rapidly induces TF by leukocyte-platelet complex formation. Therefore, the appearance of TF-bearing leukocytes and their effect on promoting coagulation were investigated in 5 patients undergoing coronary bypass surgery. Neutrophils and monocytes positive for CD41a and TF increased abruptly in circulating blood during CPB.Their increase was most prominent in blood pooled in the pericardial cavity. Monocytes, but not neutrophils positive for TF showed a second peak one day after operation, which accords with the increase in TF mRNA levels in leukocytes. Similarly, an increase in leukocytes positive for TF accords with the activated factor X generation assay using isolated leukocytes, and with an increase in thrombin-antithrombin complex in circulating blood. The second increase in TF-positive monocytes seems to be responsible for these coagulation parameters that remained high one day after operation. After 10 min of blood incubation stimulated by collagen in vitro, simulating activation in the pericardial cavity, significant increases in neutrophils and monocytes positive for TF and platelet were observed. Our present study suggested the involvement of two distinct mechanisms for the appearance of TF-bearing leukocytes responsible for promoting coagulation: the quick appearance being partly explained by the formation of leukocyte-platelet complex that occurs mainly in the pericardial cavity, and the slow appearance via transcriptional activation in monocytes. |
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