https://cdr.lib.unc.edu/downloads/9p290c48k

ACC/AHA Guidelines for Coronary Artery Bypass Graft Surgery A Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1991 Guidelines for Coronary Artery Bypass Graft Surgery)

ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: Summary article. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (committee to update the 1999 guidelines for coronary artery bypass graft surgery)

Institutional Affiliations Chair Costanzo MR: Midwest Heart Foundation, Lombard Illinois, USA Task Force 1 Dipchand A: Hospital for Sick Children, Toronto Ontario, Canada; Starling R: Cleveland Clinic Foundation, Cleveland, Ohio, USA; Anderson A: University of Chicago, Chicago, Illinois, USA; Chan M: University of Alberta, Edmonton, Alberta, Canada; Desai S: Inova Fairfax Hospital, Fairfax, Virginia, USA; Fedson S: University of Chicago, Chicago, Illinois, USA; Fisher P: Ochsner Clinic, New Orleans, Louisiana, USA; Gonzales-Stawinski G: Cleveland Clinic Foundation, Cleveland, Ohio, USA; Martinelli L: Ospedale Niguarda, Milano, Italy; McGiffin D: University of Alabama, Birmingham, Alabama, USA; Parisi F: Ospedale Pediatrico Bambino Gesu, Rome, Italy; Smith J: Freeman Hospital, Newcastle upon Tyne, UK Task Force 2 Taylor D: Cleveland Clinic Foundation, Cleveland, Ohio, USA; Meiser B: University of Munich/Grosshaden, Munich, Germany; Baran D: Newark Beth Israel Medical Center, Newark, New Jersey, USA; Carboni M: Duke University Medical Center, Durham, North Carolina, USA; Dengler T: University of Hidelberg, Heidelberg, Germany; Feldman D: Minneapolis Heart Institute, Minneapolis, Minnesota, USA; Frigerio M: Ospedale Niguarda, Milano, Italy; Kfoury A: Intermountain Medical Center, Murray, Utah, USA; Kim D: University of Alberta, Edmonton, Alberta, Canada; Kobashigawa J: Cedar-Sinai Heart Institute, Los Angeles, California, USA; Shullo M: University of Pittsburgh, Pittsburgh, Pennsylvania, USA; Stehlik J: University of Utah, Salt Lake City, Utah, USA; Teuteberg J: University of Pittsburgh, Pittsburgh, Pennsylvania, USA; Uber P: University of Maryland, Baltimore, Maryland, USA; Zuckermann A: University of Vienna, Vienna, Austria. Task Force 3 Hunt S: Stanford University, Palo Alto, California, USA; Burch M: Great Ormond Street Hospital, London, UK; Bhat G: Advocate Christ Medical Center, Oak Lawn, Illinois, USA; Canter C: St. Louis Children Hospital, St. Louis, Missouri, USA; Chinnock R: Loma Linda University Children's Hospital, Loma Linda, California, USA; Crespo-Leiro M: Hospital Universitario A Coruna, La Coruna, Spain; Delgado R: Texas Heart Institute, Houston, Texas, USA; Dobbels F: Katholieke Universiteit Leuven, Leuven, Belgium; Grady K: Northwestern University, Chicago, Illlinois, USA; Kao W: University of Wisconsin, Madison Wisconsin, USA; Lamour J: Montefiore Medical Center, New York, New York, USA; Parry G: Freeman Hospital, Newcastle upon Tyne, UK; Patel J: Cedar-Sinai Heart Institute, Los Angeles, California, USA; Pini D: Istituto Clinico Humanitas, Rozzano, Italy; Pinney S: Mount Sinai Medical Center, New York, New York, USA; Towbin J: Cincinnati Children's Hospital, Cincinnati, Ohio, USA; Wolfel G: University of Colorado, Denver, Colorado, USA Independent Reviewers Delgado D: University of Toronto, Toronto, Ontario, Canada; Eisen H: Drexler University College of Medicine, Philadelphia, Pennsylvania, USA; Goldberg L: University of Pennsylvania, Philadelphia, Pennsylvania, USA; Hosenpud J: Mayo Clinic, Jacksonville, Florida, USA; Johnson M: University of Wisconsin, Madison, Wisconsin, USA; Keogh A: St Vincent Hospital, Sidney, New South Wales, Australia; Lewis C: Papworth Hospital Cambridge, UK; O'Connell J: St. Joseph Hospital, Atlanta, Georgia, USA; Rogers J: Duke University Medical Center, Durham, North Carolina, USA; Ross H: University of Toronto, Toronto, Ontario, Canada; Russell S: Johns Hopkins Hospital, Baltimore, Maryland, USA; Vanhaecke J: University Hospital Gasthuisberg, Leuven, Belgium.

http://www.jsht.jp/uploads/ISHLT_GL_TaskForce2_110810.pdf

The International Society of Heart and Lung Transplantation Guidelines for the care of heart transplant recipients

Bronchiolitis obliterans (BO) is a major cause of allograft dysfunction in lung and heart lung transplant recipients. Clinically, progressive airflow limitation develops because of small airway obstruction. The disease has a variable course. Some patients experience rapid loss of lung function and respiratory failure. Others experience either slow progression or intermittent loss of function with long plateaus during which pulmonary function is stable. Histologic confirmation is difficult because transbronchial biopsy specimens often are not sufficiently sensitive for diagnosis. Because BO is difficult to document histologically, in 1993 a committee sponsored by the International Society for Heart and Lung Transplantation (ISHLT) proposed a clinical description of BO, termed bronchiolitis obliterans syndrome (BOS) and defined by pulmonary function changes rather than histology. Although this system does not require histologic diagnosis, it does recognize it. Transplant centers worldwide have adopted the BOS system as a descriptor of lung allograft dysfunction. This allows centers to use a common language to compare program results. In the years since publication of the BOS system, transplant scientists have studied basic and clinical aspects of lung transplant BO. In this document, we update and summarize new information obtained from this research and incorporate, where appropriate, the results into the BOS criteria. The document will include the following topics: (1) criteria for BOS, (2) BOS considerations in pediatric patients, (3) risk factors for BOS, (4) pathology of BO, (5) surrogate markers for BOS, (6) confounding factors in making a BOS diagnosis, and (7) assessment of response to treatment of BOS.

Bronchiolitis obliterans syndrome 2001: an update of the diagnostic criteria.

Aortocoronary saphenous vein graft disease, with its increasing clinical sequelae, presents an important and unresolved dilemma in cardiological practice. During the 1st month after bypass surgery, vein graft attrition results from thrombotic occlusion, while later the dominant process is atherosclerotic obstruction occurring on a foundation of neointimal hyperplasia. Although the risk factors predisposing to vein graft atherosclerosis are broadly similar to those recognized for native coronary disease, the pathogenic effects of these risk factors are amplified by inherent deficiencies of the vein as a conduit when transposed into the coronary arterial circulation. A multifaceted strategy aimed at prevention of vein graft disease is emerging, elements of which include: continued improvements in surgical technique; more effective antiplatelet drugs; increasingly intensive risk factor modification, in particular early and aggressive lipid-lowering drug therapy; and a number of evolving therapies, such as gene transfer and nitric oxide donor administration, which target vein graft disease at an early and fundamental level. At present, a key measure is to circumvent the problem of vein graft disease by preferential selection of arterial conduits, in particular the internal mammary arteries, for coronary bypass surgery whenever possible.

Aortocoronary Saphenous Vein Graft Disease Pathogenesis, Predisposition, and Prevention

Risk factors for early mortality, acute rejection, and factors affecting first-year survival after heart transplantation.

Objective: The purpose of this study was to investigate the effect of regional infusion of carnitine on spinal cord ischemia‐reperfusion (I‐ R) in rabbits. Methods: The 36 rabbits were divided into four equal groups, group I (sham operated, no I‐R injury), group II (control, only I‐ R), group III (I‐R 1 intraaortic lactated Ringer’s, LR, during aortic occlusion), group IV (I‐R 1 LR plus 100 mg/kg carnitine). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. The spinal cord function of all animals was assessed clinically 24 h after aortic declamping. Spinal cord samples were taken to measure the levels of tissue malondialdehyde (MDA) and to evaluate the histopathological changes. Results: We found significant increases in the levels of MDA in groups II and III compared with group IOP , 0:01U; and elevation of MDA in group IV was insignificant. In group II, all animals (100%) were paraplegic with Tarlov’s score of 0 and in group III, eight animals (88%) were paraplegic with Tarlov’s score of 0 or 1. None of the animals (0%) from group IV was paraplegic. Histologic examination of spinal cords from group IV animals revealed that the appearance of the spinal cord was relatively preserved, whereas spinal cords from groups II and III had evidence of acute neuronal injury. Conclusion: The results suggest that regional infusion of carnitine during aortic clamping reduces spinal cord injury and prevents neurologic damage in rabbit spinal cord I‐R model. q 2001 Elsevier Science B.V. All rights reserved.

Neuroprotective effect of regional carnitine on spinal cord ischemia--reperfusion injury.

Donor lung procurement

Brucella endocarditis, although a rare complication of brucellosis, is the main case of death attributable to this disease. An atrial septal defect (ASD) presenting with endocarditis in an adult is also extremely rare. We report the case of a male patient who presented with an infective endocarditis and was found to have an ASD. The diagnosis was proven by means of positive serology and isolation of Brucella melitensis from blood cultures and excised vegetation arising from the border of the ASD. The patient was successfully treated by means of excision of the vegetation and specific antibiotic therapy for 3 months.

Atrial Septal Defect Presenting with Brucella Endocarditis

Objectives: To examine the role of TNF alpha (TNFα) in cardiac transplant rejection by simultaneous analysis of protein expression and its messenger RNA within serum and grafted tissue. Methods: 54 endomyocardial biopsy specimens were taken from 19 patients at various times after transplantation. TNFα messenger RNA was localised using a digoxygenin labelled complementary DNA probe. An anti-TNFα antibody was used to immunohistochemically label the protein product. Serum TNFα levels at the time of biopsy were analysed using a specific enzyme-linked immunosorbent assay. Results: TNFα mRNA was present in 22/34 endomyocardial biopsies. Eight also contained TNFα protein. None had protein alone. Expression did not relate to the grade of rejection in the present or subsequent biopsies. Serum TNFα was undetectable (assay sensitivity 30–330 pg/ml) for the majority of specimens. In the nine cases with elevated serum levels, eight samples were from cases within the first 30 days post transplant ( r = −0.379; P < 0.05). Conclusions: Neither tissue TNFα mRNA, tissue protein, nor serum TNFα relate to the grade of rejection. Furthermore, TNFα expression within endomyocardial biopsies is not reflected in the serum. These findings argue against the use of serum analysis as an indicator of cytokine profiles within cardiac tissue allografts. The demonstration of a trend in the early expression of TNFα after transplantation suggests that its release may not be specific to the process of rejection.

/pdf/tnfa-mrna-and-protein-in-cardiac-transplant-biopsies-53acsm9mvi.pdf

Ali Rahman

Papers

Risk factors for early mortality, acute rejection, and factors affecting first-year survival after heart transplantation.

Neuroprotective effect of regional carnitine on spinal cord ischemia--reperfusion injury.

Donor lung procurement

Atrial Septal Defect Presenting with Brucella Endocarditis

TNFα mRNA and protein in cardiac transplant biopsies: comparison with serum TNFα levels