Reoperative coronary surgery. Comparative analysis of 6591 patients undergoing primary bypass and 508 patients undergoing reoperative coronary artery bypass

During an 18-year period a consecutive series of 6591 patients underwent primary coronary bypass grafting and 508 patients underwent reoperative bypass. The mean patient age for the reoperative group was identical to that of the primary group, 59.8 years, but the mean age at initial operation for the reoperative group was 55.2 years. Mammary grafts were done at initial operation in 59% of patients who have had one operation versus only 46% of patients who subsequently required reoperation (p less than 0.001). The overall operative mortality rate was 2.0% (134/6591) for primary coronary bypass versus 6.9% (35/508) for reoperations (p less than 0.001). Patients with a reoperative interval of 1 to 10 years had a 6.0% (18/312) mortality rate, compared with 17.6% (13/74) for those in whom the interval between operations was greater than 10 years (p less than 0.01). Ventricular arrhythmias, excessive bleeding, prolonged ventilatory support, intraaortic balloon pump insertion (all p less than 0.05), and perioperative myocardial infarction (p less than 0.001) were all more prevalent after reoperations. Including perioperative mortality, the actuarial survival rate at 5 years was 80% for reoperations versus 90% for primary operations. The corresponding figures at 10 years were 65% and 75%. The probability of undergoing reoperation within 5 and 10 years was 0.034 +/- 0.003 and 0.055 +/- 0.005, respectively. Ten years postoperatively, 36% of patients having the initial operation had recurrent angina whereas 58% of the reoperative group had significant recurrent angina. Ten years after reoperation, 30% of operative survivors were free of heart-related morbidity and mortality compared with 50% of patients having a primary operation. Univariate analysis of factors increasing the probability of reoperation include the absence of a mammary graft and younger age at operation. Patients undergoing a second bypass operation represent a substantially higher risk subgroup than patients undergoing initial operation in terms of perioperative morbidity, mortality, decreased long-term survival, and decreased relief of recurrent cardiac morbidity.     

Effectiveness of neonatal transport in New York city in neonates less than 2500 grams—A population study

In the past two decades, there has been a gradual trend to regionalization of perinatal care, categorization of hospitals and transport services for neonatal health care. The literature alludes to both beneficial and deleterious effects of neonatal transport (T) but no controls such as a matched nontransport (NT) population have been utilized to date.The major goal of this study was to evaluate the effect of neonatal transport from Level I and II high risk 2500 gm. neonates (born in NYC in one calendar year, 1979) compared to a cohort nontransported population matched for hospital of birth, weight, race, sex and risk. All transported 2500 gm. from Level I and II (n=328) were studied and a stratified random sample of the nontransported (NT) infants 2500 gm. from these same hospitals (n=2042) was used for comparison. The principle outcome variable was survival. The major conclusion of this study is that in Level I and II hospitals the transport group had a significantly increased survival in infants who were sick (Apgar <6) compared to cohorted nontransported controls. Interhospital differences in survival were noted among Level I and II but not seen in the subdivisions of (A) and (B) hospitals.Angelo Ferrara, M.D., Ph.D., is Professor, Pediatrics, NYU Medical Center, New York, N.Y.: Melvin Schwartz, M.D., was Research Professor, Environmental Medicine, NYU Medical Center, New York, N.Y.; Helen Page, R.N., M.P.A., is Quality Assurance Reviewer, Manhattan Eye, Ear, Throat Hospital, New York, N.Y.: Morton Israel, M.A., is Research Scientist, Health Resources Administration, City of N. Y., New York, N.Y.; Yucel Atakent, M.D., M.S., is Clinical Associate Professor, NYU Medical Center, New York, N.Y.; C.E. Smith, Ph.D., is President, Health Policy Analysis & Accountability Network, Inc. (HPAAN), Edgewood, New Mexico; Leon Landovitz, Ph.D., is Vice President, Management Information Systems, Healthways System Inc., Islin, N.J.Supported by NCHSR Grant #5-R018-HSO3832     

Mnemonic coding system for clinical data entry into laboratory computers: its effect on quality and efficiency.

A simplified coding method for entering the clinical details found on pathology request cards was developed. The method uses a basic four letter code, derived from the initial character of the first four words in a clinical detail, being expanded to four characters with letters from the final word if the number of words is less than four. Rules were devised to cope with common medical terminology. In excess of 90% of clinical details on request cards are readily input by clerical staff using our coding system, and 8% of clinical details are used intelligently by the computer in scheduling further tests or automatically commenting on results. A carefully designed coding system such as the one outlined above could greatly facilitate input of clinical detail without the penalty of reduced throughput.     

Anti-inflammatory activity of salmeterol: down-regulation of cytokine production.

Elevation of intracellular cAMP levels has been shown previously to inhibit cytokine secretion by various cell types in vitro. Since salmeterol is a beta 2-agonist which activates adenylate cyclase, its ability to inhibit cytokine production was evaluated. Though salmeterol, and the related drug albuterol, did not inhibit IL-1 beta production in vitro, both drugs did inhibit tumour necrosis factor-alpha (TNF-alpha) secretion by lipopolysaccharide (LPS)-activated THP-1 cells with similar IC50s of approximately 0.1 microM. This inhibition was effectively reversed by the beta 2-antagonist oxprenolol, indicating that the inhibition was mediated through the beta 2-adrenergic receptor. A strikingly different reactivity profile was seen with T cells. Salmeterol was able to inhibit the activation of both mouse and human T cells, as measured by proliferation and IL-2 secretion in response to anti-CD3 antibody, whereas albuterol was completely inactive in these assays. This T cell inhibition by salmeterol was about 10-fold less potent than that for TNF-alpha production, and was not reversed by a beta 2-antagonist, indicating that a different mechanism was involved in the effect of salmeterol on T cells. Paralleling the TNF-alpha inhibitory activity in vitro, oral dosing of salmeterol and albuterol inhibited LPS-induced increase in murine serum TNF level in vivo, with ED50s of approximately 0.1 mg/kg. This inhibition could be abrogated by dosing orally with the beta-blocker propranolol. The long-acting pharmacological profile of salmeterol was apparent in that it maintained its efficacy for 3 h, while albuterol had a much shorter duration of action. Salmeterol also had some protective effects in the galactosamine/LPS model of endotoxic shock, which is dependent upon TNF-alpha production. Though salmeterol inhibited serum TNF-alpha levels by up to 94% in this assay, it protected less than 50% of the animals from the lethal effects of the LPS/galactosamine mixture. This observation suggests that functional levels of TNF-alpha localized in tissues may not be accurately reflected by serum levels.     

Coeliac disease, adenocarcinoma of jejunum and in situ squamous carcinoma of oesophagus

The development of both adenocarcinoma of the jejunum and in situ squamous carcinoma of the oesophagus in an adult coeliac patient is described. Good evidence that adenocarcinoma of jejunum occurs more frequently in patients with coeliac disease has recently become available though this association has been suggested for some time. While oesophageal carcinoma has long been associated with coeliac disease, in situ carcinoma of oesophagus has not been previously described in these circumstances. We feel that the risk of this complication, as calculated from published series, warrants a screening programme for oesophageal malignancy in adult coeliacs.     

Pachytene Analysis in a Human Reciprocal (10;11) Translocation

Pachytene quadrivalents are described in a male heterozygous for a balanced reciprocal translocation between the long arms of chromosomes 10 and 11. The break points of the translocation occur at 10q23 and 11q24. The main chromomere patterns of the bivalents correspond to the main G bands in mitosis and are sufficiently pronounced to allow the identification of bivalents 10 and 11 in normal spermatocytes.     

In vitro regulation of thyroglobulin (Tg) autoantibody production by Tg-specific T-cell lines and hybridomas.

To define the interactions between self thyroglobulin (Tg)-reactive T and B we co-cultured enriched B cells taken from rat or mouse Tg-primed mice with major histocompatibility complex (MHC) class II-restricted T-cell lines specific for iodinated determinants on self-Tg, or hybridomas derived from those lines. Using two clonally distinct T-cell hybridomas, ADA2 and CH9, in vitro help for Tg autoantibody responses was observed using mouse (M)Tg-primed B cells and a 100 ng/ml MTg challenge. Using rat Tg-primed B cells and the same conditions, only CH9 provided help, indicating that the fine specificity of B cells influences their ability to interact with specific anti-Tg T-cell clones. In contrast to T-cell hybridomas, their parent T-cell lines MTg9B3 and MTg12B suppressed Tg autoantibody responses in vitro, although they augmented bystander proliferation of unprimed B cells. The MTg12B cells also (i) diminished the survival of Tg-primed B cells, and (ii) inhibited the proliferation of an antigen-presenting B-cell hybridoma (LK35.2) in a cytostasis assay. These findings together support the view that their suppressive activity is mediated through cytotoxicity. While the role of class II-restricted cytotoxic cells in thyroid autoimmunity is unknown, the results suggest that such cells may act to suppress autoantibody responses as well as to mediate tissue damage to class II-expressing thyroid cells.