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1. In-Hospital Mortality After Cardiac Surgery: Patient Characteristics, Timing, and Association With Postoperative Length of Intensive Care Unit and Hospital Stay

Author

Timothy George Buchman, Michael Halkos, Michael A. Mazzeffi, and Joel Zivot

Subjects
Male, Pulmonary and Respiratory Medicine, medicine.medical_specialty, Time Factors, Single Center, law.invention, Postoperative Complications, law, Humans, Medicine, Hospital Mortality, Cardiac Surgical Procedures, Stroke, Aged, Retrospective Studies, business.industry, Mortality rate, Odds ratio, Length of Stay, Middle Aged, medicine.disease, Intensive care unit, Surgery, Cardiac surgery, Intensive Care Units, Pneumonia, Female, Cardiology and Cardiovascular Medicine, business, Hospital stay
Abstract

It is important to characterize in-hospital mortality after cardiac surgery and understand the relationships between postoperative length of intensive care unit stay, postoperative length of hospital stay, and the likelihood of in-hospital mortality.We retrospectively identified all cardiac surgery cases that resulted in in-hospital mortality over an 8-year period at a single center. For these subjects we collected demographic data, preoperative comorbidities, and postoperative complications. We performed stepwise multivariate linear regression to determine which postoperative complications were associated with mortality timing. We also analyzed the relationships between postoperative length of intensive care unit stay, postoperative length of hospital stay, and in-hospital mortality in all patients (including survivors) who had cardiac surgery during the same time period. Finally, we calculated the daily incremental observed mortality rate for patients in the hospital up to postoperative day 50.Six hundred twenty-one in-hospital mortalities occurred among 18,348 patients during the study period (3.4%). Four postoperative complications were associated with mortality timing. Cardiac arrest had a negative association with the number of days until mortality, while deep sternal wound infection, stroke, and pneumonia had a positive association (all p0.05). Postoperative complications explained 15% of the variability in mortality timing (R2 model=0.15). The odds ratio for in-hospital mortality was 1.033 for each postoperative day in the hospital and 1.071 for each postoperative day in the intensive care unit (both p0.05).Most in-hospital mortality occurs during the first week after cardiac surgery with few mortalities occurring after a protracted hospital course. Postoperative complications have a limited ability to explain the variability in mortality timing. Increased length of postoperative intensive care unit stay and hospital stay after cardiac surgery are associated with an increased likelihood of in-hospital mortality.

Published
2014

3. Immune Response of Mice Transgenic for Human Histocompatibility Leukocyte Antigen-DR to Human Thyrotropin Receptor-Extracellular Domain.

Author

Hidefumi Inaba, Deshun Pan, Young-Ha Shin, William Martin, George Buchman, and Leslie J. De Groot

Subjects
HISTOCOMPATIBILITY antigens, IMMUNOREGULATION, TRANSGENIC mice, THYROTROPIN, HORMONE receptors, EPITOPES, LABORATORY mice, GRAVES' disease
Abstract

Background:Hyperthyroidism of Graves'' disease is caused by auto-antibodies to human thyrotropin receptor (hTSH-R). To elucidate important T-cell epitopes in TSH-R, we studied three models of immunity to TSH-R in mice.Methods:Mice transgenic for histocompatibility leukocyte antigen DR3 or DR2 were immunized with cDNA for hTSH-R-extracellular domain (hTSH-R-ECD), or hTSH-R-ECD protein, or hTSH-R peptide epitopes. Proliferative responses of immunized splenocytes to epitopes derived from the hTSH-ECD sequence, anti-TSH-R antibody responses, serum thyroxine and TSH, and thyroid histology were recorded.Results:DR3 mice responded to genomic immunization with proliferative responses to several epitopes, which increased in intensity and spread to include more epitopes, during a 6-week immunization program. DR2 transgenic mice developed weak proliferative responses. Both types of mice developed anti-TSH-R antibodies measured by enzyme-linked immunosorbent assay or TSH-binding inhibition assay in 16–60% of animals. There was evidence of weak thyroid stimulation in one group of animals. Immunization of DR3 transgenic mice to hTSH-R-ECD protein induced a striking response to an epitope with sequence ISRIYVSIDVTLQQLES (aa78–94). Immunization to peptides derived from the TSH-R-ECD sequence (including aa78–94) caused strong responses to the epitopes, and development of immune responses to several other nonoverlapping epitopes within the hTSH sequence (epitope spreading) and antibodies reacting with hTSH-R. This implies that immunization with hTSH-R epitopes produced immunity to mouse TSH-R.Conclusion:T-cell and B-cell responses to genetic immunization differ in DR3 and DR2 transgenic mice, and there is less genetic control of antibody than of T-cell responses. During both genomic and peptide epitope immunization there was evidence of epitope spreading during the immunization. Several functionally important epitopes are evident, especially aa78–94. However, if similar progressive epitope recruitment occurs in human disease, epitope-based therapy will be difficult to achieve. [ABSTRACT FROM AUTHOR]

Published
2009
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