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Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology | Vol.14, Issue.4 | | Pages 219-24

Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

The relationship of nodular endocardial infiltrates (Quilty lesions) to survival, patient age, anti-HLA antibodies, and coronary artery disease following heart transplantation.

Kimberly E, Chu Eric K, Ho Ludwika, de la Torre Elena R, Vasilescu Charles C, Marboe  
Abstract

Quilty lesions are mononuclear cell infiltrates identified in human heart transplant biopsies. The biologic significance of Quilty lesions remains undetermined.We monitored acute rejection by biopsy and lymphocyte growth assay (LGA) as well as transplant-related coronary artery disease (TRCAD) by yearly angiogram in 285 recipients of primary heart allografts. Patients showing Quilty lesions on biopsies during the first year posttransplant were compared with patients without such lesions. Recipients' sera were obtained at the time of biopsy and tested for anti-HLA Class I and II antibodies.The actuarial survival of patients who developed Quilty lesions was significantly better than those who did not (P=.0074). Patients with Quilty lesions were younger and more likely to have a biopsy diagnosis of acute rejection (P=.002) and positive LGA (P<.0001) during the first posttransplant year. Among patients who do not form anti-HLA Class II antibodies, those with Quilty lesions were more likely than patients without Quilty lesions to develop TRCAD 5 years posttransplantation (P=.04). There was no correlation of Quilty status with the number of HLA donor-recipient mismatches or posttransplant development of anti-HLA antibodies.Quilty formers showed improved survival and are more likely to be diagnosed with acute rejection on biopsy and have positive LGAs. Allograft recipients who do not form anti-HLA Class II antibodies but do form Quilty lesions are more likely to develop TRCAD by 5 years posttransplantation than those who do not form Quilty lesions.

Original Text (This is the original text for your reference.)

The relationship of nodular endocardial infiltrates (Quilty lesions) to survival, patient age, anti-HLA antibodies, and coronary artery disease following heart transplantation.

Quilty lesions are mononuclear cell infiltrates identified in human heart transplant biopsies. The biologic significance of Quilty lesions remains undetermined.We monitored acute rejection by biopsy and lymphocyte growth assay (LGA) as well as transplant-related coronary artery disease (TRCAD) by yearly angiogram in 285 recipients of primary heart allografts. Patients showing Quilty lesions on biopsies during the first year posttransplant were compared with patients without such lesions. Recipients' sera were obtained at the time of biopsy and tested for anti-HLA Class I and II antibodies.The actuarial survival of patients who developed Quilty lesions was significantly better than those who did not (P=.0074). Patients with Quilty lesions were younger and more likely to have a biopsy diagnosis of acute rejection (P=.002) and positive LGA (P<.0001) during the first posttransplant year. Among patients who do not form anti-HLA Class II antibodies, those with Quilty lesions were more likely than patients without Quilty lesions to develop TRCAD 5 years posttransplantation (P=.04). There was no correlation of Quilty status with the number of HLA donor-recipient mismatches or posttransplant development of anti-HLA antibodies.Quilty formers showed improved survival and are more likely to be diagnosed with acute rejection on biopsy and have positive LGAs. Allograft recipients who do not form anti-HLA Class II antibodies but do form Quilty lesions are more likely to develop TRCAD by 5 years posttransplantation than those who do not form Quilty lesions.

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Kimberly E, Chu Eric K, Ho Ludwika, de la Torre Elena R, Vasilescu Charles C, Marboe,.The relationship of nodular endocardial infiltrates (Quilty lesions) to survival, patient age, anti-HLA antibodies, and coronary artery disease following heart transplantation.. 14 (4),219-24.

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