ABSTRACT
BACKGROUND: In heart transplantation, antibody-mediated rejection (AMR) is diagnosed and graded on the basis of immunopathologic (C4d-CD68) and histopathologic criteria found on endomyocardial biopsies (EMB). Because some pathologic AMR (pAMR) grades may be associated with clinical AMR, and because humoral responses may be affected by the intensity of immunosuppression during the first posttransplantation year, we investigated the incidence and positive predictive values (PPV) of C4d-CD68 and pAMR grades for clinical AMR as a function of time. METHODS: All 564 EMB from 40 adult heart recipients were graded for pAMR during the first posttransplantation year. Clinical AMR was diagnosed by simultaneous occurrence of pAMR on EMB, donor specific antibodies and allograft dysfunction. RESULTS: One patient demonstrated clinical AMR at postoperative day 7 and one at 6 months (1-year incidence 5%). C4d-CD68 was found on 4,7% EMB with a "decrescendo" pattern over time (7% during the first 4 months vs. 1.2% during the last 8 months; P < 0.05). Histopathologic criteria of AMR occurred on 10.3% EMB with no particular time pattern. Only the infrequent (1.4%) pAMR2 grade (simultaneous histopathologic and immunopathologic markers) was predictive for clinical AMR, particularly after the initial postoperative period (first 4 months and last 8 months PPV = 33%-100%; P < 0.05). CONCLUSION: In the first posttransplantation year, AMR immunopathologic and histopathologic markers were relatively frequent, but only their simultaneous occurrence (pAMR2) was predictive of clinical AMR. Furthermore, posttransplantation time may modulate the occurrence of C4d-CD68 on EMB and thus the incidence of pAMR2 and its relevance to the diagnosis of clinical AMR.
Subject(s)
Antibodies/chemistry , Antigens, CD/chemistry , Antigens, Differentiation, Myelomonocytic/chemistry , Complement C4b/chemistry , Graft Rejection , Heart Failure/immunology , Heart Failure/therapy , Heart Transplantation , Peptide Fragments/chemistry , Aged , Allografts , Female , Humans , Male , Middle Aged , Postoperative Period , Sensitivity and Specificity , Time Factors , Tissue Donors , Treatment OutcomeSubject(s)
Cardiomyopathy, Dilated/etiology , Cardiomyopathy, Dilated/genetics , DNA, Mitochondrial/genetics , MELAS Syndrome/complications , MELAS Syndrome/genetics , Mutation/genetics , Adrenergic beta-Antagonists/therapeutic use , Adult , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Cardiomyopathy, Dilated/drug therapy , Drug Therapy, Combination , Female , Humans , MELAS Syndrome/diagnosis , Mineralocorticoid Receptor Antagonists/therapeutic use , Treatment OutcomeABSTRACT
BACKGROUND: The apical ballooning syndrome is precipitated by emotional or physical stress but the underlying mechanism remains poorly understood. The contribution of myocardial bridging on the aetiology and the onset of the syndrome is not known. METHODS: We observed 8 patients with chest pain, T-wave inversion in several leads of the ECG, transient left ventricular apical ballooning and no significant angiographic stenosis. RESULTS: There were 7 women and I man. The median age was 67.5 years. Seven patients had an intense emotional or physical stress (87.5%). All patients presented with chest pain and aT-wave inversion in the precordial leads. The median elevation of creatine-kinase was 171 IU. In all patients, echocardiography showed an alteration of the left ventricular function with a very extensive apical akinesia. Left ventricular hypertrophy was observed in 7 patients. A myocardial bridging in the mid segment of the left anterior descending coronary artery was observed in 5 patients (62.5%). Recovery was complete in all patients. During follow-up, no patient showed recurrence. CONCLUSIONS: Our data suggest that myocardial bridging possibly enhanced by catecholamines during stress may contribute, in association with left ventricular hypertrophy, to the preferential apical localization of the apical ballooning syndrome. Further investigations are necessary to confirm