BACKGROUND The natural history, management, and outcome of takotsubo (stress) cardiomyopathy are incompletely understood. METHODS The International Takotsubo Registry, a consortium of 26 centers in Europe and the United States, was established to investigate clinical features, prognostic predictors, and outcome of takotsubo cardiomyopathy. Patients were compared with age-and sex-matched patients who had an acute coronary syndrome. RESULTS Of 1750 patients with takotsubo cardiomyopathy, 89.8% were women (mean age, 66.8 years). Emotional triggers were not as common as physical triggers (27.7% vs. 36.0%), and 28.5% of patients had no evident trigger. Among patients with takotsubo cardiomyopathy, as compared with an acute coronary syndrome, rates of neurologic or psychiatric disorders were higher (55.8% vs. 25.7%) and the mean left ventricular ejection fraction was markedly lower (40.7±11.2% vs. 51.5±12.3%) (P<0.001 for both comparisons). Rates of severe in-hospital complications including shock and death were similar in the two groups (P=0.93). Physical triggers, acute neurologic or psychiatric diseases, high troponin levels, and a low ejection fraction on admission were independent predictors for in-hospital complications. During long-term follow-up, the rate of major adverse cardiac and cerebrovascular events was 9.9% per patient-year, and the rate of death was 5.6% per patient-year. CONCLUSIONS Patients with takotsubo cardiomyopathy had a higher prevalence of neurologic or psychiatric disorders than did those with an acute coronary syndrome. This condition represents an acute heart failure syndrome with substantial morbidity and mortality. (Funded by the Mach-Gaensslen Foundation and others; ClinicalTrials.gov number, NCT01947621.).
Overall, TTS patients had long-term outcomes comparable to age- and sex-matched ACS patients. Also, we demonstrated that TTS can either be benign or a life-threating condition depending on the inciting stress factor. We propose a new classification based on triggers, which can serve as a clinical tool to predict short- and long-term outcomes of TTS. (International Takotsubo Registry [InterTAK Registry]; NCT01947621).
Atypical TTS has different characteristics than typical TTS, including younger age of onset, more frequent ST-segment depression, higher prevalence of neurologic diseases, less pronounced reduction in left ventricular ejection fraction, and lower brain natriuretic peptide values on admission. Outcomes are comparable between patients with both types after adjustment for confounders, suggesting that both should be equally monitored.
T helper type 17 (Th17) cells have been characterized based on production of interleukin-17 (IL-17) and association with autoimmune diseases. We studied the role of Th17 cells in aplastic anemia (AA) by isolating Th17 cells from patients blood (n ؍ 41) and bone marrow (BM) mononuclear cells (n ؍ 7). The frequency and total number of CD3 ؉ CD4 ؉ IL-17-producing T cells were increased in AA patients at presentation compared with healthy controls (P ؍ .0007 and .02, respectively) and IntroductionTh17 cells have been characterized recently in mice as a novel subset of CD4 ϩ T cells that produce interleukin-17A (IL-17A), IL-17-F, and IL-22, 1,2 and serve as immune effectors in various settings, including inflammation, infection, and autoimmunity. 3,4 Th17 cells produce a large amount of IL-17A, a cytokine that coordinates tissue inflammation by inducing the expression of proinflammatory cytokines (such as IL-6 and tumor necrosis factor [TNF]), chemokines (such as KC, MCP-1, and MIP-2), and matrix metalloproteases that mediate tissue infiltration and tissue destruction. 5 In mice, the differentiation program of Th17 cells from naive CD4 ϩ T cells requires the activation of the transcription factor, orphan nuclear receptor ROR␥t, 6 and the presence of IL-6 and transforming growth factor- (TGF-). 7,8 In humans, Th17 differentiation is under the control of IL-1, 10 Several studies have reported the association of IL-17 with inflammatory disorders, such as rheumatoid arthritis, asthma, multiple sclerosis, and lupus, 11 as well as hematologic disorders, such as myelodysplastic syndrome 12,13 and acute myeloid leukemia. 14 Aplastic anemia (AA), a disease characterized by peripheral blood pancytopenia and bone marrow (BM) hypoplasia, 15 is an immunemediated disorder in most cases with active destruction of hematopoietic cells by effector T lymphocytes. 16 Recovery of autologous hematopoiesis in patients who failed to engraft after conditioning and stem cell transplantation, 17 and responsiveness of patients to immunosuppressive therapies, 18 provided powerful evidence for the pivotal role of the immune system in the disease pathophysiology. Immoderate production of interferon-␥ (IFN-␥), TNF-␣, and IL-2 from patients'T cells suggests that the hematopoietic cells are destroyed through a Th1 response, [19][20][21] as illustrated by the up-regulation of the transcription factor T-bet in patient T cells. 22 The description of nonrandom skewing of the V chain families of the T-cell receptor in patient peripheral blood (PB) revealed that expanded oligoclonal or monoclonal specific V subfamilies selectively induced apoptosis of hematopoietic progenitor cells. 23 Regulatory T cells (Tregs), which control and suppress autoreactive T cells, are decreased at disease presentation in almost all patients. 24 We have developed murine models for immune-mediated BM failure by the infusion of allogeneic lymph node (LN) cells into sublethally irradiated recipients for which treatment with limited number of Treg cells, 25 or anti-IFN...
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