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Transcardiac increase in tumor necrosis factor‐α and left ventricular end‐diastolic volume in patients with dilated cardiomyopathy
Author(s) -
Tsutamoto Takayoshi,
Wada Atsuyuki,
Ohnishi Masato,
Tsutsui Takashi,
Ishii Chitose,
Ohno Keijin,
Fujii Masanori,
Matsumoto Takehiro,
Yamamoto Takashi,
Takayama Tomoyuki,
Dohke Tomohiro,
Horie Minoru
Publication year - 2004
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2003.10.004
Subject(s) - medicine , dilated cardiomyopathy , cardiology , heart failure , ejection fraction , tumor necrosis factor alpha , coronary sinus , cardiac resynchronization therapy , ventricular remodeling , diastole , blood pressure
Background: It remains unclear whether tumor necrosis factor (TNF)‐α and interleukin‐6 (IL‐6) are secreted from the failing heart and whether there is a relationship between the transcardiac gradients of these cytokines and left ventricular (LV) remodeling. Aims: This study evaluated the relationship between transcardiac gradients of cytokines and LV volume and function in congestive heart failure patients with dilated cardiomyopathy (DCM). Methods and results: We measured the plasma levels of TNF‐α and IL‐6 in the aortic root (Ao) and the coronary sinus (CS) in 60 patients with DCM. There was no difference in plasma IL‐6 between the Ao and the CS. However, the plasma TNF‐α level was significantly higher in the CS than that in the Ao. There was a significant correlation between the transcardiac gradient of plasma TNF‐α and the LV end‐diastolic volume index (LVEDVI) and LV ejection fraction. According to stepwise multivariate analyses, the transcardiac increase of TNF‐α showed an independent and significantly positive relationship with a large LVEDVI. Conclusions: These results indicate that the elevated plasma TNF‐α is partly derived from the failing heart in patients with DCM and that TNF‐α plays a potential role in structural LV remodeling in patients with DCM.