Ziad I Dibbs

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Natural history studies in heart failure have shown that increases in left ventricular (LV) volume and LV mass are directly related to future deterioration in LV performance and a less favorable clinical course. Despite the recognized importance of remodeling in heart failure, very little is known about the basic mechanisms that lead to cardiac remodeling.(More)
BACKGROUND Inflammatory mediators, especially tumor necrosis factor (TNF), have been implicated in heart failure (HF). Thalidomide has anti-inflammatory properties and selectively inhibits TNF. Thus far, thalidomide or thalidomide analogues have not been evaluated in patients with heart failure. METHODS Thalidomide was assessed in preclinical and clinical(More)
OBJECTIVES The purpose of this study was to examine the variability in cytokines and cytokine receptors in patients with heart failure in comparison with a group of healthy control subjects who were free of cardiovascular disease. BACKGROUND Despite increasing interest in cytokines as mediators of disease progression in heart failure and the recent(More)
BACKGROUND Recent studies suggest that posttranslation processing or "shedding" (ie, secretion) of tumor necrosis factor (TNF) by tumor necrosis factor-alpha converting enzyme (TACE) may contribute to the left ventricular (LV) remodeling that occurs in the failing human heart. METHODS AND RESULTS To address the functional significance of TNF shedding, we(More)
Despite repeated attempts to develop a unifying hypothesis that explains the clinical syndrome of heart failure, no single conceptual paradigm has withstood the test of time. In this regard, recent studies have shown that a class of biologically active molecules, generically referred to as cytokines, are overexposed in heart failure. This article will(More)
BACKGROUND Previous studies in isolated cardiac myocytes have shown that tumor necrosis factor (TNF)-alpha provokes increased expression of 27- and 70-kD stress proteins as well as manganese superoxide dismutase, suggesting that TNF-alpha might play a role in mediating stress responses in the heart. METHODS AND RESULTS To determine whether TNF-alpha(More)
BACKGROUND Tumor necrosis factor (TNF) is initially synthesized as a 26-kDa transmembrane protein that is enzymatically cleaved by TNF-alpha converting enzyme (TACE) to generate a 17-kDa form of "secreted" TNF. Whereas the effects of secreted TNF in the heart have been characterized extensively, the effects of transmembrane TNF in the heart are unknown. (More)
Recent studies have identified the importance of biologically active molecules such as neurohormones as mediators of disease progression in heart failure. More recently it has become apparent that in addition to neurohormones, another portfolio of biologically active molecules, termed cytokines, are also expressed in the setting of heart failure. This(More)
BACKGROUND The mechanism(s) responsible for the persistent coexpression of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) in the failing heart is unknown. METHODS AND RESULTS To determine whether NO was sufficient to provoke TNF-alpha biosynthesis, we examined the effects of an NO donor, S-nitroso-N-acetyl penicillamine (SNAP), in(More)
Recent studies have shown that patients with heart failure overexpress a class of biologically active molecules, generically referred to as pro-inflammatory cytokines. This article will review recent clinical and experimental material that suggests that pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and(More)
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