Abstract：
:Despite being relatively recent, a growing and significant accumulation of experimental and clinical evidence has been observed that points to a gradual state of immune-inflammatory activation in patients with heart failure (HF). High levels of several cytokines are found in the circulation and cardiac muscle of individuals with HF, and invariably correlate with the severity of the disease. These cytokines act on endothelial dysfunction, oxidative stress, induction of anemia, myocyte apoptosis, and on the progressive loss of skeletal muscle mass which is conventionally called the inflammatory paradigm of HF. Not only the myocardium, but also several tissues seem to synthesize these cytokines and perpetuate this continuous inflammatory state at a low degree, including leukocytes, monocytes, skeletal muscle cells and endothelial cells in response to hemodynamic and infectious stimuli, to hypoxia, to oxidative stress, to neurohumoral activation, and others. Thus, a network of molecules that interact with each other is formed, and connections with other axes that effectively contribute to the clinical deterioration of the patients are also established which fits into the pathophysiological model of multisystemic involvement that has been increasingly attributed to HF. Although the determination of these biomarkers in peripheral blood provides solid evidence of prognostic power, the results of therapeutic trials that modulated the immune-inflammatory loop in the clinical phase have been, so far, hardly encouraging. Therefore, we believe that a better understanding of the inflammatory activation and its multifaceted relation with the axes of decompensation of the disease is key for new therapeutic perspectives with a relevant impact to be established in the near future.
journal_name
Arq Bras Cardioljournal_title
Arquivos brasileiros de cardiologiaauthors
Candia AM,Villacorta H Jr,Mesquita ETdoi
10.1590/s0066-782x2007001500009subject
Has Abstractpub_date
2007-09-01 00:00:00pages
183-90, 201-8issue
3eissn
0066-782Xissn
1678-4170pii
S0066-782X2007001500009journal_volume
89pub_type
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