Abstract
The prognosis for patients with congestive heart failure (CHF) has been improved as a result of the use of angiotensin converting enzyme inhibitors and beta-adrenergic receptor blockers. The success of these therapies underscores the pathogenic role of neurohormonal activation in CHF. Clinical and experimental evidence supports a pathophysiologic role for pro-inflammatory cytokines and nitric oxide (NO) in the effects of angiotensin II and norepinephrine in CHF. Potential mechanism(s) responsible for the effects of these immunomodulators can be explained on the basis of established principles of myocardial excitation contraction coupling (E-C). A novel hypothesis is proposed that cytokines and NO-mediated alterations in E-C coupling contribute to the reversible myocardial depression and beta-adrenergic desensitization observed in a diverse group of clinical conditions that activate host inflammatory responses, including CHF. Basic studies into cytokine signaling pathways in cardiac myocytes have the potential to provide important new insights relevant to the design of new management strategies for the treatment of congestive heart failure patients.
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