Abstract

Heart failure is a worldwide health problem of ever increasing proportions, particularly amongst the elderly. It most commonly is found in association with previous myocardial infarction(s), longstanding hypertension, or a myopathic process often of uncertain origin. A failure of the heart to carry out its expected functions during systolic and/or diastolic phases of the cardiac cycle can lead to reduced renal perfusion and a resultant salt-avid state mediated largely by effector hormones of the renin-angiotensinaldosterone system (RAAS). The accompanying retention of salt and water begets characteristic signs and symptoms that comprise the clinical syndrome congestive heart failure (CHF). Pharmacologic interference with the RAAS has become an integral part of today’s standard of care in the prevention and treatment of heart failure, with and without CHF. Diuretics are used to assist the kidneys in the excretion of sodium and water when patients are decompensated with CHF. In recent years, the CHF paradigm has been broadened beyond this cardiorenal perspective to include the presence of a systemic illness which contributes to its progressive nature and all-too-often downhill clinical course. Features of this illness include: a) the presence of oxidative and nitrosative stress that overwhelm such endogenous antioxidant defenses provided by Cu/Zn superoxide dismutase and Se-glutathione peroxidase in diverse tissues that include skin, skeletal muscle, heart, peripheral blood mononuclear cells (PBMC: lymphocytes and monocytes), and blood; b) an immunostimu-

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