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A 56-year-old woman was brought to the cardiologist office for routine clinical examination. The patient showed signs of peripheral edema, denied dyspnea, New York Heart Association functional class II, and was on the following cardiac medications: angiotensin-converting enzyme (ACE) inhibitors, beta blockers, statins, mineralocorticoid receptor antagonists, and furosemide. Her focused past cardiac history is that of a prior myocardial infarction, coronary artery bypass surgery, prior heart failure hospitalizations, and a known ejection fraction of 35%. She also notes medical compliance but not dietary compliance and does not feel that her muscle strength is being maintained. Serum electrolytes were: sodium, 140 mmol/L; potassium ranges from 4.9 to 5.8 mmol/L; and creatinine, 62 μmol/L. The woman’s weight was 80 kg; height was 169 cm; body mass index (BMI) was 28 kg/m2. She and her clinical team wonder if a better focus on diet may play a role.


Chronic heart failure (HF) is a major and growing public health problem, with a tremendous impact on patients’ quality of life and a broader economic burden. Approximately 5.7 million Americans ≥20 years of age have HF, and prevalence has been projected to increase 46% from 2012 to 2030 as patients survive acute myocardial infarction, live to an older age, and have best medical and nonpharmacologic care available. Survival after HF diagnosis has improved over time; however, HF carries a 5-year mortality rate of ~50% after diagnosis, and total direct medical cost of HF was estimated to be $21 billion in 2012.


HF is a clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.1 The most common etiologies are ischemic heart disease, hypertension (HTN), and diabetes. Less common causes of HF are cardiomyopathies, infections (eg, viral myocarditis, Chagas disease), toxins (eg, alcohol, cytotoxic drugs), valvular disease, and prolonged arrhythmias.2


HF may be associated with reduced cardiac output, which leads to a decrease in mean arterial pressure and diminished renal perfusion and causes to neurohormonal activation characterized by an overexpression of the sympathetic nervous system and the renin angiotensin aldosterone system to maintain optimal tissue perfusion to vital organs. This set of complex compensatory mechanisms causes vasoconstriction and renal sodium and water retention. Chronic neurohormonal activation exacerbates the hemodynamic abnormalities present in HF, producing further remodeling and neurohormone release and progressive cardiac impairment, causing excessive sodium and fluid retention.2,3 This pathophysiologic process is in part responsible for HF signs and symptoms such as dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary congestion and peripheral edema, all of which affect functional capacity and quality of life.1...

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