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  • Image not available. Heart failure (HF) is a progressive clinical syndrome that can result from any changes in cardiac structure or function that impair the ability of the ventricle to fill with or eject blood. HF may be caused by an abnormality in systolic function, diastolic function, or both. The leading causes of HF are coronary artery disease and hypertension. The primary manifestations of the syndrome are dyspnea, fatigue, and fluid retention.
  • Image not available. In response to a decrease in cardiac output, a number of compensatory responses are activated in an attempt to maintain adequate cardiac output, including activation of the sympathetic nervous system (SNS) and the renin–angiotensin–aldosterone system (RAAS), resulting in vasoconstriction and sodium and water retention as well as ventricular hypertrophy/remodeling. These compensatory mechanisms are responsible for the symptoms of HF and contribute to disease progression.
  • Image not available. Our current understanding of HF pathophysiology is best described by the neurohormonal model. Activation of endogenous neurohormones including norepinephrine, angiotensin II, aldosterone, vasopressin, and numerous proinflammatory cytokines plays an important role in ventricular remodeling and the subsequent progression of HF. Importantly, pharmacotherapy targeted at antagonizing this neurohormonal activation has slowed the progression of HF and improved survival.
  • Image not available. Most patients with symptomatic systolic heart failure (SHF) should be routinely treated with an angiotensin-converting enzyme (ACE) inhibitor, a β-blocker, and a diuretic. The benefits of these medications on slowing HF progression, reducing morbidity and mortality, and/or improving symptoms are clearly established. Patients should be treated with a diuretic if there is evidence of fluid retention. Treatment with digoxin may also be considered to improve symptoms and reduce hospitalizations.
  • Image not available. In patients with SHF, ACE inhibitors improve survival, slow disease progression, reduce hospitalizations, and improve quality of life. The doses for these agents should be targeted at those shown in clinical trials to improve survival. When ACE inhibitors are contraindicated or not tolerated, an angiotensin II receptor blocker or the combination of hydralazine and isosorbide dinitrate is a reasonable alternative. Patients with asymptomatic left ventricular dysfunction and/or a previous myocardial infarction (MI) (Stage B of the American College of Cardiology [ACC]/American Heart Association [AHA] classification scheme) should also receive ACE inhibitors, with the goal of preventing symptomatic HF and reducing mortality.
  • Image not available. The β-blockers carvedilol, metoprolol succinate, and bisoprolol have been shown to prolong survival, decrease hospitalizations and need for transplantation, and cause “reverse remodeling” of the left ventricle. These agents are recommended for all patients with a reduced left ventricular ejection fraction. Therapy must be instituted at low doses, with slow upward titration to the target dose.
  • Image not available. Although chronic diuretic therapy frequently is used in HF patients, it is not mandatory. Diuretic therapy along with sodium restriction is required only in those patients with peripheral edema and/or pulmonary congestion. Many patients will need continued diuretic therapy to maintain euvolemia after fluid overload is resolved.
  • Image not available. Digoxin does not improve survival in patients with SHF but does provide symptomatic benefits. Digoxin doses should be adjusted to achieve plasma concentrations of 0.5 to 1 ng/mL (0.6 to 1.3 nmol/L); ...

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