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  • Image not available. Heart failure is a clinical syndrome caused by the inability of the heart to pump sufficient blood to meet the metabolic needs of the body. It can result from any disorder that reduces ventricular filling (diastolic dysfunction) and/or myocardial contractility (systolic dysfunction). The leading causes of heart failure are coronary artery disease and hypertension. The primary manifestations of the syndrome are dyspnea, fatigue, and fluid retention.
  • Image not available. Heart failure is a progressive disorder that begins with myocardial injury. In response to the injury, several 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 heart failure and contribute to disease progression.
  • Image not available. Our current understanding of heart failure 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 heart failure. Pharmacotherapy targeted at antagonizing this neurohormonal activation has slowed the progression of heart failure and improved survival.
  • Image not available. Most patients with symptomatic heart failure should be routinely treated with an angiotensin-converting enzyme (ACE) inhibitor, a β-blocker, and a diuretic. The benefits of these medications on slowing heart failure progression, reducing morbidity and mortality, and 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 heart failure, 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 and the combination of hydralazine and isosorbide dinitrate are reasonable alternatives. Patients with asymptomatic left ventricular dysfunction and/or a previous myocardial infarction (MI; stage B of the American College of Cardiology/American Heart Association [ACC/AHA] classification scheme) should also receive ACE inhibitors, with the goal of preventing symptomatic heart failure and reducing mortality.
  • Image not available. The β-blockers carvedilol, metoprolol controlled release/extended release (CR/XL), and bisoprolol have been shown to prolong survival, decrease hospitalizations and the 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 patients with heart failure, 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 heart failure but does provide symptomatic benefits. Digoxin doses should be adjusted to achieve plasma ...

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