Left ventricular dysfunction and heart failure. Mechanistic and therapeutic distinctions.
Dysfunction of the left ventricle may result from a variety of insults, all of which may initiate a self-perpetuating process of ventricular remodeling which may progress to end-stage heart disease. Symptoms of heart failure may or may not co-exist with this ventricular remodeling. Treatment and prevention of these two largely distinct entities differ. Symptoms may respond to diuretics, vasodilators and digoxin. Progressive ventricular remodeling may be slowed by angiotensin converting enzyme inhibitors, hydralazine + isosorbide dinitrate and beta blockers. Prevention of symptomatic heart failure is dependent on early recognition of ventricular dysfunction and aggressive treatment to slow its progression. Development of more effective and targeted therapies will be dependent on expanded insight into the cellular and molecular mechanisms contributing to the remodeling process.
Cohn
J N
JN
Department of Medicine, University of Minnesota Medical School, Minneapolis 55455, USA.
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D004077:Digoxin / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy / Q000209:etiology* / Q000517:prevention & control; D006801:Humans; D014665:Vasodilator Agents / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy / Q000209:etiology* / Q000517:prevention & control
D000806:Angiotensin-Converting Enzyme Inhibitors; D004232:Diuretics; D014665:Vasodilator Agents; D004077:Digoxin