Neuroendocrine activation in acute myocardial infarction.
Recent research indicates that neurohormonal responses after myocardial infarction may predict patient outcome, and alteration of this process may change etiologic factors and strengthen positive prognosticators. Because there are clinical similarities between acute myocardial infarction and heart failure, there appears to be justification for a unified treatment approach (i.e., therapies that have proved beneficial in the treatment of myocardial infarction have also showed promise in the treatment of heart failure). Conversely, some therapies that have benefited the patient with heart failure may benefit the patient who has had a myocardial infarction. For example, angiotensin-converting enzyme inhibitors have been proven to blunt detrimental neurohormonal activity seen after myocardial infarction. These therapies promise to reduce complications and improve survival.
Levine
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TB
Heart Failure and Cardiac Transplant Program, Henry Ford Hospital, Detroit, Michigan 48202.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D006333:Heart Failure / Q000378:metabolism; D006439:Hemodynamics; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011379:Prognosis; D012084:Renin-Angiotensin System / Q000502:physiology
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002395:Catecholamines; D018377:Neurotransmitter Agents