Document Detail


Recognition, pathophysiology, and management of acute myocardial infarction.
MedLine Citation:
PMID:  11571813     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
New insights into the pathophysiology of atherosclerotic plaques leading to acute myocardial infarction (MI) are discussed, along with new diagnostic and treatment strategies. Ischemic heart disease represents a continuum from stable angina to unstable angina to non-Q-wave MI to Q-wave MI. Patients whose angina becomes unstable are classified as having acute coronary syndrome (ACS). It was formerly believed that thrombosis leading to critical occlusion of coronary arteries at the site of atherosclerotic plaque rupture was the common cause of ischemic heart disease. It is now thought that even lesions that do not critically occlude coronary arteries can cause MI. ACS can be caused by the rupture of an unstable atherosclerotic plaque. Vulnerable plaques are usually those causing only mild to moderate stenosis and having a lipid-rich core and a thin, macrophage-dense, collagen-poor fibrous cap. Factors affecting plaque rupture include mechanical injury, circadian rhythm, inflammation, and infection. Progressive thrombosis and vasospasm may follow plaque rupture. The diagnosis of MI starts with the recognition of symptoms of myocardial ischemia that are new or different from the usual pattern. Agents used to prevent or treat plaque rupture and its complications include thrombolytics, antiplatelet agents, antithrombotics, beta-blockers, angiotensin-converting-enzyme (ACE) inhibitors, and nitrates. Once patients survive the acute phase of MI, long-term therapy for prevention of future events begins. Post-MI patients should receive aspirin, beta-blockers, and an ACE inhibitor indefinitely; modification of cardiovascular risk factors is also important. Greater understanding of the pathophysiology of ACS has led to strategies to limit the progression of atherosclerosis and to improve survival and function after an acute event.
Authors:
J W Cheng
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists     Volume:  58     ISSN:  1079-2082     ISO Abbreviation:  Am J Health Syst Pharm     Publication Date:  2001 Sep 
Date Detail:
Created Date:  2001-09-26     Completed Date:  2002-02-28     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  9503023     Medline TA:  Am J Health Syst Pharm     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1709-18; quiz 1719-21     Citation Subset:  IM    
Affiliation:
Arnold & Marie Schwartz College of Pharmacy and Health Sciences, Long Island University, Brooklyn, NY, USA. jcheng@liu.edu
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Antagonists / therapeutic use
Angiotensin-Converting Enzyme Inhibitors / therapeutic use
Anti-Arrhythmia Agents / therapeutic use
Humans
Myocardial Infarction / diagnosis,  drug therapy*,  physiopathology*
Nitrates / therapeutic use
Platelet Aggregation Inhibitors / therapeutic use
Risk Factors
Thrombolytic Therapy
Chemical
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Anti-Arrhythmia Agents; 0/Nitrates; 0/Platelet Aggregation Inhibitors

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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