| Recognition, pathophysiology, and management of acute myocardial infarction. | |
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MedLine Citation:
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PMID: 11571813 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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J W Cheng |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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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:
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Created Date: 2001-09-26 Completed Date: 2002-02-28 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 9503023 Medline TA: Am J Health Syst Pharm Country: United States |
Other Details:
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Languages: eng Pagination: 1709-18; quiz 1719-21 Citation Subset: IM |
Affiliation:
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Arnold & Marie Schwartz College of Pharmacy and Health Sciences, Long Island University, Brooklyn, NY, USA. jcheng@liu.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic beta-Antagonists
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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:
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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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