title: [Acute coronary syndromes: an update. I. Pathogenesis and drug therapy].
abstract: BACKGROUND
  Unstable angina accounts for more than one million hospital admissions annually. 6-8% of patients with this condition have non-fatal myocardial infarction or die within the first year after diagnosis. Recently, the term "acute coronary syndromes" has been used to describe the spectrum of conditions that includes unstable angina, non-Q-wave myocardial infarction (which generally presents without ST-segment elevation), and Q-wave myocardial infarction (which generally presents with ST-segment elevation).
  
  
  METHODS
  Disruption of a formed plaque is a complex pathologic process that is central to the initiation of the acute coronary syndromes. Local thrombosis occurring after plaque disruption results from complex interactions among the lipid core, smooth-muscle cells, macrophages, and collagen.
  
  
  METHODS
  Multiple huge clinical trials confirmed that aspirin reduces the risk of death from cardiac causes and fatal and non-fatal myocardial infarction by about 50-70% in patients presenting with unstable angina. Ticlopidine may be substituted for aspirin in patients with hypersensitivity to aspirin or gastrointestinal intolerance. Clopidogrel acts similarly to ticlopidin but has fewer side effects than ticlopidine and has not been reported to cause neutropenia. High-risk patients with refractory unstable angina and elevated troponin levels may have substantial benefit of glycoptotein (GP) IIb/IIIa inhibition. Current practice guidelines support the use of the combination of unfractionated heparin and aspirin for the treatment of unstable angina. Clinical studies have demonstrated that the incidence of the composite end point of death, myocardial infarction, or recurrent angina was lower with enoxaparin than with unfractionated heparin. Beta-blockers, nitrates, and calcium-channel blockers are useful for antiischemic therapy in patients with acute coronary syndromes.
authors.affiliation: II. Interne Abteilung mit Kardiologie und Internistischer Intensivmedizin, Allgemeines Offentliches Krankenhaus der Barmherzigen Schwestern vom Heiligen Kreuz, Wels, Osterreich. johann.auer@khwels.at
authors.forename: J
authors.initials: J
authors.lastname: Auer
authors.forename: R
authors.initials: R
authors.lastname: Berent
authors.forename: E
authors.initials: E
authors.lastname: Maurer
authors.forename: H
authors.initials: H
authors.lastname: Mayr
authors.forename: T
authors.initials: T
authors.lastname: Weber
authors.forename: B
authors.initials: B
authors.lastname: Eber
mesh_terms: D000208:Acute Disease; D000284:Administration, Oral; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000789:Angina, Unstable / Q000188:drug therapy* / Q000209:etiology*; D000925:Anticoagulants / Q000008:administration & dosage / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D002121:Calcium Channel Blockers; D002986:Clinical Trials as Topic; D000077144:Clopidogrel; D004562:Electrocardiography; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D015337:Multicenter Studies as Topic; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000209:etiology*; D009566:Nitrates / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D012307:Risk Factors; D013577:Syndrome; D009626:Terminology as Topic; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D000319:Adrenergic beta-Antagonists; D000925:Anticoagulants; D002121:Calcium Channel Blockers; D005343:Fibrinolytic Agents; D009566:Nitrates; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014443:Tyrosine; D000077144:Clopidogrel; D000077466:Tirofiban; D013988:Ticlopidine; D001241:Aspirin