Preinfarction angina does not alter infarct size and in hospital outcome after acute myocardial infarction with ST elevation

Background: Preinfarction angina has been reported to limit infarct size, in a manner analogous to experimental preconditioning. However, other studies have reported inconsistent results. We aimed to investigate prospectively the role of preinfarction angina on infarct size and in hospital outcome....

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Bibliographic Details
Published in:International journal of cardiology 2004-04, Vol.94 (2), p.187-191
Main Authors: Psychari, Stavroula N., Iliodromitis, Efstathios K., Hamodraka, Eftihia, Liakos, Georgios, Velissaridou, Angeliki, Apostolou, Thomas S., Kremastinos, Dimitrios Th
Format: Article
Language:English
Subjects:
Angina, Unstable - physiopathology
Biological and medical sciences
Biomarkers - blood
C-Reactive Protein - analysis
Cardiology. Vascular system
Coronary heart disease
Creatine Kinase - blood
Creatine Kinase, MB Form
Female
Heart
Hospital Mortality
Humans
Ischemia
Ischemic Preconditioning, Myocardial
Isoenzymes - blood
Male
Medical sciences
Middle Aged
Myocardial Infarction - mortality
Myocardial Infarction - physiopathology
Outcome Assessment (Health Care)
Preconditioning
Preinfarction angina
Prospective Studies
Troponin I - blood
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Summary:Background: Preinfarction angina has been reported to limit infarct size, in a manner analogous to experimental preconditioning. However, other studies have reported inconsistent results. We aimed to investigate prospectively the role of preinfarction angina on infarct size and in hospital outcome. Methods: Ninety-nine patients were divided into three groups according to the timing of angina: the group “48 h” earlier than 48 h and the group “acute” no angina before infarction. Myocardial injury was estimated by creatine kinase, creatine kinase-MB, troponin I and C-reactive protein. In hospital events included death, recurrent ischemia, congestive heart failure and atrioventricular block. Results: Clinical characteristics, thrombolysis administration and the magnitude of enzymes released were not statistically different among the three groups: peak creatine kinase was 2139±1714 U/l for the >48 h group, vs. 2344±1634 U/l for the acute group, vs. 2209±1384 U/l for the 48 h group, vs. 168±182 U/l for the acute group, vs. 154±108 U/l for the
ISSN:0167-5273
1874-1754
DOI:10.1016/j.ijcard.2003.03.021