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QRS mapping in the evaluation of acute anterior myocardial infarction.
Author(s) -
R. von Essen,
W. Merx,
Rolf Doerr,
S. Effert,
J. Silny,
G. Rau
Publication year - 1980
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.62.2.266
Subject(s) - medicine , qrs complex , myocardial infarction , cardiology , hemodynamics , st segment , creatine kinase , chest pain , infarction , anesthesia
In 42 patients with acute anterior myocardial infarction (AMI), we studied the course of Q-wave development and R-wave reduction during the first 48 hours after the onset of chest pain. We used precordial mapping in relation to clinical features, hemodynamic measurements and enzyme release. Q waves developed within 6-14 hours (mean 9 hours) after onset of symptoms. R-wave amplitudes demonstrated nearly a reflected image: They reduced abruptly 5-11 hours (mean 9 hours) after onset of chest pain, coinciding with ST-segment elevation. In 14 patients (group A, 33%) after initial QRS alterations, there were no further changes. Twenty patients (group B, 48%) had a distinct new increase of Q waves (delta sigma Q = 3.0 +/- 2.0 mV/hours) and further R-wave reduction (-delta sigma R = 1.0 +/- 0.6 mV/hour) simultaneous with new severe chest pain and a delayed second increase of enzyme release corresponding with extension of infarction. There were no significant differences between the groups in age, hemodynamics and infarct size calculated from creatine kinase release. Eight patients (group C, 19%) had contradictory findings. Our findings are consistent with previous results indicating that the critical period for intervention is very small except in patients with extension of necrosis.

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