TY - JOUR
T1 - When the electrocardiogram fails to define site and extent of myocardial ischemia
AU - Marzullo, P.
AU - Parodi, O.
AU - Marcassa, C.
PY - 1986
Y1 - 1986
N2 - Information on the anatomical site of myocardial ischemia and infarction is commonly derived from the 12-lead electrocardiogram; however, correspondence between an electrocardiogram lead, showing ischemic changes and actual location of ischemia is not always present. In our experience, a good correspondence between the electrocardiogram and perfusion defects was found in patients with angina at rest and anterior ST segment elevation or normalization of negative T wave while patients with transient ST segment depression showed perfusion defects which correlated less with electrocardiographic changes. In addition, patients with ischemic episodes at rest and with inferior ST segment elevation, right or left ventricular ischemia were indistinguishable on the basis of the electrocardiogram as documented by Thallium-201 scintigraphy and radionuclide ventriculography. In effort angina, the site and extension of ST segment depression, even in patients with single vessel disease, failed to localize the actual anatomical location of myocardial ischemia. In patients with persistent ST segment depression and/or negative T waves, and clinically documented myocardial necrosis, transmural and non-transmural persistent perfusion defects were found in spite of absence of Q waves. In these patients, late normalization of the electrocardiogram did not correspond to normalization of flow. In conclusion, electrocardiographic changes do not always provide correct information regarding the presence, location and extent of myocardial ischemia and a multiparametric approach is often required in order to characterize ischemic and/or necrotic areas.
AB - Information on the anatomical site of myocardial ischemia and infarction is commonly derived from the 12-lead electrocardiogram; however, correspondence between an electrocardiogram lead, showing ischemic changes and actual location of ischemia is not always present. In our experience, a good correspondence between the electrocardiogram and perfusion defects was found in patients with angina at rest and anterior ST segment elevation or normalization of negative T wave while patients with transient ST segment depression showed perfusion defects which correlated less with electrocardiographic changes. In addition, patients with ischemic episodes at rest and with inferior ST segment elevation, right or left ventricular ischemia were indistinguishable on the basis of the electrocardiogram as documented by Thallium-201 scintigraphy and radionuclide ventriculography. In effort angina, the site and extension of ST segment depression, even in patients with single vessel disease, failed to localize the actual anatomical location of myocardial ischemia. In patients with persistent ST segment depression and/or negative T waves, and clinically documented myocardial necrosis, transmural and non-transmural persistent perfusion defects were found in spite of absence of Q waves. In these patients, late normalization of the electrocardiogram did not correspond to normalization of flow. In conclusion, electrocardiographic changes do not always provide correct information regarding the presence, location and extent of myocardial ischemia and a multiparametric approach is often required in order to characterize ischemic and/or necrotic areas.
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M3 - Article
C2 - 3756603
AN - SCOPUS:0022556984
VL - 2
JO - Canadian Journal of Cardiology
JF - Canadian Journal of Cardiology
SN - 0828-282X
IS - SUPPL. A
ER -