Q-wave prediction of myocardial infarct location, size and transmural extent at magnetic resonance imaging (original) (raw)
Related papers
The Pathologic Basis of Q-Wave and Non-Q-Wave Myocardial Infarction
Journal of The American College of Cardiology, 2004
The purpose of this study was to determine the pathologic basis of Q-wave (QW) and non-Q-wave (NQW) myocardial infarction (MI). BACKGROUND The QW/NQW distinction remains in wide clinical use but the meaning of the difference remains controversial. We hypothesized that measurement of total MI size and transmural extent by late gadolinium enhancement cardiovascular magnetic resonance (CMR) would identify the pathologic basis of QWs.
Annals of Noninvasive Electrocardiology, 2007
Recently, a group of ECG experts, invited by the International Society for Holter and Noninvasive Electrocardiography (ISHNE), prepared a consensus document regarding new terminology of myocardial walls and new classification of Q-wave myocardial infarction, based on correlation between ECG findings and cardiac magnetic resonance (CMR) imaging. 1 Since this initiative was organized under auspices of ISHNE, this brief editorial provides an overview of key statements regarding new terminology of Q-wave MI in ECG for the readers of the Annals.
2007
Background Historically, Q-wave myocardial infarction (MI) has been equated with transmural MI. This association have, however, recently been rejected. The endocardial extent of MI is another potential determinant of pathological Q waves, since the first part of the QRS complex where the Q wave appears reflects depolarization of subendocardial myocardium. Therefore, the aim of the present study was to test the hypothesis that endocardial extent of MI is more predictive of pathological Q waves than is MI transmurality and to investigate the relationship between QRS scoring of the ECG and MI characteristics. Methods Twenty-nine patients with reperfused first-time MI were prospectively enrolled. One week after admission, delayed contrast-enhanced magnetic resonance imaging (DE-MRI) was performed and 12-lead ECG was recorded. Size, transmurality and endocardial extent of MI were assessed by DE-MRI. Q waves were identified with Minnesota coding and electrocardiographic MI size was estimated by QRS scoring of the ECG. Results There was a significant difference between patients with and without Q waves with regard to MI size (P ¼ 0AE03) and endocardial extent of MI (P ¼ 0AE01), but not to mean and maximum MI transmurality (P ¼ 0AE09 and P ¼ 0AE14). Endocardial extent was the only independent predictor of pathological Q waves. Endocardial extent of MI was most strongly correlated to QRS score (r ¼ 0AE86, P<0AE001) of the MI variables tested. Conclusion The endocardial extent of reperfused first-time acute MI is more predictive of pathological Q waves than is MI transmurality.
International Journal of Cardiology, 2006
We aimed to characterize the extension of Q-waves after a first ST-segment elevation myocardial infarction using body surface map (BSM) and its relationship with infarct size quantified with cardiovascular magnetic resonance imaging (CMR).Thirty-five patients were studied 6 months after a first ST-segment elevation myocardial infarction (23 anterior, 12 inferior). All cases had single-vessel disease and an open artery. The extension of Q-waves was analyzed by means of a 64-lead BSM. Infarct size was quantified with CMR. Absence of Q-waves in BSM was observed in 5 patients (14%), 2 of whom (40%) had > 1 segment with transmural necrosis. Absence of Q-waves in 12-lead ECG was observed in 8 patients (23%), 7 of whom (87%) had > 1 segment with transmural necrosis. Patients with inferior infarctions (n = 12, 34%) showed a larger number of Q-waves in BSM (18 ± 7.1 leads) than patients with anterior infarctions (n = 23, 66%; 3.7 ± 3.6 leads; p < 0.0001). When the study group was analysed as a whole, the total number of Q-waves detected in BSM did not correlate with the number of necrotic segments (r = 0.15; p = 0.4). In anterior infarctions, a number of Q-waves > median (2 leads) was related to a higher number of necrotic segments (5.1 ± 2.4 vs. 2 ± 2.2 segments; p = 0.004). The same was observed in inferior infarctions (median 20 leads: 3.5 ± 1.9 vs. 1.2 ± 1.2 segments; p = 0.03).In a stable phase after a first ST-segment elevation myocardial infarction, absence of Q-waves does not mean non-transmural necrosis. Using BSM, extension of Q-waves is much higher in inferior infarctions; a separate analysis depending on infarct location is necessary. A major BSM-derived extension of Q-waves is related to larger infarct size both in anterior and in inferior infarctions.
2010
T he ECG is the most frequently used tool for evaluating myocardial infarction (MI). The ECG provides an opportunity to describe location and extent of infarction expressed as pathological Q waves or their equivalents. The terminology used for the left ventricular (LV) walls has varied over time, 1-7 although the most currently accepted terms by electrocardiographists have been anterior, septal, lateral, and inferior. 8 -15 However, terminology has been complicated by use of posterior to refer to either the basal lateral or the basal inferior wall (see below). On the basis of correlations with the postmortem anatomic gold standard reported Ͼ50 years ago 16 and confirmed later, 17,18 the presence of abnormal Q waves in leads V 1 and V 2 was related to septal wall MI; in V 3 and V 4 to anterior wall MI; in V 5 and V 6 , I, and aVL to lateral wall MI (I, aVL high lateral; V 5 and V 6 , low lateral); and in II, III, and aVF to inferior wall MI. The presence of abnormally increased R waves in V 1 and V 2 as a mirror image of Q waves in posterior leads was called a posterior wall infarction. Although similar considerations may be applied for ECG location of ST-segment deviation, this report focuses only on ECG localization of the QRScomplex abnormalities indicative of established MI as depicted by cardiac magnetic resonance (CMR) imaging.