Background: Pathological changes in cardiac electrophysiology have been investigated in coronary artery disease using magnetocardiography. Aim of this work was to examine the structure of cardiac magnetic field maps (MFM) during ventricular depolarization and repolarization in patients with acute ST elevation myocardial infarction (STEMI).



Methods: Magnetocardiograms were recorded in 39 healthy subjects and 97 patients who had been successfully revascularized after STEMI. Using the Karhunen–Loeve transform, 12 eigenmaps were constructed for six intervals within the QT interval of each subject's signal-averaged data. The relative information content of the eigenmaps was compared between STEMI patients and healthy subjects.



Results: Relative nondipolar content was between 0.03% and 0.52% higher in the STEMI group, (P < 0.001 for the repolarization intervals). Information content of the first dipolar eigenmap in the STEMI group was reduced by 2.6%–11.7% (P < 0.001 for the repolarization intervals). STT interval was best able to discriminate between groups: area-under-the-curve for nondipolar content was 85.8% (P < 0.001), for the first eigenmap 91.7% (P < 0.001). Severity of infarction was reflected in lower STT interval map 1 content for patients with anterior versus posterior infarction (83%± 11% vs. 87%± 10%, P < 0.05), with wall motion disturbances (84%± 11% vs. 92%± 7%, P < 0.001) and with microvascular obstruction (81%± 12% vs. 87%± 10%, P < 0.05). Regression analysis showed that patients with lower ejection fraction tended to have less information content (P < 0.001).



Conclusion: STEMI is associated with a loss of spatial coherence during repolarization, as quantified by principal component analysis of cardiac MFM.



Ann Noninvasive Electrocardiol 2011;16(4):379–387

/pdf/changes-in-dipolar-structure-of-cardiac-magnetic-field-maps-4zbawpq731.pdf

Changes in dipolar structure of cardiac magnetic field maps after ST elevation myocardial infarction

The potential clinical value of QT dispersion (QTd), a measure of the interlead range of QT interval duration in the surface 12-lead ECG, remains ambiguous. The aim of the study was the temporal and spatial analysis of the QT interval in healthy subjects and in patients with coronary artery disease (CAD) using magnetocardiography (MCG) and surface ECG. Standard 12-lead ECG and 37-channel MCG were performed in 20 healthy subjects, 23 patients with CAD without prior myocardial infarction (MI), 31 MI patients and 11 MI patients with ventricular tachycardia (VT). QTd was increased in CAD without MI compared to normals (ECG 46.1 +/- 6.0 vs 42.8 +/- 5.0, P < 0.05; MCG 66.8 +/- 20.3 vs 49.7 +/- 10.8, P < 0.01) and in VT compared to MI (ECG 66.8 +/- 16.5 vs 51.9 +/- 16.6, P < 0.05; MCG 93.6 +/- 29.6 vs 66.8 +/- 20.8, P < 0.005). In MCG, spatial distribution of QT intervals in patient groups differed from those in healthy subjects in three ways: (1) greater dispersion, (2) greater local variability, and (3) a change in overall pattern. This was quantified on the basis of smoothness indexes (SI). Normalized SI was higher in CAD without MI compared to normals (3.8 +/- 1.1 vs 2.7 +/- 0.6, P < 0.001) and in VT compared to MI (6.4 +/- 1.6 vs 4.2 +/- 1.4, P < 0.0005). For the normal-CAD comparison a sensitivity of 74% and a specificity of 80% was obtained, for MI-VT, 100% and 77%, respectively. The results suggest that examining the spatial interlead variability in multichannel MCG may aid in the initial identification of CAD patients with unimpaired left ventricular function and the identification of post-MI patients with augmented risk for VT.

Spatial distribution of repolarization times in patients with coronary artery disease.

https://www.internationaljournalofcardiology.com/article/S0167-5273(99)00058-3/pdf

Spatial features in body surface potential maps of patients with ventricular tachyarrhythmias with or without coronary artery disease.

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Spatial features in body surface potential maps of patients with ventricular tachyarrhythmias with or without coronary artery disease.