Endocardial infarct scar recognition by myocardial electrical impedance is not influenced by changes in cardiac activation sequence (original) (raw)
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Myocardial electrical impedance mapping of ischemic sheep hearts and healing aneurysms
Circulation, 1993
BACKGROUND This study was designed to examine the bulk electrical properties of myocardium and their variation with the evolution of infarction after coronary occlusion. These properties may be useful in distinguishing between normal, ischemic, and infarcted tissue on the basis of electrophysiological parameters. METHODS AND RESULTS The electrical impedance of myocardial tissue was studied in a sheep model of infarction. The animal model involved a one-stage ligation of the left anterior descending and second diagonal arteries at a point 40% of the distance from the apex to the base. By use of a four-electrode probe, an epicardial mapping system was developed that allowed for cardiac cycle gated and signal-averaged measurements. Subthreshold current (15 microA) was injected through two of the electrodes at frequencies of 1, 5, and 15 kHz and the induced potential measured with the other two electrodes. Epicardial maps of the left ventricle were obtained during acute infarction and a...
American journal of physiology. Heart and circulatory physiology, 2015
Myocardial electrical impedance is influenced by the mechanical activity of the heart. Therefore, the ischemia induced mechanical dysfunction may cause specific changes in the systolic-diastolic pattern of myocardial impedance but this is not known. This study aimed to analyze the phasic changes of myocardial resistivity in normal and ischemic conditions. Myocardial resistivity was measured continuously during the cardiac cycle using 26 different simultaneous excitation frequencies (1 kHz-1 MHz) in 7 anesthetized open chest pigs. Animals were submitted to 30 minutes regional ischemia by acute left anterior descending coronary artery occlusion. The electrocardiogram, left ventricular (LV) pressure, LV dP/dt and aortic blood flow were recorded simultaneously. Baseline myocardial resistivity depicted a phasic pattern during the cardiac cycle with higher values at the pre-ejection period (4.19±1.09% increase above the mean,p<0.001) and lower values during relaxation phase (5.01±0.85%...
JACC: Clinical Electrophysiology, 2020
OBJECTIVES This study sought to investigate the sensitivity of electroanatomical mapping (EAM) to detect scar as identified by late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR). BACKGROUND Previous studies have shown correlation between low voltage electrogram amplitude and myocardial scar. However, voltage amplitude is influenced by the distance between the scar and the mapping surface and its extent. The aim of this study is to examine the reliability of low voltage EAM as a surrogate for myocardial scar using LGE-derived scar as the reference. METHODS Twelve swine underwent anterior wall infarction by occlusion of the left anterior descending artery (LAD) (n ¼ 6) or inferior wall infarction by occlusion of the left circumflex artery (LCx) (n ¼ 6). Subsequently, animals underwent CMR and EAM using a multielectrode mapping catheter. CMR characteristics, including wall thickness, LGE location and extent, and EAM maps, were independently analyzed, and concordance between voltage maps and CMR characteristics was assessed. RESULTS LGE volume was similar between the LCx and LAD groups (8.5 AE 2.2 ml vs. 8.3 AE 2.5 ml, respectively; p ¼ 0.852). LGE scarring in the LAD group was more subendocardial, affected a larger surface area, and resulted in significant wall thinning (4.88 AE 0.43 mm). LGE scarring in the LCx group extended from the endocardium to the epicardium with minimal reduction in wall thickness (scarred: 5.4 AE 0.67 mm vs. remote: 6.75 AE 0.38 mm). In all the animals in the LAD group, areas of low voltage corresponded with LGE and wall thinning, whereas only 2 of 6 animals in the LCx group had low voltage areas on EAM. Bipolar and unipolar voltage amplitudes were higher in thick inferior walls in the LCx group than in thin anterior walls in the LAD group, despite a similar LGE volume. CONCLUSIONS Discordances between LGE-detected scar areas and low voltage areas by EAM highlighted the limitations of the current EAM system to detect scar in thick myocardial wall regions.
IEEE Transactions on Biomedical Engineering, 2004
Electrical properties of myocardial tissue are anisotropic due to the complex structure of the myocardial fiber orientation and the distribution of gap junctions. For this reason, measured myocardial impedance may differ depending on the current distribution and direction with respect to myocardial fiber orientation and, consequently, according to the measurement method. The objective of this study is to compare the specific impedance spectra of the myocardium measured using two different methods. One method consisted of transmural measurements using an intracavitary catheter and the other method consisted of nontransmural measurements using a four-needle probe inserted into the epicardium. Using both methods, we provide the in situ specific impedance spectrum (magnitude and phase angle) of normal, ischemic, and infarcted pig myocardium tissue from 1 kHz to 1 MHz. Magnitude spectra showed no significant differences between the measurement techniques. However, the phase angle spectra showed significant differences for normal and ischemic tissues according to the measurement technique. The main difference is encountered after 60 min of acute ischemia in the phase angle spectrum. Healed myocardial tissue showed a small and flat phase angle spectrum in both methods due to the low content of cells in the transmural infarct scar. In conclusion, both transmural and nontransmural measurements of phase angle spectrum allow the differentiation among normal, ischemic, and infarcted tissue.
Journal of Applied Physiology, 2005
Changes in myocardial electrical impedance (MEI) and physiological end points have been correlated during acute ischemia. However, the importance of MEI's early time course is not clear. This study evaluates such significance, by comparing the temporal behavior of MEI during acute total occlusion of the left anterior descending coronary artery in anesthetized humans, dogs, and pigs. Here, interspecies differences in three MEI parameters (baseline, time to plateau onset, and plateau value normalized by baseline) were evaluated using Kruskal-Wallis ANOVA and post hoc tests ( P < 0.05). Noteworthy differences in the MEI time to plateau onset were observed: In dogs, MEI ischemic plateau was reached after 46.3 min (SD 12.9) min of occlusion, a significantly longer period compared with that of pigs and humans [4.7 (SD 1.2) and 4.1 min (SD 1.9), respectively]. However, no differences could be observed between both animal species regarding the normalized MEI ischemic plateau value (1...
To analyze the passive electrical properties of a healed infarction and assess their role on transmission of contiguous ischemic ST segment potential changes. Methods: We measured tissue resistivity (Vcm) at 1 kHz and the epicardial ST segment during 1 h of proximal reocclusion of the left anterior descending (LAD) coronary artery in 12 anesthetized pigs with one-month-old transmural infarction elicited by LAD ligature below the first branch. The impedance spectrum (1 to 1000 kHz) of normal and infarcted myocardium was measured in seven other pigs with similar infarctions. Electrical transmission of current pulses (30 mA) in infarcted tissue and in test solutions was also investigated. Results: The infarct scar has a lower than normal resistivity (110630 Vcm vs. 235660 Vcm, p,0.0001) and, unlike the normal myocardium, resistivity and phase angle of the scar did not change at increasing current frequencies, reflecting no capacitative response. LAD reocclusion induced a resistivity rise (5106135 Vcm, p,0.01) and a ST segment elevation (0.660.7 to 9.565.1 mV, p50.002) in the ischemic peri-infarction zone, whereas the infarcted area showed ST segment elevation (0.560.5 to 3.862.6 mV, p50.03) with no resistivity changes. Potential decay of both ST segment and current pulses in the scar and in 0.9% NaCl solution was less than 1 mV/ mm. Transmural deposition of connective tissue was seen in the center of the infarction. Conclusions: A one-month-old transmural infarction is a low resistance, noncapacitative medium that allows a good transmission of current pulses and of ST segment potential changes generated by contiguous peri-infarction ischemia.
IEEE Transactions on Biomedical Engineering, 2013
Catheter ablation of ventricular tachycardia (VT) is preceded by characterization of the myocardial substrate via electroanatomical voltage mapping (EAVM). The purpose of this study was to characterize the relationship between chronic myocardial fibrotic scar detected by multicontrast late enhancement (MCLE) MRI and by EAVM obtained using an MR-guided electrophysiology system, with a final aim to better understand how these measures may improve identification of potentially arrhythmogenic substrates. Real-time MR-guided EAVM was performed in six chronically infarcted animals in a 1.5T MR system. The MCLE images were analyzed to identify the location and extent of the fibrotic infarct. Voltage maps of the left ventricle (LV) were created with an average of 231 ± 35 points per LV. Correlation analysis was conducted between bipolar voltage and three MR parameters (infarct transmurality, tissue categorization into healthy and scar classes, and normalized relaxation rate R1 *). In general, tissue regions classified as scar by normalized R1 * values were well correlated with locations with low bipolar voltage values. Moreover, our results demonstrate that MRI information (transmurality, tissue classification, and relaxation rate) can accurately predict areas of myocardial fibrosis identified with bipolar voltage mapping, as demonstrated by ROC analysis. MCLE can help overcome limitations of bipolar voltage mapping including long durations and lower spatial discrimination and may help identify the sites within scars, which are commonly believed to trigger arrhythmic events in postinfarction patients.