Abstract
Myocardial electrical impedance is a biophysical property of the heart that is influenced by the intrinsic structural characteristics of the tissue. Therefore, the structural derangements elicited in a chronic myocardial infarction should cause specific changes in the local systolic-diastolic myocardial impedance, but this is not known. This study aimed to characterize the local changes of systolic-diastolic myocardial impedance in a healed myocardial infarction model. Six pigs were successfully submitted to 150 min of left anterior descending (LAD) coronary artery occlusion followed by reperfusion. 4 weeks later, myocardial impedance spectroscopy (1–1000 kHz) was measured at different infarction sites. The electrocardiogram, left ventricular (LV) pressure, LV dP/dt, and aortic blood flow (ABF) were also recorded. A total of 59 LV tissue samples were obtained and histopathological studies were performed to quantify the percentage of fibrosis. Samples were categorized as normal myocardium (<10% fibrosis), heterogeneous scar (10–50%) and dense scar (>50%). Resistivity of normal myocardium depicted phasic changes during the cardiac cycle and its amplitude markedly decreased in dense scar (18 ± 2 Ω·cm vs. 10 ± 1 Ω·cm, at 41 kHz; P < 0.001, respectively). The mean phasic resistivity decreased progressively from normal to heterogeneous and dense scar regions (285 ± 10 Ω·cm, 225 ± 25 Ω·cm, and 162 ± 6 Ω·cm, at 41 kHz; P < 0.001 respectively). Moreover, myocardial resistivity and phase angle correlated significantly with the degree of local fibrosis (resistivity: r = 0.86 at 1 kHz, P < 0.001; phase angle: r = 0.84 at 41 kHz, P < 0.001). Myocardial infarcted regions with greater fibrotic content show lower mean impedance values and more depressed systolic-diastolic dynamic impedance changes. In conclusion, this study reveals that differences in the degree of myocardial fibrosis can be detected in vivo by local measurement of phasic systolic-diastolic bioimpedance spectrum. Once this new bioimpedance method could be used via a catheter-based device, it would be of potential clinical applicability for the recognition of fibrotic tissue to guide the ablation of atrial or ventricular arrhythmias.
Highlights
Myocardial electrical impedance is a biophysical marker of the state of integrity of the myocardial tissue (Sperelakis and Hoshiko, 1961)
Studies conducted in experimental animal models have consistently shown that acute myocardial ischemia induced by coronary artery ligation increased dramatically the myocardial impedance (Cinca et al, 1998; Padilla et al, 2003; Rodriguez-Sinovas et al, 2005)
The technique of measuring the changes in myocardial impedance did not allow to delineate the sequential impedance variations elicited during the systole and diastole phases of the cardiac cycle because of the long time required for the whole impedance spectrum acquisition (Gersing, 1998; Casas et al, 1999; Warren et al, 2000; Cinca et al, 2008)
Summary
Myocardial electrical impedance is a biophysical marker of the state of integrity of the myocardial tissue (Sperelakis and Hoshiko, 1961). As compared with the classical technique, the new EIS-based method permitted a prompt detection of local myocardial ischemia based on the occurrence of specific changes in the phasic systolic-diastolic impedance curve These were characterized by an holosystolic resistivity rise leading to a bell-shaped impedance waveform and a reduction of the area under the left ventricular (LV) pressureimpedance curve. During the healing-over process the acute ischemic myocardium suffers a profound structural and functional remodeling, with collagen deposition and fibroblasts proliferation These structural alterations will affect the pattern of systolic-diastolic impedance of the infarct scar region, but this has not yet been investigated
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