Recognition of Fibrotic Infarct Density by the Pattern of Local Systolic-Diastolic Myocardial Electrical Impedance

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.

Keywords: healed myocardial infarction; hemodynamics; myocardial electrical impedance; novel bioimpedance device; swine.

Figures

Figure 1

Schematic representation of the experimental model. (A) Photograph of a swine heart illustrating the location of the infarcted region in the anterior wall of the left ventricle and the sites where the impedance electrode was sequentially inserted (asterisks). The inset box depicts a schematic representation of the 4-needle impedance electrode (5 mm length spaced 1.27 mm, 0.4 mm diameter). (B) Representative microphotographs (at 1x and 20x magnification) of myocardial samples from normal zones (N) and from heterogeneous and dense infarct scar regions (ISH and ISD, respectively) stained with Masson's trichrome.

Figure 2

Time-relationship between resistivity at 1 kHz, left ventricular (LV) pressure, LV dP/dt, aortic blood flow (ABF), and ECG in three representative LV regions: healthy tissue (A), heterogeneous (B) and dense infarct scar (C).

Figure 3

Impedance spectroscopy of 1 month old myocardial infarction in the six studied pigs. (A) Mean values of resistivity (top) and phase angle (bottom) of myocardial impedance at different excitation frequencies in normal (N), heterogeneous (ISH), and dense infarcted myocardial regions (ISD). (B) Mean resistivity (top) and phase angle (bottom) at 4 selected frequencies (1 kHz, 41 kHz, 307 kHz, and 1000 kHz). *Significantly different from N (** < 0.01, *** < 0.001). +Significantly different from ISH (++ < 0.01, +++ < 0.001).

Figure 4

Linear correlation between the local degree of myocardial fibrosis and myocardial resistivity (upper panel) or phase angle (lower panel) in 59 samples from six pigs. Resistivity values are measured at 1 kHz and phase angle at 41 kHz.

Figure 5

Effects of infarct fibrotic content on myocardial resistivity curve. (A) Systolic-diastolic myocardial resistivity waveform in healthy myocardial tissue (left), heterogeneous scar (middle) and dense scar tissue (right). Arrows indicate the time interval between the R wave peak and the max peak of the resistivity curve. (B) Mean values of the systolic-diastolic resistivity curve amplitude -Δρ- at 4 selected frequencies (1 kHz, 41 kHz, 307 kHz, 1000 kHz). (C) Mean temporal delays between the peak of the systolic-diastolic resistivity curve and its corresponding R wave peak of the ECG. Resistivity waveforms and delays are shown at 41 kHz. * Significantly different from N (* < 0.05, ** < 0.01, *** < 0.001). +Significantly different from ISH (+ < 0.05, ++ < 0.01).

Figure 6

Time relationship between the systolic-diastolic changes in myocardial impedance and left ventricular pressure. (A) Representative LV pressure-impedance curves at sites with < 10% of fibrosis (white), 10–50% of fibrosis (gray) and >50% of fibrosis (black). (B) Mean values of the area under the curve at different current frequencies. *Significantly different from set N (* < 0.05, ** < 0.01, *** < 0.001). +Significantly different from set ISH (+ < 0.05, ++ < 0.01).