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Abstract

The electrical impedance properties of healthy and infarcted left ventricular myocardium differ markedly. The properties of the infarction border zone are intermediate between healthy and infarcted myocardium. Impedance may be a useful assay of cardiac tissue content and adaptable for cardiac mapping in vivo. Condensed Abstract. To delineate the electrical impedance properties of healthy and chronically infarcted left ventricular myocardium emphasizing the infarction border zone, impedance was measured in chronically infarcted ovine hearts. Densely infarcted myocardial impedance was significantly lower than healthy myocardium. Impedance gradually decreased in the infarction border zone in transition between healthy myocardium and dense infarction. This correlated with a decreasing myocyte content. The magnitude of the difference in impedance between densely infarcted and healthy myocardium increased as measurement frequency decreased. There was a direct association between impedance and electrogram characteristics. Endocardial impedance, measured in vivo using an electrode catheter inserted percutaneously, distinguished between healthy and infarcted myocardium

Iron Deposition following Chronic Myocardial Infarction as a Substrate for Cardiac Electrical Anomalies: Initial Findings in a Canine Model

“…A capacitor cell consisting of two parallel square electrodes (each of 1.5 cm 2 surface area) with variable distance between them [26] was custom built to measure bulk electrical impedance of each sample using alternating-current (AC) impedance spectroscopy (Fig. 1).…”

Cardiac resynchronization therapy guided by cardiovascular magnetic resonance

“…This notion is supported by the fact that a pacing stimulus in scarred myocardium leads to a prolonged and fragmented QRS complex [91,92] as well as electrical and mechanical dyssynchrony. Furthermore, it is known that myocardial scars are not readily excitable [93] and that they effectively reduce the volume of myocardium available to a LV pacing stimulus [94].…”

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

“…Previous studies in sheep showed the 200% increase in myocardial impedance after 4 h of permanent coronary occlusion that turned to a 60% decrease 1 week later, and this was maintained 6 weeks after (Fallert et al, 1993). The mechanisms implicated in the progressive reduction of tissue resistivity during infarct healing are likely related to the sequential occurrence of interstitial edema, loss of myocyte content, and collagen and fat deposition in the ischemic region (Fallert et al, 1993; Schwartzman et al, 1999; Del Rio et al, 2008; Farraha et al, 2014). These structural derangements will be less marked in infarction areas with surviving myocardial cells and therefore could be detected by bioimpedance techniques.…”

“…These structural derangements will be less marked in infarction areas with surviving myocardial cells and therefore could be detected by bioimpedance techniques. In 4 sheep with 60-days old anterior myocardial infarction induced by permanent ligature of the LAD coronary artery, epicardial impedance measured with the 4-electrode technique at 1 kHz was lower in the visually defined dense infarction than in the border zone or in the healthy myocardium (Schwartzman et al, 1999). Using a 3 h LAD occlusion-reperfusion model in three sheep it has been reported that areas with greater myocardial injury (<50% viability), assessed by histologic examination, had greatest attenuation of impedance magnitude compared with areas with >50% viability in a 5 weeks-myocardial infarction (Farraha et al, 2014).…”