Electrochemical impedance spectroscopy unmasks high-risk atherosclerotic features in human coronary artery disease

Michael Chen; Krit Suwannaphoom; Yas Sanaiha; Yuan Luo; Peyman Benharash; Michael C Fishbein; René R Sevag Packard

doi:10.1096/fj.202401200R

Electrochemical impedance spectroscopy unmasks high-risk atherosclerotic features in human coronary artery disease

FASEB J. 2024 Sep 30;38(18):e70069. doi: 10.1096/fj.202401200R.

Authors

Michael Chen¹, Krit Suwannaphoom², Yas Sanaiha^{3

4}, Yuan Luo⁵, Peyman Benharash^{3

4}, Michael C Fishbein², René R Sevag Packard^{1

6

7

8

9

10

11

12}

Affiliations

¹ Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California, USA.
² Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, California, USA.
³ Cardiovascular Outcomes Research Laboratories, University of California, Los Angeles, California, USA.
⁴ Division of Cardiac Surgery, Department of Surgery, David Geffen School of Medicine, University of California, Los Angeles, California, USA.
⁵ State Key Laboratory of Transducer Technology, Shanghai Institute of Microsystem and Information Technology, Chinese Academy of Sciences, Shanghai, People's Republic of China.
⁶ Ronald Reagan UCLA Medical Center, Los Angeles, California, USA.
⁷ West Los Angeles Veterans Affairs Medical Center, Los Angeles, California, USA.
⁸ Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.
⁹ Department of Bioengineering, Henry Samueli School of Engineering and Applied Science, University of California, Los Angeles, California, USA.
¹⁰ Jonsson Comprehensive Cancer Center, University of California, Los Angeles, California, USA.
¹¹ Molecular Biology Institute, University of California, Los Angeles, California, USA.
¹² California NanoSystems Institute, University of California, Los Angeles, California, USA.

PMID: 39315853
DOI: 10.1096/fj.202401200R

Abstract

Coronary plaque rupture remains the prominent mechanism of myocardial infarction. Accurate identification of rupture-prone plaque may improve clinical management. This study assessed the discriminatory performance of electrochemical impedance spectroscopy (EIS) in human cardiac explants to detect high-risk atherosclerotic features that portend rupture risk. In this single-center, prospective study, n = 26 cardiac explants were collected for EIS interrogation of the three major coronary arteries. Vessels in which advancement of the EIS catheter without iatrogenic plaque disruption was rendered impossible were not assessed. N = 61 vessels underwent EIS measurement and histological analyses. Plaques were dichotomized according to previously established high rupture-risk parameter thresholds. Diagnostic performance was determined via receiver operating characteristic areas-under-the-curve (AUC). Necrotic cores were identified in n = 19 vessels (median area 1.53 mm²) with a median fibrous cap thickness of 62 μm. Impedance was significantly greater in plaques with necrotic core area ≥1.75 mm² versus <1.75 mm² (19.8 ± 4.4 kΩ vs. 7.2 ± 1.0 kΩ, p = .019), fibrous cap thickness ≤65 μm versus >65 μm (19.1 ± 3.5 kΩ vs. 6.5 ± 0.9 kΩ, p = .004), and ≥20 macrophages per 0.3 mm-diameter high-power field (HPF) versus <20 macrophages per HPF (19.8 ± 4.1 kΩ vs. 10.2 ± 0.9 kΩ, p = .002). Impedance identified necrotic core area ≥1.75 mm², fibrous cap thickness ≤65 μm, and ≥20 macrophages per HPF with AUCs of 0.889 (95% CI: 0.716-1.000) (p = .013), 0.852 (0.646-1.000) (p = .025), and 0.835 (0.577-1.000) (p = .028), respectively. Further, phase delay discriminated severe stenosis (≥70%) with an AUC of 0.767 (0.573-0.962) (p = .035). EIS discriminates high-risk atherosclerotic features that portend plaque rupture in human coronary artery disease and may serve as a complementary modality for angiography-guided atherosclerosis evaluation.

Keywords: electrochemical impedance spectroscopy; fibrous cap; high‐risk plaque; human coronary artery disease; inflammation; invasive sensor; necrotic core.

Abstract

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