Coronary Spasm Due to Pulsed Field Ablation: A State-of-the-Art Review

Abstract

With the ever-growing population of patients undergoing cardiac ablation with pulsed electric fields, there is a need to understand secondary effects from the therapy. Coronary artery spasm is one such effect that has recently emerged as the subject of further investigation in electrophysiology literature. This review aims to elucidate the basic anatomy underlying vascular spasm due to pulsed electric fields and the effects of irreversible electroporation on coronary arteries. This review also aims to gather the current preclinical and clinical data regarding the physiology and function of coronary arteries following electroporation.

Keywords: coronary spasm; irreversible electroporation; pulsed field ablation; vascular smooth muscle.

FIGURE 1

Gross anatomy and cross section of a coronary artery. The smooth muscle cells are mainly located in the tunica media of the artery. Note the direction of the actin‐myosin crisscrossing within the cell. Activation of contractility does not take orientation in its regard. [Colour figure can be viewed at wileyonlinelibrary.com]

FIGURE 2

Control (left), Day 7 (middle), and Day 35 (right). Top row shows the absence of VSM cells in the PFA‐treated arteries when compared with the control. Tunica media at Day 7 is marked with asterisks, and regenerated cellular components at Day 35 are marked with an arrow. The middle row shows the absence of multiplying cells at 7 days (asterisks) and a relatively active process at 35 days, with some cells staining positive (arrow). Lower row shows that the endothelial layer at 35 days is regenerated and regular in shape, with the endothelial cells producing the vWF molecule (arrow). Reproduced from Maor et al., “Vascular smooth muscle cells ablation with endovascular nonthermal IRE,” Journal of Vascular and Interventional Radiology 21, no. 11 (2010): 1708–1715, with permission from Elsevier. SMA = smooth muscle actin, vWF = Von Willebrand factor. [Colour figure can be viewed at wileyonlinelibrary.com]

FIGURE 3

(A) The focal pulsed field ablation (PFA) catheter. (B) Angiography before, spasm (arrowheads) after, and resolution at 50 min. (C) Right coronary artery (RCA) spasm (arrowheads) following endocardial PFA. (D) Histology at the site of the spasm reveals a preserved lumen and a shallow myocardial lesion (double‐headed arrow). (Inset) Left anterior descending coronary artery (LAD) demonstrating tunica media fibrosis (TMF), intimal hyperplasia (IH), epicardial lymphocytic inflammation (EI), and epicardial fibrosis (EF). (E) Histology through the lateral right atrium: RCA is seen with preserved lumen, adjacent to the myocardial lesion (double‐headed arrow). (Inset) RCA demonstrates TMF, IH, EI, and EF. Reproduced from Koruth et al., “Coronary Arterial Spasm and Pulsed Field Ablation: Preclinical Insights,” Clinical Electrophysiology 8, no. 12 (2022): 1579–1580, with permission from Elsevier. [Colour figure can be viewed at wileyonlinelibrary.com]

FIGURE 4

Shown is the preablation baseline coronary angiography (A) to (C), and postablation angiography (D) to (F). The arrows indicate areas of vasospasm. Reproduced from Malyshev et al., “Nitroglycerin to Ameliorate Coronary Artery Spasm During Focal Pulsed‐Field Ablation for Atrial Fibrillation,” JACC: Clinical Electrophysiology 10, no. 5 (2024): 885–896, with permission from Elsevier. [Colour figure can be viewed at wileyonlinelibrary.com]