Refractory ventricular tachycardia caused by inflow cannula mechanical injury in a patient with left ventricular assist device: Catheter ablation and pathological findings

Abstract

In patients with left ventricular assist device (LVAD), a minority of post-operative ventricular tachycardias (VTs) is caused by contact between the inflow cannula and the endocardium. Currently, electrophysiologic characteristics and pathologic features of this condition are lacking. We report on a case of a successfully ablated mechanical VT. After VT recurrence, heart transplantation took place. Pathologic observations were consistent with direct tissue injury and inflammation, eventually contributing to persisting arrhythmias. Radiofrequency catheter ablation can be a safe and effective option to treat arrhythmias caused by inflow cannula interference in the short term, although a high recurrence rate is expected.

Keywords: Cardiac pathology; Catheter ablation; Heart transplantation; Left ventricular assist device; Ventricular tachycardia.

Fig. 1

Ventricular tachycardia activation mapping, (A) Fluoroscopic 30° right anterior oblique view of the mapping catheter at the effective radiofrequency ablation site. (B) Electroanatomic activation map merged with the left ventricle-cannula shield obtained from angio-computed tomography (isochrone set at 5 ms). (C) Mapping catheter at the effective radiofrequency site. Contact artifacts with the inflow cannula are indicated with white asterisks. (D) Maximal anticipation of bipolar potential on surface electrocardiogram and initial downslope of the unipolar potential.

Fig. 2

(A) Gross view of the endocardial aspect of the mid-lateral left ventricular wall from the explanted heart with the inflow cannula; black asterisks: subendocardial thickening and fibrosis reproducing the shape of the cannula; grey arrowheads: confluent, yet discontinue ecchymotic lesions ascribable to radiofrequency ablation lesions. (B) Electroanatomic internal view of the ablation sites. (C–F) Histologic preparations of the ablation sites and surrounding tissue (hematoxylin and eosin). (C) Endocardial disruption with underneath coagulative necrosis of myocardial cells and granulation tissue characterizing an ablation site; adjacent dense fibrotic tissue; vital cardiomyocytes visible at the upper right site of the picture (25× magnification). (D) A magnified image from C, showing macrophage infiltration at the edge of necrotic myocardial tissue (100× magnification). (E) Macrophage infiltration at the interface between viable myocardium and fibrotic tissue (100× magnification). (F) Macrophage infiltration network interspersed into fibrotic reparative tissue (400× magnification). E: endocardial layer. C: coagulative necrosis of myocardial cells. G: granulation tissue. F: fibrotic reparative tissue. VC: vital cardiomyocytes. M: macrophage infiltration.