Estimating an embolic source in peripheral artery disease using non-obstructive general angioscopy and histopathology

Abstract

Spontaneously ruptured aortic plaques are known to scatter frequently. Peripheral artery disease (PAD) is assumed to be exacerbated by aortic embolism besides local atherosclerosis. However, it has been challenging to show where the embolic plug came from. We estimated the embolic source of PAD in a 78-year-old male with a history of repetitive occlusion in the right peroneal artery by demonstrating and sampling using non-obstructive angioscopy (NOGA) for peripheral arteries and the aorta. Screening of the aorta, the iliac artery, and the femoral artery by computed tomography angiography, and NOGA revealed aortic dissection in the infrarenal abdominal artery. Four puff-chandelier ruptures that scattered like puffs were detected, and sampling was successful from puff-chandelier ruptures in the thoracic aorta, in the suprarenal abdominal artery, and in the dissected infrarenal abdominal artery. Among three puff-chandelier ruptures, a puff-chandelier rupture in the dissected infrarenal abdominal artery had the highest homology regarding the structure and the degree of fatty globules and cholesterol crystals. Endovascular graft replacement in the infrarenal dissected abdominal artery stopped the patient's repeated worsening of PAD.

Learning objective

The potential cause of peripheral artery disease is embolism from the upstream arteries beside local atherosclerosis. Homological comparison between materials from the occluded site and scattering plaques at the aorta and upstream arteries may suggest the embolic mechanism. In this case, repetitive occlusion in the right peritoneal artery was attributed to the embolism from the dissected infrarenal aorta because the highest homology was shown between the dissected infrarenal aorta where stent graft replacement stopped worsening of peripheral artery disease.