Authors
P Barsoum, D Bazin, B Grine, R Geha, F Walylo, H Colboc
Published in
Annales de cardiologie et d'angeiologie. Aug 19, 2026. Epub Aug 19, 2026.
Abstract
Rotational atherectomy is an established strategy for the treatment of severely calcified coronary lesions. Although reduced burr efficiency is not uncommon during complex procedures, the structural changes responsible for this phenomenon have not been investigated following rotational atherectomy of native coronary lesions.
In a patient undergoing rotational atherectomy for a massively calcified native coronary lesion, we encountered failure of the burr to cross the lesion despite preserved rotational speed. Macroscopic examination suggested surface alteration of the burr. Replacement with a new burr resulted in immediate lesion crossing. To investigate the underlying mechanism, the surface of a new burr was compared with that of a clinically used burr using high-resolution field-emission scanning electron microscopy (FE-SEM).
FE-SEM demonstrated marked thinning of the cobalt binding matrix and multiple cavities indicating loss of diamond particles. In contrast, the remaining exposed diamond particles showed no obvious structural damage. These observations indicate that progressive degradation of the cobalt matrix, rather than damage of the diamond particles themselves, is the most likely mechanism responsible for reduced abrasive performance of the rotational atherectomy burr.
This report provides the first ultrastructural evidence of rotational atherectomy burr degradation following treatment of a severely calcified native coronary lesion. FE-SEM provides novel mechanistic insight into the progressive loss of the burr's abrasive performance, offering a plausible explanation for a situation frequently encountered by interventional cardiologists in which plaque modification becomes ineffective. Recognition of this mechanism may help operators identify burr wear and consider its replacement.
PMID:
42618441
Bibliographic data and abstract were imported from PubMed on 20 Aug 2026.
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