Determining the quantity and character of carotid artery embolic debris by electron microscopy and energy dispersive spectroscopy.

Objectives: Carotid artery angioplasty and stenting (CAS) is now routinely performed with embolic protection devices, yet little is known about the compositional characteristics of the captured embolic debris and whether the type or quantity of debris correlates with patient, lesion, or operator characteristics. This study examined the embolic debris generated during CAS using electron microscopy and energy dispersive spectroscopy (EDS) for symptomatic and asymptomatic patients.

Methods: Between 2003 and 2005, CAS for carotid stenosis was performed in 175 patients. Cerebral protection devices were used in all but three cases. Sixty-four consecutive unselected microporous filters from procedures performed by a single vascular surgeon were obtained for analysis. Captured particulate debris within the protection devices was quantified (number and mean size of particles) by light microscopy for all filters. Twenty protection devices (9 symptomatic, 11 asymptomatic patients) were processed for electron microscopy and EDS to assess morphology, cellular composition, and calcium content of debris.

Results: Captured particulate matter was present in 49 filters (77%) and included particles measuring 200 to 500 mum in 72%, 500 to 1000 mum in 53%, and >1000 mum in 33%. The mean number of captured particles was 6.9, and mean size was 248 +/- 150 mum. Univariate analysis revealed that sequential patient cohort and filter type were correlated with the number (but not size) of captured particles. The number of particles significantly decreased after the first cohort of 20 patients (11.5 particles) compared with the second (5.0 particles, P = .023) and third (5.2 particles, P = .029) cohorts. The type of captured debris ranged from sheets of damaged red blood cells without other components to clumps of recently activated platelets with early fibrin crosslinking to plaque debris coated with well-organized coalescing areas of platelet thrombus. Platelet activation was more common in symptomatic patients (78%) than asymptomatic patients (27%; P < .05). Despite the presence of calcified lesions in six patients whose filters were analyzed by EDS, <1% of energy emission on EDS of scanned particulate debris fell within the emission range of calcium, indicating the presence of minimal calcium in the embolic particles.

Conclusions: Particulate embolic debris is released in most patients during CAS and can measure >1000 mum in one third of patients. The number of particles may decrease with increasing operator experience with CAS. Debris captured during CAS with embolic protection exhibits a range of cellular and acellular components on electron microscopy, with a higher prevalence of platelet activation evident in symptomatic patients.