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Plaque Vulnerability and Cerebral Embolization After Carotid Stenting
Andrew Unzeitig, MD, David E. Timaran, MD, Eric B. Rosero, MD, Adriana J. Higuera, MD, R James Valentine, MD, Carlos H. Timaran, MD.
University of Texas Southwestern Medical Center, Dallas, TX, USA.
Objectives: The large necrotic core and thin fibrous cap of vulnerable plaques render them prone to rupture and cerebral embolization. Whether vulnerable plaques represent unfavorable lesions for carotid artery stenting (CAS) is unknown. The purpose of this study was to assess the occurrence of cerebral embolization after CAS of vulnerable vs. nonvulnerable plaques identified with virtual histology intravascular ultrasound (VH-IVUS).
Methods: During an 18-month period, 40 patients undergoing CAS were prospectively evaluated. All patients underwent VH-IVUS at the time of the intervention. Transcranial Doppler (TCD) monitoring during CAS and pre- and 24-hour postprocedural diffusion-weighted magnetic resonance imaging (DW-MRI) were used to assess cerebral embolization. Using VH-IVUS, lesions with large necrotic core (>10%) and thin fibrous cap were identified as vulnerable plaques. Univariate and nonparametric analyses were used to compare the degree of cerebral embolization between vulnerable and nonvulnerable plaques.
Results: CAS was performed for 15 (38%) vulnerable and 25 (42%) nonvulnerable plaques. The median MES counts detected by TCD were 313 (interquartile range [IQR], 251-404) for vulnerable plaques and 239 (IQR, 160-378) for nonvulnerable plaques (P=.2). New acute cerebral emboli detected with DW-MRI occurred in 57% and 56% of patients undergoing CAS of vulnerable and nonvulnerable plaques, respectively (P=.9). The total and ipsilateral median number of DW-MRI lesions between groups were not statistically significantly different, i.e. 1 (IQR, 0-3) and 1 (IQR, 0-2) for vulnerable and nonvulnerable plaques, respectively (P=.8). One asymptomatic patient undergoing CAS of a vulnerable plaque sustained a minor stroke; the 30-day stroke-death rate in this series was 2.5%.
Conclusions: Cerebral embolization, as detected by TCD and DW-MRI, occurs with similar frequency after CAS of vulnerable and nonvulnerable plaques. Because acute brain injury occurs in more than half of patients undergoing CAS under filter embolic protection for both vulnerable and nonvulnerable plaques, further improvements to prevent distal embolization is necessary to optimize CAS safety.
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