Intraplaque hemorrhage in carotid artery atherosclerotic plaque has been shown to be a marker of risk, associated with prior and future ischemic events, and has been associated with regions of intraplaque high-intensity signal on 3D-TOF MRA. We assessed the association of intraplaque high-intensity signal determined on 3D-TOF MRA with the incidence of prior ipsilateral stroke or TIA.
MATERIALS AND METHODS:
We assessed intraplaque hemorrhage by evaluating for intraplaque high-intensity signal adapting a recently validated technique on 3D-TOF source images in participants with high-grade (≥70%) extracranial carotid stenosis. Logistic regression analyses were used to assess the strength of association between the presence of intraplaque high-intensity signal on routine MRA sequences and prior stroke or TIA.
RESULTS:
Intraplaque high-intensity signal was present in 22 (41.5%) of 53 carotid arteries studied in 51 patients. Ipsilateral ischemic events occurred in 15 (68.1%) of 22 in the intraplaque high-intensity signal–positive group (10 strokes, 5 TIAs) and in 4 (12.9%) of 31 in the intraplaque high-intensity signal–negative group (3 strokes, 1 TIA). Ischemic events occurred within the 6-month period preceding imaging in 18 (94.7%) of 19 cases. The univariate odds ratio of the association of intraplaque high-intensity signal with any prior ischemic event was 14.5 (95% CI, 3.6–57.6), and the multivariate age- and sex-adjusted odds ratio was 14.2 (95% CI, 3.3–60.5). The association remained present across 1.5T and 3T magnet field strengths.
CONCLUSIONS:
Intraplaque high-intensity signal determined from MRA sequences already in place to measure luminal stenosis is strongly associated with prior ipsilateral ischemic events. Prospective validation of these findings to predict outcome in carotid artery stenosis could provide a valuable and widely accessible stroke risk stratification tool.
Global cerebral edema is an independent predictor of mortality and poor outcomes after aneurysmal SAH. Global cerebral edema, a complex disease process, is thought to be associated with an altered cerebral autoregulatory response. We studied the association between cerebral hemodynamics and early global cerebral edema by using CTP.
MATERIALS AND METHODS:
We retrospectively studied consecutive patients with aneurysmal SAH with admission CTP performed at days 0–3. Two neuroradiologists classified global cerebral edema and hydrocephalus on NCCT performed concurrently with CTP. Global cerebral edema was defined as diffuse effacement of the sulci and/or basal cisterns or diffuse disruption of the cerebral gray-white matter junction. CTP was postprocessed into CBF and MTT maps by using a standardized method. Quantitative analysis of CTP was performed by using standard protocol with ROI sampling of the cerebral cortex. The Fisher exact test, Mann-Whitney test, and independent-samples t test were used to determine statistical associations.
RESULTS:
Of the 45 patients included, 42% (19/45) had global cerebral edema and 58% (26/45) did not. Patient groups with and without global cerebral edema were well-matched for demographic and clinical data. Patients with global cerebral edema were more likely to have qualitative global CTP deficits than those without global cerebral edema (P = .001) with an OR = 13.3 (95% CI, 2.09–138.63). Patients with global cerebral edema also had a very strong trend toward statistical significance, with reduced quantitative CBF compared with patients without global cerebral edema (P = .064).
CONCLUSIONS:
Global perfusion deficits are significantly associated with global cerebral edema in the early phase after aneurysmal SAH, supporting the theory that hemodynamic disturbances occur in global cerebral edema.
