109 3T MRI of acute atherosclerotic plaque rupture and downstream embolic injury

Abstract

<h3>Introduction</h3> Luminal stenosis is a poor predictor of the risk posed by any given atherosclerotic plaque, therefore current angiographic imaging techniques cannot reliably determine which patients are most likely to suffer future ischaemic events. However, MRI may be able to detect features of atherosclerotic plaque rupture that have been associated with an increased risk of recurrent atherothrombosis. <h3>Hypothesis</h3> 3T MRI of the carotid artery can identify atherosclerotic plaque rupture in patients presenting with TIA or minor stroke. <h3>Methods</h3> 81 patients with carotid artery disease were recruited; 41 presented acutely with TIA or minor stroke and 40 asymptomatic patients acted as the control group. Median time from symptom onset to MRI in the symptomatic group was 2.1 days (range 0.17–7.0). All patients underwent T1, T2 and proton density-weighted turbo spin echo MRI to 10 mm either side of the carotid. As part of a combined scan protocol, study participants then underwent diffusion-weighted imaging (DWI) and Fluid-Attenuated Inversion Recovery (FLAIR) imaging of the brain to assess acute and chronic injury, respectively. If physically able, patients underwent follow-up scanning a minimum of six weeks later. Plaques were graded according to the MRI modified American Heart Association (AHA) system by two independent reviewers blinded to the clinical status of the patient. Statistical analysis was performed using the Wilcoxon sign rank test and Fisher′s exact test to compare plaques, in addition to the Mann Whitney U test to compare cerebral injury. <h3>Results</h3> AHA type VI (ruptured) plaque was seen in 22/41(54%) in the symptomatic group vs 8/41(20%) in the asymptomatic group (p&lt;0.05), either due to intra-plaque haemorrhage (34% vs 18%, p=0.08; Abstract 109 figure 1A), surface rupture (24% vs 5%, p=0.03; Abstract 109 figure 1B), or luminal thrombus (7% vs 0%, p=0.24; Abstract 109 figure 1C). Of particular note, 17/30 (57%) cases of AHA VI (ruptured) plaque were seen to cause &lt;70% stenosis―the current cut-off for surgical treatment. At follow-up scanning a minimum of 6 weeks later, only two cases of AHA VI plaque showed evidence of full healing. Of the 41 patients in the acute group, evidence of cerebral injury on DWI imaging was seen in 32/41 patients; the median number of lesions per patient was 7 and the median total lesion volume was 10.62 ml (range 0–522 ml). No significant associations were noted between AHA plaque type and downstream cerebral injury, however the presence of plaque surface rupture independently predicted a higher number of DWI lesions, a higher total DWI burden at presentation, and higher total cerebral FLAIR signal at follow-up when compared to all other plaque types (p&lt;0.05). <h3>Conclusion</h3> Acute atherosclerotic plaque rupture can be visualised using 3T MRI. In particular, MRI can provide detailed information on plaque morphology that can predict downstream embolic injury, independent of the degree of luminal stenosis caused.