Management of carotid atherosclerosis in stroke.

Internal carotid artery atherosclerosis is a major risk factor for stroke, accounting for 15-20% of ischaemic strokes. Revascularisation procedures-either carotid endarterectomy or carotid artery stenting-can reduce the risk of stroke for those with significant (>50%) luminal stenosis but particularly for those with more severe (70-99%) stenosis. However, advances in medical pharmacotherapy have implications for the relative benefit from surgery for symptomatic carotid atherosclerosis, as well as our approach to asymptomatic disease. This review considers the evidence underpinning the current medical and surgical management of symptomatic carotid atherosclerosis, the importance of factors beyond the degree of luminal stenosis, and developments in therapeutic strategies. We also discuss the importance of non-stenotic but high-risk carotid atherosclerotic plaques on the cause of stroke, and their implications for clinical practice.

Carotid atherosclerotic plaque microcalcification is independently associated with recurrent neurovascular events: A pilot study.

BACKGROUND: Microcalcification and macrocalcification are critical processes in atherosclerotic plaque progression, though how these processes relate to the risk of stroke recurrence in symptomatic carotid atherosclerosis is poorly understood. METHODS: We performed a post hoc analysis of data from the ICARUSS (Imaging Carotid Atherosclerosis in the Recovery and Understanding of Stroke Severity) study, where individuals with acute ischemic stroke originating from ipsilateral carotid stenosis of ⩾ 50% underwent 18F-sodium fluoride positron emission tomography (NaF-PET) to measure microcalcification. Tracer uptake was quantified using maximum tissue-to-background ratio (TBRmax). Macrocalcification was measured on computed tomography (CT) using Agatston scoring. Patients were followed up for 6 months for recurrent ipsilateral neurovascular events. RESULTS: Five (27.8%) of 18 individuals had a recurrent ischemic stroke or transient ischemic attack. Ipsilateral carotid plaque NaF uptake at baseline was higher in those with recurrent events compared to those without, and this association remained after adjustment for other vascular risk factors (adjusted odds ratio (aOR) = 1.24, 1.03-1.50). Macrocalcification score in the symptomatic artery was also significantly independently associated with ipsilateral recurrence, but the effect size was relatively smaller (aOR = 1.12, 1.06-1.17 for each 100 unit increase). CONCLUSIONS: Our findings indicate that microcalcification in symptomatic carotid plaques is independently associated with ipsilateral ischemic stroke recurrence. Furthermore, differences in the extent of active microcalcification in macrocalcified plaques may help explain variation in the relationship between calcified carotid plaques and stroke recurrence reported in the literature. Our pilot study indicates that evaluation of carotid artery microcalcification using NaF-PET may be a useful method for risk-stratification of carotid atherosclerosis, though our findings require confirmation in larger cohorts.

Recurrent vascular events and mortality outcomes in patients with known atrial fibrillation, compared to atrial fibrillation detected early after stroke.

INTRODUCTION: Atrial fibrillation (AF) detected after stroke (AFDAS) may represent a distinct clinical entity to that of known AF (KAF). However, there is limited long-term outcome data available for patients with AFDAS. More information regarding prognosis in AFDAS is required to inform future trial design in these patients. PATIENTS AND METHODS: We used data (2015-2019) from a national prospective stroke registry of consecutive patients with acute ischaemic stroke and AF. AFDAS was defined as a new diagnosis of AF after stroke detected on electrocardiograph or cardiac monitoring. The co-primary endpoints were: (1) all-cause mortality; (2) recurrent major adverse cardiovascular events (MACE) at 3 years. Secondary endpoints were: (1) recurrent stroke; (2) functional outcome at discharge; (3) presence of co-existing stroke mechanisms. RESULTS: 583 patients were included. After a median follow-up of 2.65 years (cumulative 1064 person-years) 309 patients died and 23 had recurrent MACE. Compared with AFDAS, KAF was associated with a higher risk of all-cause mortality (adjusted Hazard Ratio (aHR) 1.56, 95% CI 1.12-2.18), a higher prevalence of co-existing stroke mechanisms (adjusted odds ratio (aOR) 2.28, 95% CI 1.14-4.59), but not poor functional outcome (aOR 1.61, 95% CI 0.98-2.64). A trend towards a higher risk of MACE was observed in patients with KAF, but this was limited by statistical power (aHR 2.90, 95% CI 0.67-12.51). All 14 recurrent strokes occurred in the KAF group (Log-rank p = 0.03). DISCUSSION AND CONCLUSION: These data provide further evidence that AFDAS differs to KAF with respect to risk of recurrent stroke, MACE, and all-cause mortality.

Imaging Carotid Plaque Inflammation Using Positron Emission Tomography: Emerging Role in Clinical Stroke Care, Research Applications, and Future Directions.

Atherosclerosis is a chronic systemic inflammatory condition of the vasculature and a leading cause of stroke. Luminal stenosis severity is an important factor in determining vascular risk. Conventional imaging modalities, such as angiography or duplex ultrasonography, are used to quantify stenosis severity and inform clinical care but provide limited information on plaque biology. Inflammatory processes are central to atherosclerotic plaque progression and destabilization. 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) is a validated technique for quantifying plaque inflammation. In this review, we discuss the evolution of FDG-PET as an imaging modality to quantify plaque vulnerability, challenges in standardization of image acquisition and analysis, its potential application to routine clinical care after stroke, and the possible role it will play in future drug discovery.