Abstract
BackgroundThe posterior wall of the proximal internal carotid artery (ICA) is the predilection site for the development of stenosis. To optimally prevent stroke, identification of new risk factors for plaque progression is of high interest. Therefore, we studied the impact of carotid geometry and wall shear stress on cardiovascular magnetic resonance (CMR)-depicted wall thickness in the ICA of patients with high cardiovascular disease risk.MethodsOne hundred twenty-one consecutive patients ≥50 years with hypertension, ≥1 additional cardiovascular risk factor and ICA plaque ≥1.5 mm thickness and < 50% stenosis were prospectively included. High-resolution 3D-multi-contrast (time of flight, T1, T2, proton density) and 4D flow CMR were performed for the assessment of morphological (bifurcation angle, ICA/common carotid artery (CCA) diameter ratio, tortuosity, and wall thickness) and hemodynamic parameters (absolute/systolic wall shear stress (WSS), oscillatory shear index (OSI)) in 242 carotid bifurcations.ResultsWe found lower absolute/systolic WSS, higher OSI and increased wall thickness in the posterior compared to the anterior wall of the ICA bulb (p < 0.001), whereas this correlation disappeared in ≥10% stenosis. Higher carotid tortuosity (regression coefficient = 0.764; p < 0.001) and lower ICA/CCA diameter ratio (regression coefficient = − 0.302; p < 0.001) were independent predictors of increased wall thickness even after adjustment for cardiovascular risk factors. This association was not found for bifurcation angle, WSS or OSI in multivariate regression analysis.ConclusionsHigh carotid tortuosity and low ICA diameter were independent predictors for wall thickness of the ICA bulb in this cross-sectional study, whereas this association was not present for WSS or OSI. Thus, consideration of geometric parameters of the carotid bifurcation could be helpful to identify patients at increased risk of carotid plaque generation. However, this association and the potential benefit of WSS measurement need to be further explored in a longitudinal study.
Highlights
The posterior wall of the proximal internal carotid artery (ICA) is the predilection site for the development of stenosis
Previous studies have shown that individual geometry, low wall shear stress (WSS) and high oscillatory shear index (OSI) at the carotid bifurcation could play a role in the development of atherosclerotic lesions [7,8,9]
Exclusion criteria were: contraindications to 3 T cardiovascular magnetic resonance (CMR) such as ferromagnetic implants, claustrophobia, poor clinical condition (modified ranking scale > 3), atrial fibrillation or other relevant cardiac arrhythmias interfering with the electrocardiographic (ECG)-trigger), ICA-stenosis > 50% or ICA-occlusion according to North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria [18], expectation of life < 2 years, pregnancy, distance to place of residence > 100 km and refusal of study participation
Summary
The posterior wall of the proximal internal carotid artery (ICA) is the predilection site for the development of stenosis. ICA stenoses often develop asymmetrically [2], suggesting that additional parameters such as carotid geometry and the specific distribution of wall shear stress (WSS) may be responsible for the development and progression of atherosclerosis [3] This is further supported by the observation that atherosclerosis is concentrated at the outlet of arteries such as the carotid bulb while straight segments such as the common carotid artery or abdominal aorta are far less affected [4,5,6]. Studies in healthy subjects using computational fluid dynamics (CFD) and 4D flow cardiovascular magnetic resonance (CMR) demonstrated that these potentially atherogenic flow conditions predominantly occur at the posterior wall of the proximal ICA (bulb) [4, 8, 10] This coincides with the area where atherosclerotic plaques and stenoses typically occur [7, 8, 10]. There is emerging evidence that high WSS possibly promotes intra-plaque hemorrhage, thinning of the fibrous cap and leads to plaque rupture [3, 7, 13, 14]
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