Abnormal shear stress and residence time are associated with proximal coronary atheroma in the presence of myocardial bridging.

BACKGROUND: Atheromatous plaques tend to form in the coronary segments proximal to a myocardial bridge (MB), but the mechanism of this occurrence remains unclear. This study evaluates the relationship between blood flow perturbations and plaque formation in patients with an MB. METHODS AND RESULTS: A total of 92 patients with an MB in the mid left anterior descending artery (LAD) and 20 patients without an MB were included. Coronary angiography, intravascular ultrasound, and coronary physiology measurements were performed. A moving-boundary computational fluid dynamics algorithm was used to derive wall shear stress (WSS) and peak residence time (PRT). Patients with an MB had lower WSS (0.46 ± 0.21 vs. 0.96 ± 0.33 Pa, p < 0.001) and higher maximal plaque burden (33.6 ± 15.0 vs. 14.2 ± 5.8%, p < 0.001) within the proximal LAD compared to those without. Plaque burden in the proximal LAD correlated significantly with proximal WSS (r = -0.51, p < 0.001) and PRT (r = 0.60, p < 0.001). In patients with an MB, the site of maximal plaque burden occurred 23.4 ± 13.3 mm proximal to the entrance of the MB, corresponding to the site of PRT. CONCLUSIONS: Regions of low WSS and high PRT occur in arterial segments proximal to an MB, and this is associated with the degree and location of coronary atheroma formation.

Laminar Wall Shear Stress in Brain Arteriovenous Malformations: Systematic Review of Literature.

BACKGROUND: Laminar wall sheer stress (LWSS) modulates inflammatory activity of the endothelium and may be a contributing factor in many cerebrovascular pathologies. There is a lack of consensus whether significant differences in LWSS exist between feeding vessels in brain arteriovenous malformation (bAVM) and healthy vessels. A systematic review of LWSS research in bAVM was undertaken, including the methods used and the assumptions made in determining LWSS. METHODS: Ovid MEDLINE, EMBASE, and Scopus electronic databases were systematically searched from inception for articles calculating LWSS in bAVM cases. LWSS values were extracted for comparison between ipsilateral bAVM feeding arteries and healthy contralateral vessels or healthy normative data. RESULTS: Three retrospective cohort studies were identified, reporting on 42 adult and pediatric bAVM cases. Mean LWSS (mLWSS) in healthy vessels (contralateral vessels or normative controls) typically ranged from 1.2-2.7 Pa, while mLWSS values in untreated bAVM feeding arteries typically ranged from 1.6-3.6 Pa. All studies had mixed cohorts of ruptured and unruptured cases, obscuring the relationship between LWSS and bAVM history. CONCLUSIONS: mLWSS values in healthy arteries and bAVM feeding vessels tend to be low and overlapping. Further research of high scientific and methodologic quality is necessary to improve understanding of how LWSS hemodynamics relate to bAVM formation, rupture, and treatment.