Key result
Baseline wall shear stress was directly related to endothelium-dependent epicardial coronary vasomotion (coefficient 17.2, p=0.004) and inversely related to remodeling and eccentricity indices.
Why the study?
Is coronary artery wall shear stress associated with endothelial dysfunction and arterial remodelling in patients with minor coronary artery disease?
Observational (n=24)
Is coronary artery wall shear stress associated with endothelial dysfunction and arterial remodelling in patients with minor coronary artery disease?
Effect estimate: coefficient 17.2
p-value: p=0.004
Lower in vivo coronary wall shear stress is associated with endothelial dysfunction and morphological features of plaque vulnerability in patients with minor coronary disease.
Low wall shear stress was associated with endothelial dysfunction and plaque vulnerability features in minor CAD; leaves open its role in risk stratification.
AIMS: To investigate in vivo relationships between segmental wall shear stress (WSS), endothelium-dependent vasoreactivity and arterial remodelling. METHODS AND RESULTS: Twenty-four patients with minor angiographic coronary arterial disease (≤30% stenosis severity) underwent intracoronary (IC) salbutamol provocation during intravascular ultrasound (IVUS)-upon-Doppler guidewire imaging. Macrovascular response (change in segmental lumen volume [SLV] at baseline and following IC salbutamol), plaque burden (percent atheroma volume [PAV]), remodelling indices (RI), eccentricity indices (EI) and WSS were evaluated in 179 consecutive 5 mm coronary segments. Baseline WSS was directly related to endothelium-dependent epicardial coronary vasomotion (% change SLV, coefficient 17.2, p=0.004), and inversely related to RI (coefficient -0.23, p=0.02) and EI (coefficient -10.0, p=0.001). Baseline WSS was lower in segments displaying endothelial dysfunction (defined as any change in SLV ≤0) compared with preserved function (0.66±0.33 vs. 0.71±0.22 N/m2, p=0.046). Independent of plaque burden, segments with the lowest tertile of WSS displayed less vasodilatation, or vasoconstriction, than segments with the highest tertile of WSS. Higher plaque burden segments harbouring the lowest tertiles of WSS displayed vasoconstriction, expansive arterial remodelling and greater plaque eccentricity. CONCLUSIONS: In patients with stable coronary syndromes and minor angiographic coronary disease, coronary segments with lower in vivo WSS values display functional and morphological features of plaque vulnerability.
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Puri et al. (2015) conducted an observational in minor angiographic coronary arterial disease (n=24). Segmental wall shear stress (WSS) was evaluated on endothelium-dependent epicardial coronary vasomotion (% change SLV) (coefficient 17.2, p=0.004). Baseline wall shear stress was directly related to endothelium-dependent epicardial coronary vasomotion (coefficient 17.2, p=0.004) and inversely related to remodeling and eccentricity indices.
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