Is spontaneous coronary artery dissection (SCAD) related to local anatomy and hemodynamics? An exploratory study.

Aims: Spontaneous coronary artery dissection (SCAD) is an increasingly diagnosed cause of myocardial infarction with unclear pathophysiology. The aim of the study was to test if vascular segments site of SCAD present distinctive local anatomy and hemodynamic profiles.
Methods: Coronary arteries with spontaneously healed SCAD (confirmed by follow-up angiography) underwent three-dimensional reconstruction, morphometric analysis with definition of vessel local curvature and torsion, and computational fluid dynamics (CFD) simulations with derivation of time-averaged wall shear stress (TAWSS) and topological shear variation index (TSVI). The (reconstructed) healed proximal SCAD segment was visually inspected for co-localization with curvature, torsion, and CFD-derived quantities hot spots.
Results: Thirteen vessels with healed SCAD underwent the morpho-functional analysis. Median time between baseline and follow-up coronary angiograms was 57 (interquartile range [IQR] 45-95) days. In seven cases (53.8%), SCAD was classified as type 2b and occurred in the left anterior descending artery or near a bifurcation. In all cases (100%), at least one hot spot co-localized within the healed proximal SCAD segment, in 9 cases (69.2%) ≥ 3 hot spots were identified. Healed SCAD in proximity of a coronary bifurcation presented lower TAWSS peak values (6.65 [IQR 6.20-13.20] vs. 3.81 [2.53-5.17] Pa, p = 0.008) and hosted less frequently TSVI hot spots (100% vs. 57.1%, p = 0.034).
Conclusion: Vascular segments of healed SCAD were characterized by high curvature/torsion and WSS profiles reflecting increased local flow disturbances. Hence, a pathophysiological role of the interaction between vessel anatomy and shear forces in SCAD is hypothesized.
Competing Interests: Conflict of interest AC has consultancy agreements with Medyria, HiD-Imaging and Nanoflex. JS is supported by a Monash University scholarship and received speaker's fees from Abbott and Edwards Lifesciences and a travel grant from Abbott. BS received research grants to the institution from the OPO Foundation, the Iten-Kohaut Foundation, the German Center for Cardiovascular Research (DZHK), Boston Scientific, and Edwards Lifesciences and has received consulting and speaker fees from Boston Scientific and Abbott Vascular. CT received institutional grants from Abbott Vascular, Medtronic, SMT, the Iten-Kohaut Foundation and the Swiss Heart Foundation as well as consulting grants from Biotronik, Microport, Schnell Medical. CT and BS have been supported by the H.H. Sheikh Khalifa bin Hamad Al-Thani Research Programme. The remaining authors have nothing to disclose.
(Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)