M. Zhang, L. McGrath-Cadell, S. Hesselson, C. Shen, R. Gharleghi, N. Collins, D. W. Muller, J. C. Kovacic, R. M. Graham, S. Beier
BackgroundSpontaneous coronary artery dissection (SCAD) causes acute coronary syndrome that predominantly affects women. It is not known why SCAD occurs in specific coronary artery segments. We aimed to identify anatomical and hemodynamic factors that lead to SCAD.
MethodsWe studied 36 women with angiographically-confirmed SCAD from more than 20 hospital sites and 75 sex- and ethnicity-matched control participants with normal coronary anatomy. Coronary arteries were reconstructed from computed tomography coronary angiography (CTCA) to quantify vessel geometry (curvature, diameter, torsion) and flow-derived metrics (time-averaged endothelial shear stress [TAESS], topological shear variation index [TSVI], oscillatory shear index [OSI], and relative residence time [RRT]) at the tree (left/right), territory (LAD, LCx, RCA), and lesion levels.
ResultsCompared with controls, SCAD-affected coronary arteries had greater curvature and higher TAESS and TSVI at the whole-tree level (all p[≤]0.007). At the vessel (territory) level, SCAD-affected arteries were smaller in average diameter and showed higher curvature, TAESS, and TSVI than matched control vessels (all p[≤]0.047). Within the same patient, SCAD lesion segments were characterized by smaller diameter, lower torsion, and higher TAESS and TSVI than non-affected segments from the same coronary tree (all p[≤]0.001; curvature borderline). A model combining curvature, TAESS, and TSVI discriminated SCAD from controls with AUC 0.95 (left tree) and 0.97 (right tree); adding diameter yielded AUCs >0.91 at the territory level.
ConclusionsSCAD was associated with a reproducible multi-scale signature of smaller vessel caliber and higher, more variable endothelial shear stress supporting a hemodynamic contribution to SCAD clustering in specific coronary arteries and segments.
Graphical abstract
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