Background. The calcified segment of a coronary atherosclerotic lesion can
affect final stent diameter and symmetry, even at high inflation pressures.
However, how the spatial distribution of each plaque element, defined by
virtual histology intravascular ultrasound (VH-IVUS), could affect stent
deployment, has not been studied. Methods. Fourty three patients (25 males,
62±9 years, 7 females, 64±7 years) undergoing direct percutaneous coronary
intervention and IVUS examination, were evaluated. In those pts, 73 lesions
were treated with drug-eluting stents. Lumen area pre-stenting and Real
cross-sectional stent lumen area (Rcssla) were measured along the whole lesion.
The average cross-sectional stent lumen area (Acssla) (sum of total Real
measured cross-sectional stent lumen areas number of Real cross-sectional
areas that were summed) was also calculated. For the whole lesion the
percentage and area of calcium, lipid core, fibrous and fibro-fatty tissue
inside the plaque were defined by VH-IVUS. Parameters associated with the
spatial distribution of each plaque element, as the area and percentage of each
individual plaque component that was adjacent to the lumen, were also estimated
in a subset of 52 out of 73 lesions, by a recently developed computational
algorithm. The tightest area and the segments with maximum calcium, maximum
luminal calcium and maximum necrotic core area, were analyzed. Average stent
deployment was defined as a percentage of Acssla in comparison to ideal
cross-sectional stent lumen area (Icssla). Stent deployment =
[1-(Icssla-Acssla)/Icssla]*100%. Results. In the total population stent
expansion was significantly less at the site of maximum calcification compared
to the average stent deployment (74±12% vs 80±13%, P=0.048, respectively). In
contrast, at the site of maximum necrotic core, stent deployment was less
compromised, compared to the average stent deployment (88±17% vs 80%±13%
P=.003, respectively). Furthermore, in the subset of the 52 patients mentioned
before, at the sites where calcium was adjacent to the lumen, stent expansion
was more impaired compared to sites where calcium was non luminal (70±23% vs
79±11%, P=.036, respectively).
Conclusions. Our results reveal an interaction between plaque components and
their distribution on stent expansion deployed at high inflation pressures.
This could explain the heterogeneity observed in stent deployment along
coronary atherosclerotic plaques and stresses the need for proper lesion
preparation, when stent strut fracture or under-deployment could occur.