Evidence map›Paper›PMID 39836287›Full record

ArticleBiomechanics and modeling in mechanobiology2025

Impact of lesion preparation-induced calcified plaque defects in vascular intervention for atherosclerotic disease: in silico assessment.

Jonas Sogbadji, Karim Kadry, Gianluca Poletti, Francesca Berti, Elazer R Edelman, Farhad R Nezami

Abstract read
In one paragraph

Article in Biomechanics and modeling in mechanobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Jonas Sogbadji *Institute for Medical Engineering and Science, Massachusetts Institute of Technology, 77 Massachusetts Ave, Cambridge, MA, 02139, USA. jonassog@mit.edu.
Karim Kadry *Institute for Medical Engineering and Science, Massachusetts Institute of Technology, 77 Massachusetts Ave, Cambridge, MA, 02139, USA.
Gianluca PolettiLaBS-Department of Chemistry, Materials and Chemical Engineering, Politecnico di Milano, Piazza Leonardo da Vinci 32, Milano, 20133, Italy.
Francesca BertiLaBS-Department of Chemistry, Materials and Chemical Engineering, Politecnico di Milano, Piazza Leonardo da Vinci 32, Milano, 20133, Italy.
Elazer R EdelmanInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, 77 Massachusetts Ave, Cambridge, MA, 02139, USA.
Farhad R NezamiCardiac Surgery Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA. frikhtegarnezami@bwh.harvard.edu.

Funding

Personalized lesion modification optimizes atherosclerosis interventionR01HL161069 · NHLBI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI EDELMAN, ELAZER R · 2022 to 2025
$2.8M
NHLBI NIH HHS R01 HL161069U.S. National Institutes of Health R01 HL161069
6 · The paper itself

Abstract

Percutaneous coronary interventions in highly calcified atherosclerotic lesions are challenging due to the high mechanical stiffness that significantly restricts stent expansion. Intravascular lithotripsy (IVL) is a novel vessel preparation technique with the potential to improve interventional outcomes by inducing microscopic and macroscopic cracks to enhance stent expansion. However, the exact mechanism of action for IVL is poorly understood, and it remains unclear whether the improvement in-stent expansion is caused by either the macro-cracks allowing the vessel to open or the micro-cracks altering the bulk material properties. In silico models offer a robust means to examine (a) diverse lesion morphologies, (b) a range of lesion modifications to address these deficiencies, and (c) the correlation between calcium morphology alteration and improved stenting outcomes. These models also help identify which lesions would benefit the most from IVL. In this study, we develop an in silico model of stent expansion to study the effect of macro-crack morphology on interventional outcomes in clinically inspired geometries. Larger IVL-induced defects promote more post-stent lumen gain. IVL seems to induce better stenting outcomes for large calcified lesions. IVL defects that split calcified plaque in two parts are the most beneficial for stenting angioplasty, regardless of the calcified plaque size. Location of the IVL defect does not seem to matter with respect to lumen gain. These findings underscore the potential of IVL to enhance lesion compliance and improve clinical outcomes in PCI. The macroscopic defects induced by IVL seem to have a substantial impact on post-stent outcomes.

Indexed as

AtherosclerosisCalcinosisComputer SimulationPlaque, AtheroscleroticVascular CalcificationHumansLithotripsyModels, CardiovascularStentsComputational biomechanicsFinite element analysisIntravascular lithotripsyStent expansionVessel preparationVirtual angioplasty

Identifiers

PMID39836287
PMCPMC12055935

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.