A transcriptomic model to predict increase in fibrous cap thickness in response to high-dose statin treatment: Validation by serial intracoronary OCT imaging.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Jun 2019
Historique:
received: 15 02 2019
revised: 15 04 2019
accepted: 03 05 2019
pubmed: 28 5 2019
medline: 19 12 2019
entrez: 26 5 2019
Statut: ppublish

Résumé

Fibrous cap thickness (FCT), best measured by intravascular optical coherence tomography (OCT), is the most important determinant of plaque rupture in the coronary arteries. Statin treatment increases FCT and thus reduces the likelihood of acute coronary events. However, substantial statin-related FCT increase occurs in only a subset of patients. Currently, there are no methods to predict which patients will benefit. We use transcriptomic data from a clinical trial of rosuvastatin to predict if a patient's FCT will increase in response to statin therapy. FCT was measured using OCT in 69 patients at (1) baseline and (2) after 8-10 weeks of 40  mg rosuvastatin. Peripheral blood mononuclear cells were assayed via microarray. We constructed machine learning models with baseline gene expression data to predict change in FCT. Finally, we ascertained the biological functions of the most predictive transcriptomic markers. Machine learning models were able to predict FCT responders using baseline gene expression with high fidelity (Classification AUC = 0.969 and 0.972). The first model (elastic net) using 73 genes had an accuracy of 92.8%, sensitivity of 94.1%, and specificity of 91.4%. The second model (KTSP) using 18 genes has an accuracy of 95.7%, sensitivity of 94.3%, and specificity of 97.1%. We found 58 enriched gene ontology terms, including many involved with immune cell function and cholesterol biometabolism. In this pilot study, transcriptomic models could predict if FCT increased following 8-10 weeks of rosuvastatin. These findings may have significance for therapy selection and could supplement invasive imaging modalities.

Sections du résumé

BACKGROUND BACKGROUND
Fibrous cap thickness (FCT), best measured by intravascular optical coherence tomography (OCT), is the most important determinant of plaque rupture in the coronary arteries. Statin treatment increases FCT and thus reduces the likelihood of acute coronary events. However, substantial statin-related FCT increase occurs in only a subset of patients. Currently, there are no methods to predict which patients will benefit. We use transcriptomic data from a clinical trial of rosuvastatin to predict if a patient's FCT will increase in response to statin therapy.
METHODS METHODS
FCT was measured using OCT in 69 patients at (1) baseline and (2) after 8-10 weeks of 40  mg rosuvastatin. Peripheral blood mononuclear cells were assayed via microarray. We constructed machine learning models with baseline gene expression data to predict change in FCT. Finally, we ascertained the biological functions of the most predictive transcriptomic markers.
FINDINGS RESULTS
Machine learning models were able to predict FCT responders using baseline gene expression with high fidelity (Classification AUC = 0.969 and 0.972). The first model (elastic net) using 73 genes had an accuracy of 92.8%, sensitivity of 94.1%, and specificity of 91.4%. The second model (KTSP) using 18 genes has an accuracy of 95.7%, sensitivity of 94.3%, and specificity of 97.1%. We found 58 enriched gene ontology terms, including many involved with immune cell function and cholesterol biometabolism.
INTERPRETATION CONCLUSIONS
In this pilot study, transcriptomic models could predict if FCT increased following 8-10 weeks of rosuvastatin. These findings may have significance for therapy selection and could supplement invasive imaging modalities.

Identifiants

pubmed: 31126891
pii: S2352-3964(19)30308-1
doi: 10.1016/j.ebiom.2019.05.007
pmc: PMC6607084
pii:
doi:

Substances chimiques

Biomarkers 0
Hydroxymethylglutaryl-CoA Reductase Inhibitors 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

41-49

Informations de copyright

Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.

Auteurs

Kipp W Johnson (KW)

Institute for Next Generation Healthcare, Mount Sinai Health System, New York, NY, United States of America; Department of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, United States of America.

Benjamin S Glicksberg (BS)

Bakar Computational Health Sciences Institute, The University of California, San Francisco, San Francisco, CA, United States of America.

Khader Shameer (K)

Advanced Analytics Center, AstraZeneca, Gaithersburg, MD, United States of America.

Yuliya Vengrenyuk (Y)

Mount Sinai Heart, Mount Sinai Health System, New York, NY, United States of America.

Chayakrit Krittanawong (C)

Department of Internal Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States of America.

Adam J Russak (AJ)

Institute for Next Generation Healthcare, Mount Sinai Health System, New York, NY, United States of America; Department of Internal Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States of America.

Samin K Sharma (SK)

Mount Sinai Heart, Mount Sinai Health System, New York, NY, United States of America.

Jagat N Narula (JN)

Mount Sinai Heart, Mount Sinai Health System, New York, NY, United States of America.

Joel T Dudley (JT)

Institute for Next Generation Healthcare, Mount Sinai Health System, New York, NY, United States of America; Department of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, United States of America.

Annapoorna S Kini (AS)

Mount Sinai Heart, Mount Sinai Health System, New York, NY, United States of America. Electronic address: annapoorna.kini@mountsinai.org.

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Classifications MeSH