Intrinsic calcification angle: a novel feature of the vulnerable coronary plaque in patients with type 2 diabetes: an optical coherence tomography study.


Journal

Cardiovascular diabetology
ISSN: 1475-2840
Titre abrégé: Cardiovasc Diabetol
Pays: England
ID NLM: 101147637

Informations de publication

Date de publication:
24 09 2019
Historique:
received: 28 05 2019
accepted: 11 09 2019
entrez: 26 9 2019
pubmed: 26 9 2019
medline: 12 5 2020
Statut: epublish

Résumé

Coronary calcification is associated with high risk for cardiovascular events. However, its impact on plaque vulnerability is incompletely understood. In the present study we defined the intrinsic calcification angle (ICA) as the angle externally projected by a vascular calcification and analyzed its role as novel feature of coronary plaque vulnerability in patients with type 2 diabetes. Optical coherence tomography was used to determine ICA in 219 calcifications from 56 patients with stable coronary artery disease (CAD) and 143 calcifications from 36 patients with acute coronary syndrome (ACS). We then used finite elements analysis to gain mechanistic insight into the effects of ICA. Minimal (139.8 ± 32.8° vs. 165.6 ± 21.6°, p < 0.001) and mean ICA (164.1 ± 14.3° vs. 176.0 ± 8.4°, p < 0.001) were lower in ACS vs. stable CAD patients. Mean ICA predicted ACS with very good diagnostic efficiency (AUC = 0.840, 95% CI 0.797-0.882, p < 0.001, optimal cut-off 175.9°); younger age (OR 0.95 per year, 95% CI 0.92-0.98, p = 0.002), male sex (OR 2.18, 95% CI 1.41-3.38, p < 0.001), lower HDL-cholesterol (OR 0.82 per 10 mg/dl, 95% CI 0.68-0.98, p = 0.029) and ACS (OR 14.71, 95% CI 8.47-25.64, p < 0.001) were determinants of ICA < 175.9°. A lower ICA predicted ACS (OR for 10°-variation 0.25, 95% CI 0.13-0.52, p < 0.001) independently from fibrous cap thickness, presence of macrophages or extension of lipid core. In finite elements analysis we confirmed that lower ICA causes increased stress on a lesion's fibrous cap; this effect was potentiated in more superficial calcifications and adds to the destabilizing role of smaller calcifications. Our clinical and mechanistic data for the first time identify ICA as a novel feature of coronary plaque vulnerability.

Sections du résumé

BACKGROUND
Coronary calcification is associated with high risk for cardiovascular events. However, its impact on plaque vulnerability is incompletely understood. In the present study we defined the intrinsic calcification angle (ICA) as the angle externally projected by a vascular calcification and analyzed its role as novel feature of coronary plaque vulnerability in patients with type 2 diabetes.
METHODS
Optical coherence tomography was used to determine ICA in 219 calcifications from 56 patients with stable coronary artery disease (CAD) and 143 calcifications from 36 patients with acute coronary syndrome (ACS). We then used finite elements analysis to gain mechanistic insight into the effects of ICA.
RESULTS
Minimal (139.8 ± 32.8° vs. 165.6 ± 21.6°, p < 0.001) and mean ICA (164.1 ± 14.3° vs. 176.0 ± 8.4°, p < 0.001) were lower in ACS vs. stable CAD patients. Mean ICA predicted ACS with very good diagnostic efficiency (AUC = 0.840, 95% CI 0.797-0.882, p < 0.001, optimal cut-off 175.9°); younger age (OR 0.95 per year, 95% CI 0.92-0.98, p = 0.002), male sex (OR 2.18, 95% CI 1.41-3.38, p < 0.001), lower HDL-cholesterol (OR 0.82 per 10 mg/dl, 95% CI 0.68-0.98, p = 0.029) and ACS (OR 14.71, 95% CI 8.47-25.64, p < 0.001) were determinants of ICA < 175.9°. A lower ICA predicted ACS (OR for 10°-variation 0.25, 95% CI 0.13-0.52, p < 0.001) independently from fibrous cap thickness, presence of macrophages or extension of lipid core. In finite elements analysis we confirmed that lower ICA causes increased stress on a lesion's fibrous cap; this effect was potentiated in more superficial calcifications and adds to the destabilizing role of smaller calcifications.
CONCLUSION
Our clinical and mechanistic data for the first time identify ICA as a novel feature of coronary plaque vulnerability.

Identifiants

pubmed: 31551093
doi: 10.1186/s12933-019-0926-x
pii: 10.1186/s12933-019-0926-x
pmc: PMC6760065
doi:

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

122

Commentaires et corrections

Type : CommentIn

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Auteurs

Sebastian Reith (S)

Department of Cardiology, Medical Clinic I, University Hospital of the RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.

Andrea Milzi (A)

Department of Cardiology, Medical Clinic I, University Hospital of the RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.

Enrico Domenico Lemma (ED)

Zoological Institute, Department of Cell- and Neurobiology, Karlsruhe Institute of Technology (KIT), Karlsruhe, Germany.

Rosalia Dettori (R)

Department of Cardiology, Medical Clinic I, University Hospital of the RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.

Kathrin Burgmaier (K)

Department of Pediatrics, University Hospital of Cologne, Cologne, Germany.

Nikolaus Marx (N)

Department of Cardiology, Medical Clinic I, University Hospital of the RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.

Mathias Burgmaier (M)

Department of Cardiology, Medical Clinic I, University Hospital of the RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany. mburgmaier@ukaachen.de.

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