Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Dec 1;16(1):152.
doi: 10.1186/s12933-017-0635-2.

Type 2 diabetes mellitus is associated with a lower fibrous cap thickness but has no impact on calcification morphology: an intracoronary optical coherence tomography study

Affiliations

Type 2 diabetes mellitus is associated with a lower fibrous cap thickness but has no impact on calcification morphology: an intracoronary optical coherence tomography study

Andrea Milzi et al. Cardiovasc Diabetol. .

Abstract

Background: Patients with type 2 diabetes (T2DM) are at high risk for cardiovascular events, which usually arise from the rupture of a vulnerable coronary plaque. The minimal fibrous cap thickness (FCT) overlying a necrotic lipid core is an established predictor for plaque rupture. Recently, coronary calcification has emerged as a relevant feature of plaque vulnerability. However, the impact of T2DM on these morphological plaque parameters is largely unexplored. Therefore, this study aimed to compare differences of coronary plaque morphology in patients with and without T2DM with a particular focus on coronary calcification.

Methods: In 91 patients (T2DM = 56, non-T2DM = 35) with 105 coronary de novo lesions (T2DM = 56, non-T2DM = 49) plaque morphology and calcification were analyzed using optical coherence tomography (OCT) prior to coronary intervention.

Results: Patients with T2DM had a lower minimal FCT (80.4 ± 27.0 µm vs. 106.8 ± 27.8 µm, p < 0.001) and a higher percent area stenosis (77.9 ± 8.1% vs. 71.7 ± 11.2%, p = 0.001) compared to non-diabetic subjects. However, patients with and without T2DM had a similar total number of calcifications (4.0 ± 2.6 vs. 4.2 ± 3.1, p = ns) and no significant difference was detected in the number of micro- (0.34 ± 0.79 vs. 0.31 ± 0.71), spotty (2.11 ± 1.77 vs. 2.37 ± 1.89) or macro-calcifications (1.55 ± 1.13 vs. 1.53 ± 0.71, all p = ns). The mean calcium arc (82.3 ± 44.8° vs. 73.7 ± 31.6), the mean thickness of calcification (0.54 ± 0.13 mm vs. 0.51 ± 0.15 mm), the mean calcified area (0.99 ± 0.72 mm2 vs. 0.78 ± 0.49 mm2), the mean depth of calcification (172 ± 192 μm vs. 160 ± 76 μm) and the cap thickness overlying the calcification (50 ± 71 μm vs. 62 ± 61 μm) did not differ between the diabetic and non-diabetic groups (all p = ns).

Conclusion: T2DM has an impact on the minimal FCT of the coronary target lesion, but not on localization, size, shape or extent of calcification. Thus, the minimal FCT overlying the necrotic lipid core but not calcification is likely to contribute to the increased plaque vulnerability observed in patients with T2DM.

Keywords: Coronary calcification; Diabetes mellitus; Optical coherence tomography; Plaque vulnerability.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Study design algorithm including inclusion and exclusion criteria is depicted. ACS, acute coronary syndrome; CAD, coronary artery disease; OCT, optical coherence tomography
Fig. 2
Fig. 2
Details of calcification analysis in short (a) and long axis (b). Quantitative analysis of various parameters for the assessment of localization, size, shape and extent of calcifications in a transverse (a) and longitudinal (b) section of an OCT—image of a fibrocalcific coronary plaque
Fig. 3
Fig. 3
Lipid plaques in patients with (b) and without diabetes (a). In the presence of diabetes a thinner minimal fibrous cap thickness can be identified. In (a) a spotty calcification is visible (marked with the yellow arrow). FCT, fibrous cap thickness

References

    1. Kannel WB, McGee DL. Diabetes and cardiovascular disease. The Framingham study. JAMA. 1979;241:2035–2038. doi: 10.1001/jama.1979.03290450033020. - DOI - PubMed
    1. Paneni F, Beckman JA, Creager MA, Cosentino F. Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I. Eur Heart J. 2013;34:2436–2443. doi: 10.1093/eurheartj/eht149. - DOI - PMC - PubMed
    1. Haffner SM, Lehto S, Rönnemaa T, Pyörälä K, Laakso M. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med. 1998;339:229–234. doi: 10.1056/NEJM199807233390404. - DOI - PubMed
    1. Falk E, Nakano M, Bentzon JF, Finn AV, Virmani R. Update on acute coronary syndromes: the pathologists’ view. Eur Heart J. 2013;34:719–728. doi: 10.1093/eurheartj/ehs411. - DOI - PubMed
    1. Sinclair H, Bourantas C, Bagnall A, Mintz GS, Kunadian V. OCT for the identification of vulnerable plaque in acute coronary syndrome. JACC Cardiovasc Imaging. 2015;8:198–209. doi: 10.1016/j.jcmg.2014.12.005. - DOI - PubMed

MeSH terms