Coronary Artery Lesion Lipid Content and Plaque Burden in Diabetic and Nondiabetic Patients: PROSPECT II

Author:

Gyldenkerne Christine1ORCID,Maeng Michael1ORCID,Kjøller-Hansen Lars2ORCID,Maehara Akiko34ORCID,Zhou Zhipeng4,Ben-Yehuda Ori45,Erik Bøtker Hans1,Engstrøm Thomas6,Matsumura Mitsuaki4ORCID,Mintz Gary S.4ORCID,Fröbert Ole7ORCID,Persson Jonas8,Wiseth Rune9ORCID,Larsen Alf I.10ORCID,Jensen Lisette O.11ORCID,Nordrehaug Jan E.12,Bleie Øyvind12ORCID,Omerovic Elmir13ORCID,Held Claes14ORCID,James Stefan K.14ORCID,Ali Ziad A.3ORCID,Rosen Hans C.15ORCID,Stone Gregg W.16ORCID,Erlinge David15ORCID

Affiliation:

1. Department of Cardiology, Aarhus University Hospital, Aarhus University, Denmark (C.G., M. Maeng, H.E.B.).

2. Department of Cardiology, Zealand University Hospital, Roskilde, Denmark (L.K.-H.).

3. New York-Presbyterian Hospital and Division of Cardiology, Columbia University Irving Medical Center, New York, NY (A.M., Z.A.A.).

4. Clinical Trials Center, Cardiovascular Research Foundation, New York, NY (A.M., Z.Z., O.B.-Y., M. Matsumura, G.S.M.).

5. Division of Cardiology, University of California San Diego (O.B.-Y.).

6. University of Copenhagen, Denmark (T.E.).

7. Department of Cardiology, Faculty of Health, Örebro University, Sweden (O.F.).

8. Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden (J.P.).

9. Clinic of Cardiology, St Olavs University Hospital, Trondheim, Norway (R.W.).

10. Department of Cardiology, Stavanger University Hospital, Norway (A.I.L.).

11. Department of Cardiology, Odense University Hospital, Denmark (L.O.J.).

12. Department of Clinical Science, University of Bergen, Norway (J.E.N., Ø.B.).

13. Department of Molecular and Clinical Medicine/Cardiology, Sahlgrenska University Hospital, Gothenburg, Sweden (E.O.).

14. Department of Medical Sciences and Cardiology, Uppsala University and Uppsala Clinical Research Center, Sweden (C.H., S.K.J.).

15. Lund University, Sweden (H.C.R., D.E.).

16. The Zena and Michael A Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY (G.W.S.).

Abstract

Background: Patients with diabetes have increased rates of major adverse cardiac events (MACEs). We hypothesized that this is explained by diabetes-associated differences in coronary plaque morphology and lipid content. Methods: In PROSPECT II (Providing Regional Observations to Study Predictors of Events in the Coronary Tree), 898 patients with acute myocardial infarction with or without ST-segment elevation underwent 3-vessel quantitative coronary angiography and coregistered near-infrared spectroscopy and intravascular ultrasound imaging after successful percutaneous coronary intervention. Subsequent MACEs were adjudicated to either treated culprit lesions or untreated nonculprit lesions. This substudy stratified patients by diabetes status and assessed baseline culprit and nonculprit prevalence of high-risk plaque characteristics defined as maximum plaque burden ≥70% and maximum lipid core burden index ≥324.7. Separate covariate-adjusted multivariable models were performed to identify whether diabetes was associated with nonculprit lesion–related MACEs and high-risk plaque characteristics. Results: Diabetes was present in 109 of 898 patients (12.1%). During a median 3.7-year follow-up, MACEs occurred more frequently in patients with versus without diabetes (20.1% versus 13.5% [odds ratio (OR), 1.94 (95% CI, 1.14–3.30)]), primarily attributable to increased risk of myocardial infarction related to culprit lesion restenosis (4.3% versus 1.1% [OR, 3.78 (95% CI, 1.12–12.77)]) and nonculprit lesion–related spontaneous myocardial infarction (9.3% versus 3.8% [OR, 2.74 (95% CI, 1.25–6.04)]). However, baseline prevalence of high-risk plaque characteristics was similar for patients with versus without diabetes concerning culprit (maximum plaque burden ≥70%: 90% versus 93%, P =0.34; maximum lipid core burden index ≥324.7: 66% versus 70%, P =0.49) and nonculprit lesions (maximum plaque burden ≥70%: 23% versus 22%, P =0.37; maximum lipid core burden index ≥324.7: 26% versus 24%, P =0.47). In multivariable models, diabetes was associated with MACEs in nonculprit lesions (adjusted OR, 2.47 [95% CI, 1.21–5.04]) but not with prevalence of high-risk plaque characteristics (adjusted OR, 1.21 [95% CI, 0.86–1.69]). Conclusions: Among patients with recent myocardial infarction, both treated and untreated lesions contributed to the diabetes-associated ≈2-fold increased MACE rate during the 3.7-year follow-up. Diabetes-related plaque characteristics that might underlie this increased risk were not identified by multimodality imaging. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02171065.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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