Coronary Plaque Ulcerations - Novel Features of Plaque Vulnerability in ACS with Intact Fibrous Cap? – Insights from the OPTICO-ACS Study Program
C. Seppelt1, D. Meteva1, Y. Abdelwahed1, L. Sieronski1, H. Rai2, M. Riedel1, N. Kränkel1, C. Skurk1, H.-C. Mochmann1, A. Lauten1, B. Stähli3, U. Rauch-Kröhnert1, G. Fröhlich1, A. Haghikia1, D. Sinning1, M. Reinthaler1, M. Krisper4, T. D. Trippel4, H. Dreger5, F. Knebel5, M. Joner6, U. Landmesser1, D. Leistner1
1CC 11: Med. Klinik für Kardiologie, Charité - Universitätsmedizin Berlin, Berlin; 2Klinik für Herz- und Kreislauferkrankungen, Deutsches Herzzentrum München, München; 3Universitäres Herzzentrum, UniversitätsSpital Zürich, Zürich, CH; 4CC11: Med. Klinik m.S. Kardiologie, Charité - Universitätsmedizin Berlin, Berlin; 5CC11: Med. Klinik m. S. Kardiologie und Angiologie, Charité - Universitätsmedizin Berlin, Berlin; 6Deutsches Herzzentrum München, München;

Background and Methods:

Coronary plaque ulcerations (PU) represent markers of advanced plaque remodeling. However, despite the possibility for an in-vivo detection of PU by optical coherence tomography (OCT) their contribution to plaque destabilization resulting in an ACS-causing culprit lesion is yet unknown. To examine PU as a potential marker of plaque vulnerability, the first 316 consecutive patients within the prospective, translational, multicentric OPTICO-ACS-study were analyzed by two independent OCT core labs. For the entire analysis, the incidence of PU and its associations with other coronary plaque features were compared between ACS-causing culprit plaques (CP) and non-culprit plaques (NCP) within the culprit vessel.

Results:

The presence of PU is significantly higher (p<0.001) in ACS-causing culprit plaques (CP: 33.2%) as compared to non-culprit plaques (NCP: 11.2%). ACS-patients with culprit plaques with PU are significantly older as compared to non-ulcerated culprit plaques. (66 ± 11 years CP with PU vs. 63 ± 13 years CP without PU; p=0.04), but show similar clinical ACS characteristics such as presentation as STE-ACS (p=0.20), pain-to-balloon time (p=0.85) and extent of ischaemic myocardial injury (p=0.38).

PU within ACS-causing culprit lesions is predominant (p=0.01) associated with ACS with intact fibrous cap (IFC-ACS; 49%) whereas only 25% of ACS with ruptured fibrous cap (RFC-ACS) exhibited PU. Importantly no differences for established criteria of plaque vulnerability are detectable among CP with PU, such as the presence of thin cap fibroatheromas (TCFA; 75% CP with PU vs. 78% CP without PU; p=0.6), CP lipid index (4343 ± 2007 vs. 4001 ± 2008; p=0.8) and the minimum fibrous cap thickness of the CP (73µm ± 44µm vs. 67µm ± 35µm; p=0.3). Likewise, minimum lumen area was comparable among culprit lesions with and without PU (1.8mm2 ± 1.3mm2 vs. 2.0mm2 ± 1.0mm2; p=0.3). CP with PU are characterized by a significantly higher presence of macrophages (99% vs. 89%; p=0.025), indicating that PU could be a result of excessive inflammatory mechanisms causing plaque destabilization as expressed by ulceration of the ACS-causing culprit plaque.

Conclusions:

The present study identifies for the first-time coronary plaque ulcerations as novel markers representing advanced coronary plaque vulnerability above the established markers, especially in those plaques prone to cause IFC-ACS.
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