Abdelwahed Youssef S, Nelles Gregor, Frick Clara, Seppelt Claudio, Meteva Denitsa, Stähli Barbara E, Rai Himanshu, Riedel Matthias, Skurk Carsten, Rauch-Kröhnert Ursula, Haghikia Arash, Sinning David, Dreger Henryk, Knebel Fabian, Trippel Tobias, Krisper Maximillian, Klotsche Jens, Joner Michael, Landmesser Ulf, Leistner David M
Department of Cardiology, Charité University Medicine Berlin, Campus Benjamin-Franklin (CBF), Hindenburgdamm 30, 12203 Berlin, Germany.
DZHK (German Centre for Cardiovascular Research) Partner Site Berlin, 12203 Berlin, Germany.
Eur Heart J Cardiovasc Imaging. 2022 Nov 17;23(12):1598-1605. doi: 10.1093/ehjci/jeab247.
AIMS: Rupture of the fibrous cap (RFC) represents the main pathophysiological mechanism causing acute coronary syndromes (ACS). Destabilization due to plaque biomechanics is considered to be importantly involved, exact mechanisms triggering plaque ruptures are, however, unknown. This study aims at characterizing the relation between plaque components and rupture points at ACS-causing culprit lesions in a large cohort of ACS-patients assessed by high-resolution intracoronary imaging. METHODS AND RESULTS: Within the prospective, multicentric OPTICO-ACS study program, the ACS-causing culprit plaques of 282 consecutive patients were investigated following a standardized optical coherence tomography (OCT) imaging protocol. Each pullback was assessed on a frame-by-frame basis for the presence of lipid components (LC), calcium components (CC), and coexistence of both LC and CC (LCC) by two independent OCT-core labs. Of the 282 ACS-patients, 204 patients (72.3%) presented with ACS caused by culprit lesions with rupture of the fibrous cap (RFC-ACS) and 27.7% patients had ACS caused by culprit lesions with intact fibrous cap (IFC-ACS). When comparing RFC-ACS to IFC-ACS, a preferential occurrence of all three plaque components (LC, CC, and LCC) in RFC-ACS became apparent (P < 0.001). Within ruptured culprit lesions, the zone straight at the rupture point [extended rupture zone (RZ)] was characterized by similar (24.7% vs. 24.0%; P = ns) calcium content when compared with the proximal and distal border of the culprit lesion [border zone (BZ)]. The RZ displayed a significantly higher amount of both, LC (100% vs. 69.8%; P < 0.001) and LCC (22.7% vs. 6.8%; P < 0.001), when compared with the BZ. The relative component increase towards the RZ was particularly evident for LCC (+233.8%), while LC showed only a modest increase (+43.3%). CONCLUSIONS: Calcified- and lipid-containing components characterize ruptured fibrous cap ACS-causing culprit lesions. Their coexistence is accelerated directly at the ruptured point, suggesting a pathophysiological contribution in the development of RFC-ACS.
Zotero 插件