Abdelwahed YS, Nelles G, Frick C, et al. - Ruptured fibrous cap acute coronary syndromes (ACS)-causing culprit lesions are characterized by calcified- and lipid-containing components, and direct acceleration of their coexistence was evident at the ruptured point, indicating a pathophysiological contribution in RFC-ACS (ACS caused by culprit lesions with rupture of the fibrous cap) development.

• Within the prospective, multicentric OPTICO-ACS study program, a large cohort of ACS-patients (n=282) was evaluated using high-resolution intracoronary imaging in order to characterize the association between plaque components and rupture points at ACS-causing culprit lesions.

• Of participants, 72.3% had RFC-ACS and 27.7% had ACS due to culprit lesions with intact fibrous cap (IFC-ACS).

• On comparing RFC-ACS to IFC-ACS, a preferential occurrence of all three plaque components (LC [lipid components], CC [calcium components], and LCC [coexistence of both LC and CC]) in RFC-ACS was apparent.

• The zone straight at the rupture point [extended rupture zone (RZ)] within ruptured culprit lesions was characterized by similar (24.7% vs 24.0%) calcium content vs the proximal and distal border of the culprit lesion [border zone (BZ)].

• A significantly higher amount of both, LC (100% vs 69.8%) and LCC (22.7% vs 6.8%) was exhibited by RZ vs BZ.

• For LCC, relative component increase towards the RZ was especially seen (+233.8%), while LC displayed only a modest increase (+43.3%).