Abstract 205 Prognostic implications of spotty calcium at ACS-causing culprit lesions – insights from the OPTICO-ACS study program

Background: Coronary calcifications represent a feature of advanced plaque remodeling and can be broadly categorized into spotty- and macrocalcifications. Spotty calcifications, i.e. with a maximum arc of <90° and a length of <4mm, have been described as a novel feature of plaque vulnerability, whereas macrocalcifications seem to have no impact on plaque destabilization. Optical coherence tomography (OCT) allows the morphometric assessment of coronary plaque calcium in vivo. Therefore, the aim of the present study was to comprehensively characterize culprit plaque calcification patterns in a large cohort of patients with acute coronary syndrome (ACS).

Methods: Within the OPTICO-ACS study program, 155 ACS-patients were included into the entire analysis. OCT-characteristics, including a comprehensive analysis of calcium patterns of the ACS-causing culprit lesion were assessed by standardized CoreLab analysis following universal consensus standards for OCT-derived plaque features. All patients were followed up for 12 months after ACS and major adverse cardiac events (MACE) consisting of death, myocardial infarction, target vessel revascularization plus re-hospitalization due to angina pectoris were documented.

Results: 75 patients (45.2%) presented with spotty calcium (SC) at the culprit lesion. Plaque rupture (RFC-ACS) was the predominately ACS-causing pathophysiology (77.1%) in those patients. The presence of spotty calcifications was associated with other high-risk features within the culprit lesion, such as the presence of thin cap fibroatheroma (86.6% vs. 72.8%; p=0.041), thinner fibrous cap (65.2 µm vs. 79.6 µm; p=0.013) and greater maximum lipid arc (282.7° vs. 259.0°; p=0.030) as compared to culprit lesions without spotty calcium. Furthermore, SC-patients showed increased levels of total cholesterol (191.7 mg/dl vs. 172.4 mg/dl; p=0.009), LDL-cholesterol (127.1 mg/dl vs. 114.4 mg/dl; p=0.021) and had larger myocardial injury during ACS (peak creatin-kinase 1485.1 U/l vs. 1273.2 U/l; p=0.041). Finally, importantly MACE plus (MACE + re-hospitalization due to instable angina) during 12 months follow-up after ACS occurred significantly more often in SC-patients (16.4% vs. 5.3%; p=0.028) as compared to patients without spotty calcium at the culprit site.

Conclusion: The findings from the present study distinguish for the first-time spotty calcium within ACS-causing culprit lesions as an additional high-risk feature associated with adverse outcome after ACS.

Clin Res Cardiol (2021) DOI DOI https://doi.org/10.1007/s00392-021-01843-w
Prognostic implications of spotty calcium at ACS-causing culprit lesions – insights from the OPTICO-ACS study program
G. Nelles¹, Y. Abdelwahed¹, C. Seppelt¹, L. Sieronski¹, A. Heuberger¹, D. Meteva¹, C. Skurk¹, A. Haghikia¹, U. Rauch-Kröhnert¹, H. Dreger², F. Knebel², T. D. Trippel³, M. Krisper⁴, N. Kränkel¹, M. Joner⁵, U. Landmesser¹, D. Leistner¹
¹CC 11: Med. Klinik für Kardiologie, Charité - Universitätsmedizin Berlin, Berlin; ²CC11: Med. Klinik m. S. Kardiologie und Angiologie, Charité - Universitätsmedizin Berlin, Berlin; ³CC11: Med. Klinik m.S. Kardiologie, Charité - Universitätsmedizin Berlin, Berlin; ⁴Kardiologisch-Angiologisch-Internistische Praxisgemeinschaft, Praxis Rankestrasse, Berlin; ⁵Deutsches Herzzentrum München, München;
Background: Coronary calcifications represent a feature of advanced plaque remodeling and can be broadly categorized into spotty- and macrocalcifications. Spotty calcifications, i.e. with a maximum arc of <90° and a length of <4mm, have been described as a novel feature of plaque vulnerability, whereas macrocalcifications seem to have no impact on plaque destabilization. Optical coherence tomography (OCT) allows the morphometric assessment of coronary plaque calcium in vivo. Therefore, the aim of the present study was to comprehensively characterize culprit plaque calcification patterns in a large cohort of patients with acute coronary syndrome (ACS). Methods: Within the OPTICO-ACS study program, 155 ACS-patients were included into the entire analysis. OCT-characteristics, including a comprehensive analysis of calcium patterns of the ACS-causing culprit lesion were assessed by standardized CoreLab analysis following universal consensus standards for OCT-derived plaque features. All patients were followed up for 12 months after ACS and major adverse cardiac events (MACE) consisting of death, myocardial infarction, target vessel revascularization plus re-hospitalization due to angina pectoris were documented. Results: 75 patients (45.2%) presented with spotty calcium (SC) at the culprit lesion. Plaque rupture (RFC-ACS) was the predominately ACS-causing pathophysiology (77.1%) in those patients. The presence of spotty calcifications was associated with other high-risk features within the culprit lesion, such as the presence of thin cap fibroatheroma (86.6% vs. 72.8%; p=0.041), thinner fibrous cap (65.2 µm vs. 79.6 µm; p=0.013) and greater maximum lipid arc (282.7° vs. 259.0°; p=0.030) as compared to culprit lesions without spotty calcium. Furthermore, SC-patients showed increased levels of total cholesterol (191.7 mg/dl vs. 172.4 mg/dl; p=0.009), LDL-cholesterol (127.1 mg/dl vs. 114.4 mg/dl; p=0.021) and had larger myocardial injury during ACS (peak creatin-kinase 1485.1 U/l vs. 1273.2 U/l; p=0.041). Finally, importantly MACE plus (MACE + re-hospitalization due to instable angina) during 12 months follow-up after ACS occurred significantly more often in SC-patients (16.4% vs. 5.3%; p=0.028) as compared to patients without spotty calcium at the culprit site. Conclusion: The findings from the present study distinguish for the first-time spotty calcium within ACS-causing culprit lesions as an additional high-risk feature associated with adverse outcome after ACS.
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