Key result
Coronary microevaginations linked to ~236% higher risk of intact fibrous cap ACS independent of bifurcations.
Why the study?
The role of coronary microevaginations in atherosclerosis and plaque destabilization in the absence of coronary intervention was unknown.
Are coronary microevaginations associated with plaque vulnerability and specific inflammatory microenvironments in patients with acute coronary syndrome?
Observational (n=557)
Are coronary microevaginations associated with plaque vulnerability and specific inflammatory microenvironments in patients with acute coronary syndrome?
Relative Risk: 3.36 (95% CI 1.67–6.76)
p-value: p=0.001
Coronary microevaginations are a novel feature of plaque vulnerability strongly associated with intact fibrous cap acute coronary syndromes and innate immune system activation.
Coronary microevaginations may identify high-risk plaques in ACS; hypothesis-generating and requires prospective validation before clinical adoption.
AIMS: Coronary microevaginations (CMEs) represent an outward bulge of coronary plaques and have been introduced as a sign of adverse vascular remodelling following coronary device implantation. However, their role in atherosclerosis and plaque destabilization in the absence of coronary intervention is unknown. This study aimed to investigate CME as a novel feature of plaque vulnerability and to characterize its associated inflammatory cell-vessel-wall interactions. METHODS AND RESULTS: A total of 557 patients from the translational OPTICO-ACS study programme underwent optical coherence tomography imaging of the culprit vessel and simultaneous immunophenotyping of the culprit lesion (CL). Two hundred and fifty-eight CLs had a ruptured fibrous cap (RFC) and one hundred had intact fibrous cap (IFC) acute coronary syndrome (ACS) as an underlying pathophysiology. CMEs were significantly more frequent in CL when compared with non-CL (25 vs. 4%, P < 0.001) and were more frequently observed in lesions with IFC-ACS when compared with RFC-ACS (55.0 vs. 12.7%, P < 0.001). CMEs were particularly prevalent in IFC-ACS-causing CLs independent of a coronary bifurcation (IFC-ICB) when compared with IFC-ACS with an association to a coronary bifurcation (IFC-ACB, 65.4 vs. 43.7%, P = 0.030). CME emerged as the strongest independent predictor of IFC-ICB (relative risk 3.36, 95% confidence interval 1.67-6.76, P = 0.001) by multivariable regression analysis. IFC-ICB demonstrated an enrichment of monocytes in both culprit blood analysis (culprit ratio: 1.1 ± 0.2 vs. 0.9 ± 0.2, P = 0.048) and aspirated culprit thrombi (326 ± 162 vs. 96 ± 87 cells/mm2, P = 0.017), while IFC-ACB confirmed the accumulation of CD4+ T cells, as recently described. CONCLUSION: This study provides novel evidence for a pathophysiological involvement of CME in the development of IFC-ACS and provides first evidence for a distinct pathophysiological pathway for IFC-ICB, driven by CME-derived flow disturbances and inflammatory activation involving the innate immune system. TRIAL REGISTRATION: Registration of the study at clinicalTrials.gov (NCT03129503).
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Seppelt et al. (2023) conducted an observational in Acute coronary syndrome (n=557). Coronary microevaginations vs. Absence of coronary microevaginations was evaluated on Intact fibrous cap acute coronary syndrome independent of a coronary bifurcation (IFC-ICB) (RR 3.36, 95% CI 1.67-6.76, p=0.001). Coronary microevaginations emerged as a strong independent predictor of intact fibrous cap acute coronary syndrome independent of a coronary bifurcation (RR 3.36; 95% CI 1.67-6.76; P=0.001).
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