scholarly journals A case report of cocaine abuse, acute coronary syndrome, and eroded plaque: stent or not stent?

2021 ◽  
Vol 5 (6) ◽  
Author(s):  
Isabel Muñoz Pousa ◽  
Ubaldo Hernández ◽  
Victor A Jiménez Díaz

Abstract Background Intracoronary imaging techniques have allowed characterizing atherosclerotic plaques morphologically in patients with the acute coronary syndrome (ACS). Although the main feature described is plaque rupture, the use of optical coherence tomography has made it possible to objectify that the eroded plaque is not uncommon in this setting. Case summary We presented a case of a 45-year-old man with active smoking and cocaine user, admitted to the emergency department for chest pain. The electrocardiogram showed ST-segment elevation myocardial infarction (STEMI) in the inferior leads. Emergent coronary angiography was performed, showing thrombotic occlusion of mid-distal right coronary artery. After successful thromboaspiration, no areas of significant angiographic stenosis were observed. Optical coherence tomography imaging at the occlusion site revealed an eroded plaque and a remaining small thrombusburden. Conservative management without stent implantation was decided. Treatments consisted of an acute phase glycoprotein IIb/IIIa inhibitor and subsequently dual antiplatelet therapy with Aspirin (ASA) and Ticagrelor 90 mg b.i.d. for 12 months. The patient remains asymptomatic and uneventful at 9-month follow-up. Discussion Young age, history of active smoking, and cocaine use are common clinical features in patients with ACS due to an eroded plaque. These patients frequently display a STEMI with the involvement of a single coronary vessel. Optical coherence tomography imaging aids to a precise diagnosis and to define a proper treatment.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Fukuyama ◽  
H Otake ◽  
F Seike ◽  
H Kawamori ◽  
T Toba ◽  
...  

Abstract Background The direct relationship between plaque rupture (PR) that cause acute coronary syndrome (ACS) and wall shear stress (WSS) remains uncertain. Methods From the Kobe University ACS-OCT registry, one hundred ACS patients whose culprit lesions had PR documented by optical coherence tomography (OCT) were enrolled. Lesion-specific 3D coronary artery models were created using OCT data. Specifically, at the ruptured portion, the tracing of the luminal edge of the residual fibrous cap was smoothly extrapolated to reconstruct the luminal contour before PR. Then, WSS was computed from computational fluid dynamics (CFD) analysis by a single core laboratory. Relationships between WSS and the location of PR were assessed with 1) longitudinal 3-mm segmental analysis and 2) circumferential analysis. In the longitudinal segmental analysis, each culprit lesion was subdivided into five 3-mm segments with respect to the minimum lumen area (MLA) location at the centered segment (Figure. 1). In the circumferential analysis, we measured WSS values at five points from PR site and non-PR site on the cross-sections with PR. Also, each ruptured plaque was categorized into the lateral type PR (L-PR), central type PR (C-PR), and others according to the relation between the site of tearing and the cavity (Figure. 2). Results In the longitudinal 3-mm segmental analysis, the incidences of PR at upstream (UP1 and 2), MLA, and downstream (DN1 and 2) were 45%, 40%, and 15%, respectively. The highest average WSS was located in UP1 in the upstream PR (UP1: 15.5 (10.4–26.3) vs. others: 6.8 (3.3–14.7) Pa, p<0.001) and MLA segment in the MLA PR (MLA: 18.8 (6.0–34.3) vs. others: 6.5 (3.1–11.8) Pa, p<0.001), and the second highest WSS was located at DN1 in the downstream PR (DN1: 5.8 (3.7–11.5) vs. others: 5.5 (3.7–16.5) Pa, p=0.035). In the circumferential analysis, the average WSS at PR site was significantly higher than that of non-PR site (18.7 (7.2–35.1) vs. 13.9 (5.2–30.3) Pa, p<0.001). The incidence of L-PR, C-PR, and others were 51%, 42%, and 7%, respectively. In the L-PR, the peak WSS was most frequently observed in the lateral site (66.7%), whereas that in the C-PR was most frequently observed in the center site (70%) (Figure. 3). In the L-PR, the peak WSS value was significantly lower (44.6 (19.6–65.2) vs. 84.7 (36.6–177.5) Pa, p<0.001), and the thickness of broken fibrous cap was significantly thinner (40 (30–50) vs. 80 (67.5–100) μm, p<0.001), and the lumen area at peak WSS site was significantly larger than those of C-PR (1.5 (1.3–2.0) vs. 1.4 (1.1–1.6) mm2, p=0.008). Multivariate analysis demonstrated that the presence of peak WSS at lateral site, thinner broken fibrous cap thickness, and larger lumen area at peak WSS site were independently associated with the development of the L-PR. Conclusions A combined approach with CFD simulation and morphological plaque evaluation by using OCT might be helpful to predict future ACS events induced by PR. Funding Acknowledgement Type of funding source: None


Author(s):  
Krishna Prasad ◽  
Sreeniavs Reddy S ◽  
Jaspreet Kaur ◽  
Raghavendra Rao k ◽  
Suraj Kumar ◽  
...  

Introduction: Women perform worse after acute coronary syndrome (ACS) than men. The reason for these differences is unclear. The aim was to ascertain gender differences in the culprit plaque characteristics in ACS. Methods:Patients with ACS undergoing percutaneous coronary intervention for the culprit vessel underwent optical coherence tomography (OCT) imaging. Culprit plaque was identified as lipid rich,fibrous, and calcific plaque. Mechanisms underlying ACS are classified as plaque rupture, erosion,or calcified nodule. A lipid rich plaque along with thin-cap fibroatheroma (TCFA) was a vulnerable plaque. Plaque microstructures including cholesterol crystals, macrophages, and microvessels were noted. Results: A total of 52 patients were enrolled (men=29 and women=23). Baseline demographic features were similar in both the groups except men largely were current smokers (P<0.001). Plaque morphology,men vs. women: lipid rich 88.0% vs. 90.5%; fibrous 4% vs 0%; calcific 8.0% vs. 9.5% (P = 0.64). Of the ACS mechanisms in males versus females; plaque rupture (76.9 % vs. 50 %), plaque erosion (15.4 % vs.40 %) and calcified nodule (7.7 % vs. 10 %) was noted (P = 0.139). Fibrous cap thickness was (50.19 ±11.17 vs. 49.00 ± 10.71 mm, P = 0.71) and thin-cap fibroatheroma (96.2% vs. 95.0%, P = 1.0) in men and women respectively. Likewise no significant difference in presence of macrophages (42.3 % vs. 30%, P = 0.76), microvessels (73.1% vs. 60 %, P = 0.52) and cholesterol crystals (92.3% vs. 80%, P = 0.38). Conclusion: No significant gender-based in-vivo differences could be discerned in ACS patients’ culprit plaques morphology, characteristics, and underlying mechanisms.


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