Showing papers by "Ik-Kyung Jang published in 2023"
1 citations
TL;DR: In this article , the authors examined the relationship between the level of coronary artery inflammation assessed by peri-coronary adipose tissue (PCAT) attenuation and coronary plaque characteristics by optical coherence tomography.
Abstract: Background: Vascular inflammation plays a key role in atherogenesis and in the development of acute coronary syndromes. Coronary inflammation can be measured by peri-coronary adipose tissue (PCAT) attenuation on computed tomography angiography. We examined the relationships between the level of coronary artery inflammation assessed by PCAT attenuation and coronary plaque characteristics by optical coherence tomography. Methods: A total of 474 patients (198 acute coronary syndromes and 276 stable angina pectoris) who underwent preintervention coronary computed tomography angiography and optical coherence tomography were included. To compare the relationships between the level of coronary artery inflammation and detailed plaque characteristics, we divided the subjects into high (n=244) and low (n=230) PCAT attenuation groups using a threshold value of −70.1 Hounsfield units. Results: The high PCAT attenuation group, compared with the low PCAT attenuation group, had more males (90.6% versus 69.6%; P<0.001), more non-ST-segment elevation myocardial infarction (38.5% versus 25.7%; P=0.003), and less stable angina pectoris (51.6% versus 65.2%; P=0.003). Aspirin, dual antiplatelet, and statins were less frequently used in the high PCAT attenuation group compared to the low PCAT attenuation group. Patients with high PCAT attenuation, compared with those with low PCAT attenuation, had lower ejection fraction (median 64% versus 65%; P=0.014) and lower levels of high-density lipoprotein cholesterol (median 45 versus 48 mg/dL; P=0.027). Optical coherence tomography features of plaque vulnerability were significantly more common in patients with high PCAT attenuation, compared to those with low PCAT attenuation, including lipid-rich plaque (87.3% versus 77.8%; P=0.006), macrophage (76.2% versus 67.8%; P=0.041), microchannels (61.9% versus 48.3%; P=0.003), plaque rupture (38.1% versus 23.9%; P<0.001), and layered plaque (60.2% versus 50.0%; P=0.025). Conclusions: Optical coherence tomography features of plaque vulnerability were significantly more common in patients with high PCAT attenuation, compared with those with low PCAT attenuation. Vascular inflammation and plaque vulnerability are intimately related in patients with coronary artery disease. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04523194.
TL;DR: In this article , the authors performed a systematic review and meta-analysis of randomized and observational studies to assess the association between acute and persistent stent malapposition detected using intravascular ultrasound (IVUS) or optical coherence tomography (OCT) and adverse cardiovascular outcomes.
Abstract: INTRODUCTION
The association of coronary stent malapposition (SM) and adverse clinical outcomes after percutaneous coronary intervention (PCI) remains unclear. We aimed to perform a systematic review and meta-analysis of randomized and observational studies to assess the association between acute and persistent SM detected using intravascular ultrasound (IVUS) or optical coherence tomography (OCT) and adverse cardiovascular outcomes.
EVIDENCE ACQUISITION
Available studies were identified through a systematic search of PubMed, reference lists of relevant articles, and Medline. Main efficacy outcomes of interest were: device-oriented composite endpoint (DoCE, including cardiac death, myocardial infarction [MI], target lesion revascularization [TLR], and stent thrombosis [ST]), major safety events (MSE, including cardiac death, MI and ST), TLR, and ST. A sensitivity analysis regarding the impact of major malapposition was also performed.
EVIDENCE SYNTHESIS
A total of 9 studies enrolling 6497 patients were included in the meta-analysis. After a mean follow up of 24±14 months, overall acute and/or persistent malapposition was not significantly associated with the occurrence of all the outcomes of interest, including DoCE (risk ratio [RR] 1.00, 95% confidence interval [CI, 0.79-1.26], P=0.99), MSE (RR 1.42, 95%CI [0.81-2.50], P=0.22), TLR (RR 0.84, 95%CI [0.59-1.19], P=0.33), and ST (RR 1.16, 95%CI [0.48-2.85], P=0.74). In the sensitivity analysis, we found a significant increase of MSE in patients with major malapposition (RR 2.97, 95%CI [1.51-5.87], P=0.001).
CONCLUSIONS
Acute and persistent SM were not overall associated with adverse cardiovascular clinical outcomes at follow-up. However, major malapposition was associated with an increased risk of major safety events, including cardiac death, MI and ST. These findings should be taken into account during stent implantation and PCI optimization.
TL;DR: Nida et al. as discussed by the authors reported the first case of recurrent plaque erosion in a different vessel 9 years after the initial episode, which can be differentiated in vivo by optical coherence tomography (OCT).
Abstract: Case Reports21 March 2023Recurrent Plaque Erosion in a Young PatientTakayuki Niida, MD, PhD, Maya Serhal, MD, Rahul Sakhuja, MD, Robert Yeh, MD, MSc, MBA, and Ik-Kyung Jang, MD, PhDTakayuki Niida, MD, PhDCardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MassachusettsSearch for more papers by this author, Maya Serhal, MDCardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MassachusettsSearch for more papers by this author, Rahul Sakhuja, MDCardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MassachusettsSearch for more papers by this author, Robert Yeh, MD, MSc, MBARichard A. and Susan F. Smith Center for Outcomes Research in Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MassachusettsSearch for more papers by this author, and Ik-Kyung Jang, MD, PhDCardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MassachusettsSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/aimcc.2022.1068 SectionsSupplemental MaterialAboutVisual AbstractAbstractPDF ToolsAdd to favoritesDownload CitationsTrack Citations ShareFacebookTwitterLinkedInRedditEmail AbstractPlaque erosion is one of the important mechanisms of acute coronary syndromes. We report the first case of recurrent plaque erosion in a different vessel 9 years after the initial episode.BackgroundAcute coronary syndromes (ACS) are one of the most common causes of mortality and morbidity worldwide (1). Pathology studies have reported 2 primary mechanisms of ACS: plaque rupture and plaque erosion, which can be differentiated in vivo by optical coherence tomography (OCT) (2). Although plaque rupture has been the most frequent mechanism of ACS, widespread use of lipid-lowering therapy has changed the clinical landscape of ACS in recent years: the incidence of ST-segment elevation myocardial infarction (STEMI) has been declining, whereas the incidence of non–ST-segment elevation myocardial infarction (NSTEMI) has been slightly rising (3). Plaque erosion is a common underlying pathology in NSTEMI. Currently, plaque erosion accounts for one-third of ACS cases (4, 5), and it is becoming increasingly important to have better understanding of plaque erosion.ObjectiveTo learn the pathobiology of plaque erosion in patients with ACS.To understand that conservative management without coronary stenting may be an option in patients with ACS and plaque erosion.Case ReportA 39-year-old Hispanic man with a history of acute myocardial infarction presented with chest pain and shortness of breath for 12 to 24 hours. His vital signs were stable: blood pressure 127/86 mm Hg, heart rate 56 beats/min, respiratory rate 17 breaths/min, and oxygen saturation was 97% on room air. Findings of the physical examination were unremarkable, without signs of acute heart failure.He had a history of inferior STEMI 9 years ago at the age of 30 years (Figure 1). The coronary angiogram revealed a hazy thrombotic lesion in the proximal right coronary artery (RCA) with evidence of embolization to the posterolateral branch (Figure 2, A). Left coronary arteries showed no significant narrowing (Figure 2, B). OCT findings of the culprit lesion were consistent with plaque erosion without evidence of superficial lipid or plaque rupture (Figure 2, C). The patient was treated conservatively with aspirin, ticagrelor, intravenous eptifibatide, and unfractionated heparin. Follow-up coronary angiogram on day 4 showed smaller thrombus and Thrombolysis In Myocardial Infarction flow grade 3 with restoration of flow to the posterolateral branch (Figure 2, D). Hypercoagulability work-up did not reveal any abnormalities. Echocardiogram with a bubble study to rule out paradoxical embolism was negative. He was discharged on day 5 on aspirin, ticagrelor, statin, and a beta-blocker.Figure 1. Electrocardiogram during initial presentation 9 years ago. Electrocardiogram shows ST-segment elevation in II, III, aVF, V5, and V6 leads. Download figure Download PowerPoint Figure 2. Coronary angiogram and OCT at the culprit lesion 9 years ago. (A) Angiogram shows a filling defect in the proximal RCA and total occlusion in the posterolateral branch possibly due to distal embolization. (B) Angiogram shows no significant stenosis in left coronary arteries. (C) An OCT image of the culprit lesion. OCT shows no superficial lipid or evidence of plaque rupture. A mixed thrombus is present between the 10:00- and 12:00-o'clock position (arrowheads). (D) Angiogram shows a smaller residual thrombus in the proximal RCA, and the posterolateral branch has recanalized. OCT = optical coherence tomography; RCA = right coronary artery. Download figure Download PowerPoint On this admission, an electrocardiogram showed no apparent abnormalities. However, high-sensitivity troponin T was elevated at 888 ng/L (normal range, 0–14 ng/L). An echocardiogram showed normal biventricular size and systolic function without regional wall motion abnormalities and no evidence of pericardial effusion. Although chest pain had improved with nitroglycerin, considering the elevated troponin T level, an urgent coronary angiogram was performed, which showed a widely patent RCA (Figure 3, A). The left anterior descending artery showed a large filling defect in the proximal segment with Thrombolysis In Myocardial Infarction flow grade 3 (Figure 3, B). OCT showed no evidence of superficial lipid or plaque rupture: a finding consistent with plaque erosion (Figure 3, C, and Video 1). With a diagnosis of probable plaque erosion, immediate percutaneous coronary intervention was deferred, and the patient was treated with aspirin, unfractionated heparin, and eptifibatide. A follow-up coronary angiogram on day 3 showed persistent large thrombus burden. Because of the large residual thrombus burden without significant improvement, the treating cardiologist decided to proceed with stenting. A drug-eluting stent (XIENCE Skypoint 2.75 × 23 mm; Abbott, USA) was implanted. The patient was discharged on day 4.Figure 3. Angiogram and OCT at recurrent NSTEMI. (A) Angiogram shows the widely patent right coronary artery. (B) Angiogram shows a large eccentric filling defect in the proximal LAD. (C) An OCT image of probable plaque erosion. OCT shows no superficial lipid or plaque rupture. A mixed thrombus was visualized between 8:00- and 2:00-o'clock position (white asterisks). LAD = left anterior descending artery; NSTEMI = non–ST-segment elevation myocardial infarction; OCT = optical coherence tomography. Download figure Download PowerPoint Video 1. OCT at recurrent non–ST-segment elevation myocardial infarction. OCT shows attenuation of underlying plaque by thrombus without superficial lipid or calcification immediately proximal or distal to the thrombus. OCT = optical coherence tomography. (Duration: 0:51)DiscussionThe underlying mechanisms of plaque erosion are complex (4, 5). When the local blood flow pattern is disturbed with subsequent changes in endothelial shear stress (ESS), expression of Toll-like receptor 2 and hyaluronidase 2 are upregulated, and myeloperoxidase is produced from polymorphonucleates. Toll-like receptor 2 expression causes inflammation and leads to desquamation of endothelial cells. Hyaluronidase 2 degrades hyaluronic acid into its proinflammatory isoforms, causing endothelial cell activation and desquamation, as well as also causing neutrophil mobilization. Myeloperoxidase produces hypochlorous acid and causes apoptosis of endothelial cells. Neutrophils accumulate at the site of endothelial erosion and create net-like structures, called neutrophil extracellular traps. Neutrophil extracellular traps also contain neutrophil-derived cytokines and tissue factors that attract platelets and promote thrombus formation.Yahagi and colleagues (6) performed 3-vessel OCT imaging and a histology examination in a 34-year-old man who died suddenly. They showed multiple plaque erosions in 3 coronary arteries, as well as a platelet-rich (white) thrombus in left circumflex artery and fibrin-rich (red) thrombi in RCA and diagonal branch. Typically, a white thrombus is found on an eroded plaque, but a red thrombus also has been reported (7).Yamamoto and colleagues (8) reported 5 independent predictors of plaque erosion: age younger than 68 years, anterior ischemia, no diabetes mellitus, hemoglobin >15.0 g/dL, and normal renal function. Young age, absence of diabetes, and normal renal function may be related to lower levels of vascular inflammation, whereas left anterior descending coronary artery location and high blood viscosity would be related to ESS. When all 5 variables were present in a patient with NSTEMI, the probability of plaque erosion increased to 73.1%. This case met all 5 of these predictors. Thus, the underlying pathobiology of plaque erosion may be complex, including endothelial factor, local fluid dynamics, and systemic factors, whereas vascular inflammation plays a major role in plaque rupture.The EROSION (Effective Anti-Thrombotic Therapy Without Stenting: Intravascular Optical Coherence Tomography-Based Management in Plaque Erosion) study demonstrated that patients with ACS caused by plaque erosion might be treated conservatively without stent implantation. A follow-up study showed most patients without stenting did not develop a major adverse cardiovascular event on dual antiplatelet therapy (DAPT) up to 1 year (4, 5). In our case, the site of the previous STEMI secondary to plaque erosion in the RCA looked fine 9 years after conservative treatment, supporting the notion that conservative treatment may indeed be an option for patients with plaque erosion.Kotoku and colleagues (9) reported a 46-year-old man with STEMI due to plaque erosion who initially was treated conservatively but developed recurrent plaque erosion at the same lesion 6 months later. Kim and colleagues (10) showed that elevated ESS and ESS gradient at the site of plaque erosion persisted up to 1 year, indicating that the hemodynamic thrombogenic millieu persists up to 1 year. Taken together, these cases indicate that patients with plaque erosion may have diffuse endothelial dysfunction and/or systemic and local hypercoagulability, thus remaining at high risk for recurrent plaque erosion.To our knowledge, this is the first report of recurrent plaque erosion in a previously nonculprit vessel resulting in ACS. In addition, the widely patent RCA, which had caused ACS as the result of plaque erosion 9 years ago and was treated conservatively, supports the notion that conservative management without stenting may be an option for patients with ACS and plaque erosion.References1. Virani SS, Alonso A, Benjamin EJ, et al. Heart disease and stroke statistics—2020 update: a report from the American Heart Association. Circulation. 2020;141:e139-596. [PMID: 31992061] doi:10.1161/CIR.0000000000000757 CrossrefMedlineGoogle Scholar2. Araki M, Park SJ, Dauerman HL, et al. Optical coherence tomography in coronary atherosclerosis assessment and intervention. Nat Rev Cardiol. 2022;19:684-703. [PMID: 35449407] doi:10.1038/s41569-022-00687-9 CrossrefMedlineGoogle Scholar3. Libby P, Pasterkamp G, Crea F, et al. Reassessing the mechanisms of acute coronary syndromes. Circ Res. 2019;124:150-60. [PMID: 30605419] doi:10.1161/CIRCRESAHA.118.311098 CrossrefMedlineGoogle Scholar4. Fahed AC, Jang IK. Plaque erosion and acute coronary syndromes: phenotype, molecular characteristics and future directions. Nat Rev Cardiol. 2021:724-34. [PMID: 33953381] doi:10.1038/s41569-021-00542-3 CrossrefMedlineGoogle Scholar5. Kolte D, Yonetsu T, Ye JC, et al. Optical coherence tomography of plaque erosion: JACC focus seminar part 2/3. J Am Coll Cardiol. 2021;78:1266-74. [PMID: 34531028] doi:10.1016/j.jacc.2021.07.030 CrossrefMedlineGoogle Scholar6. Yahagi K, Zarpak R, Sakakura K, et al. Multiple simultaneous plaque erosion in 3 coronary arteries. JACC Cardiovasc Imaging. 2014;7:1172-4. [PMID: 25459599] doi:10.1016/j.jcmg.2014.08.005 CrossrefMedlineGoogle Scholar7. Jia H, Abtahian F, Aguirre AD, et al. In vivo diagnosis of plaque erosion and calcified nodule in patients with acute coronary syndrome by intravascular optical coherence tomography. J Am Coll Cardiol. 2013;62:1748-58. [PMID: 23810884] doi:10.1016/j.jacc.2013.05.071 CrossrefMedlineGoogle Scholar8. Yamamoto E, Yonetsu T, Kakuta T, et al. Clinical and laboratory predictors for plaque erosion in patients with acute coronary syndromes. J Am Heart Assoc. 2019;8:e012322. [PMID: 31640466] doi:10.1161/JAHA.119.012322 CrossrefMedlineGoogle Scholar9. Kotoku N, Higuma T, Ishibashi Y, et al. Recurrence of ST-segment elevation myocardial infarction caused by plaque erosion after discontinuing dual antiplatelet therapy. Coron Artery Dis. 2022;31:66-7. [PMID: 33899758] doi:10.1097/MCA.0000000000001055 CrossrefMedlineGoogle Scholar10. Kim HO, Jiang B, Poon EKW, et al. High endothelial shear stress and stress gradient at plaque erosion persist up to 12 months. Int J Cardiol. 2022;357:1-7. [PMID: 35306029] doi:10.1016/j.ijcard.2022.03.035 CrossrefMedlineGoogle Scholar Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAuthors: 1Takayuki Niida, MD, PhD; 1Maya Serhal, MD; 1Rahul Sakhuja, MD; 2Robert Yeh, MD, MSc, MBA; 1Ik-Kyung Jang, MD, PhDAffiliations: 1Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts2Richard A. and Susan F. Smith Center for Outcomes Research in Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MassachusettsFundingDr. Ik-Kyung Jang's research has been supported by Mrs. Gillian Gray through the Allan Gray Fellowship Fund in Cardiology.DisclosuresDisclosure forms are available with the article online.Corresponding AuthorIk-Kyung Jang, MD, PhD; Allan and Gill Gray Professor of Medicine, Harvard Medical School, Cardiology Division, Massachusetts General Hospital, 55 Fruit St, GRB 800, Boston, MA 02114; e-mail, [email protected]. PreviousarticleNextarticle FiguresReferencesRelatedDetails Metrics March 2023Volume 2, Issue 3KeywordsAcute coronary syndromeAngiographyLipidsNeutrophilsNon st segment elevation myocardial infarctionOptical coherence tomographySt segment elevation myocardial infarctionThrombosis ePublished: 21 March 2023 Issue Published: March 2023 Copyright & PermissionsCopyright © 2023 by Authors. Published in partnership by the American College of Physicians and American Heart Association. All Rights Reserved.licensesThis is an open access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND), which allows reusers to copy and distribute the material in any medium or format in unadapted form only, for noncommercial purposes only, and only so long as attribution is given to the creator. See: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode.PDF downloadLoading ...