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Showing papers by "Ik-Kyung Jang published in 2020"


Journal ArticleDOI
TL;DR: In ACS patients, those with layered phenotype at the culprit lesion demonstrated greater macrophage infiltration at the non-culprit sites and was associated with more features of plaque vulnerability, particularly when the culpritLesion also had a layered pattern.
Abstract: AIMS Layered plaques represent signs of previous plaque destabilization. A recent study showed that acute coronary syndrome (ACS) patients with layered culprit plaque have more vulnerability at the culprit lesion and systemic inflammation. We aimed to compare the characteristics of non-culprit plaques between patients with or without layered plaque at the culprit lesion. We also evaluated the characteristics of layered non-culprit plaques, irrespective of culprit plaque phenotype. METHODS AND RESULTS We studied ACS patients who had undergone pre-intervention optical coherence tomography (OCT) imaging. The number of non-culprit lesions was evaluated on coronary angiogram and morphological characteristics of plaques were studied by OCT. In 349 patients, 99 (28.4%) had layered culprit plaque. The number of non-culprit plaques in patients with or without layered culprit plaque was similar (3.2 ± 0.8 and 2.8 ± 0.8, P = 0.23). Among 465 non-culprit plaques, 145 from patients with layered culprit plaque showed a higher prevalence of macrophage infiltration (71.0% vs. 60.9%, P = 0.050). When analysed irrespective of culprit plaque phenotype, layered non-culprit plaques showed higher prevalence of lipid (93.3% vs. 86.0%, P = 0.028), thin cap fibroatheroma (29.7% vs. 13.7%, P < 0.001), and macrophage infiltration (82.4% vs. 54.0%, P < 0.001) than non-layered plaques. Plaques with layered phenotype at both culprit and non-culprit lesions had the highest vulnerability. CONCLUSION In ACS patients, those with layered phenotype at the culprit lesion demonstrated greater macrophage infiltration at the non-culprit sites. Layered plaque at the non-culprit lesions was associated with more features of plaque vulnerability, particularly when the culprit lesion also had a layered pattern.

30 citations


Journal ArticleDOI
TL;DR: In patients with stable angina pectoris, healed culprit plaques are common and have more features of vulnerability and advanced atherosclerosis both at culprit and nonculprit lesions.
Abstract: Objective: Healed plaques, signs of previous plaque destabilization, are frequently found in the coronary arteries. Healed plaques can now be diagnosed in living patients. We investigated the preva...

29 citations


Journal ArticleDOI
TL;DR: The recent evolving concepts about management of non-culprit plaques in STEMI patients are discussed, proposing a diagnostic and therapeutic algorithm to guide physicians in clinical practice and the several knowledge gaps to address are underscore.
Abstract: Approximately 50% of patients with ST-segment elevation myocardial infarction (STEMI) have multivessel coronary artery disease, a condition associated with an increased incidence of recurrent ischaemic events and higher mortality. Based on recent evidences, a strategy of staged percutaneous coronary intervention (PCI) of obstructive non-culprit lesions should be considered the gold standard for the management of these patients. However, several issues remain still unresolved. Indeed, what is the optimal timing of staged PCI is not completely defined. Moreover, assessment of intermediate non-culprit lesions represent still a clinical conundrum, as pressure-wire indexes do not seem able to correctly identify those patients in whom deferral is safe. Intracoronary imaging may help to identify untreated non-culprit lesions containing vulnerable plaques that may portend a higher risk of future cardiovascular events. However, there are hitherto no studies demonstrating that preventive PCI of vulnerable plaques or more intensive pharmacological treatment is associated with an improved clinical outcome. In this review, we discuss the recent evolving concepts about management of non-culprit plaques in STEMI patients, proposing a diagnostic and therapeutic algorithm to guide physicians in clinical practice. We also underscore the several knowledge gaps to address in future studies.

28 citations


Journal ArticleDOI
TL;DR: The present 3-vessel OCT study showed that TCFAs cluster at specific locations in the epicardial coronary arteries, especially in patients with ACS, and was more prevalent in segments with tight stenosis.
Abstract: Background Previous pathology studies demonstrated that thin-cap fibroatheroma (TCFA) is localized in specific segments of the epicardial coronary arteries. A detailed description of in vivo coronary plaques of various phenotypes has not been reported. Objectives We performed a comprehensive analysis on the distribution of coronary plaques with different phenotypes from our 3-vessel optical coherence tomography (OCT) database. Methods OCT images of all 3 coronary arteries in 131 patients were analyzed every 1 mm to assess plaque phenotype and features of vulnerability. In addition, plaques were divided into tertiles according to percent area stenosis (%AS). Results Among 534 plaques identified in 393 coronary arteries, 27.0% were fibrous plaques, 13.3% fibrocalcific plaques, 40.8% thick-cap fibroatheromas, and 18.9% thin-cap fibroatheromas (TCFA). TCFAs showed clustering in the proximal segment, particularly in the left anterior descending (LAD) artery. On the other hand, fibrous plaques were relatively evenly distributed throughout the entire length of the coronary arteries. In patients with acute coronary syndromes (ACS), TCFAs showed stronger proximal clustering in the LAD, two clustering peaks in the right coronary artery, and one clustering peak in the circumflex artery. The pattern of TCFA distribution was less obvious in non-ACS patients. The prevalence of TCFA was higher in the highest %AS tertile, compared to the lowest %AS tertile (30% vs. 9%, p Conclusions The present 3-vessel OCT study demonstrated that TCFAs cluster at specific locations in the epicardial coronary arteries, especially in ACS patients. TCFA was more prevalent in segments with tight stenosis.

17 citations


Book ChapterDOI
01 Jan 2020
TL;DR: This chapter reviews the early history of OCT development with an emphasis on basic concepts and the process of technology translation, as well as advances in imaging speed using swept source/Fourier domain detection.
Abstract: Optical coherence tomography (OCT) enables cross-sectional, volumetric, and functional imaging of internal microstructure and pathology in biological tissues. OCT can perform an “optical biopsy”, imaging pathology in situ and in real time without the need for excisional biopsy. OCT imaging has become a standard of care in ophthalmology and is an emerging imaging modality in cardiology, dermatology, gastroenterology and other specialties where it provides information that often cannot be obtained by any other means. This chapter reviews the early history of OCT development with an emphasis on basic concepts and the process of technology translation. Early OCT technology and catheter imaging devices as well as advances in imaging speed using swept source/Fourier domain detection are reviewed. The process of clinical translation, beginning with ex vivo imaging and histology, preclinical animal studies and progressing to clinical studies in patients is discussed. The history of commercial intravascular OCT development is also summarized.

13 citations


Journal ArticleDOI
TL;DR: Seasonal variations in the incidence of ACS reflect differences in the underlying pathobiology, with the proportion of plaque rupture highest in winter, whereas that of plaque erosion is highest in summer.
Abstract: Background Seasonal variations in acute coronary syndromes (ACS) have been reported, with incidence and mortality peaking in the winter. However, the underlying pathophysiology for these variations...

13 citations


Journal ArticleDOI
TL;DR: Patients with healed plaque in the culprit vessel had a higher incidence of revascularization, as compared to those without healed plaque, at 2 years, and presence of layered plaque and low-density lipoprotein cholesterol levels were independently associated with an increased risk ofRevascularization.
Abstract: Recent studies have shown that healed plaque at the culprit lesion detected by optical coherence tomography (OCT) is a sign of pan-vascular vulnerability and advanced atherosclerosis. However, the clinical significance of healed plaque is unknown. A total of 265 patients who had OCT imaging of a culprit vessel and 2-year clinical follow-up data were included. Patients were stratified based on the presence or absence of a layered plaque phenotype, defined as layers of different optical density by OCT at either culprit or non-culprit lesions. The association between layered plaque and major adverse cardiac events (MACE), defined as cardiac death, acute coronary syndromes (ACS), or revascularization, was studied. Among 265 patients, 96 (36.2%) had the layered plaque phenotype. Layered plaque was more frequently observed in stable angina pectoris patients than in ACS patients (57.8%vs. 25.1%, p < 0.001). The average clinical follow-up period was 672 ± 172 days. Cumulative MACE was significantly higher in patients with layered plaque (p = 0.041), which was primarily driven by the high revascularization rate at 2 years (p = 0.002). Multivariate regression analysis showed that presence of layered plaque and low-density lipoprotein cholesterol levels were independently associated with an increased risk of revascularization (p = 0.026, p = 0.008, respectively). Patients with healed plaque in the culprit vessel had a higher incidence of revascularization, as compared to those without healed plaque, at 2 years.

12 citations


Journal ArticleDOI
TL;DR: Investigation of the prevalence of plaque erosion by age and sex among acute coronary syndromes (ACS) patients found plaque erosion risk was increased in the males age ≤ 50 and in the females age‚¬70 among ACS patients, and rupture was the dominant etiology in both sexes.
Abstract: Postmortem studies reported plaque erosion is frequent in young women. Recent in vivo studies failed to show age and sex differences in the plaque erosion prevalence. The aim of this study was to investigate the prevalence of plaque erosion by age and sex among acute coronary syndromes (ACS) patients. From 1699 ACS patients, 1083 with plaque erosion or rupture were analyzed. Patients were categorized as 5 age groups (≤ 50, 51–60, 61–70, 71–80, ≥ 81 years). Overall prevalence of plaque erosion was similar between males and females (p = 0.831). Males age ≤ 50 had higher (p = 0.018) and age 71–80 had lower (p = 0.006) prevalence of plaque erosion. Females age 61–70 had higher (p = 0.021) and age 71–80 had lower (p = 0.045) prevalence of plaque erosion. In advanced age groups (≥ 71 years), rupture was the dominant etiology in both sexes. In multivariate analysis of males, age ≤ 50 demonstrated a trend to increase (OR 1.418, 95% CI 0.961–2.093, p = 0.078) the erosion risk. Females age ≤ 70 independently increased (OR 2.138, 95% CI 1.249–3.661, p = 0.006) the risk for erosion. The prevalence of plaque erosion was similar between males and females. Plaque erosion risk was increased in the males age ≤ 50 and in the females age ≤ 70 among ACS patients.

12 citations


Journal ArticleDOI
TL;DR: Assessment of stenosis degree and plaque type using CCTA provided additional prognostic value over CACS and FRS to risk stratify stroke patients without prior history of CAD better.
Abstract: Objective To assess the incremental prognostic value of coronary computed tomography angiography (CCTA) in comparison to a clinical risk model (Framingham risk score, FRS) and coronary artery calcium score (CACS) for future cardiac events in ischemic stroke patients without chest pain. Materials and methods This retrospective study included 1418 patients with acute stroke who had no previous cardiac disease and underwent CCTA, including CACS. Stenosis degree and plaque types (high-risk, non-calcified, mixed, or calcified plaques) were assessed as CCTA variables. High-risk plaque was defined when at least two of the following characteristics were observed: low-density plaque, positive remodeling, spotty calcification, or napkin-ring sign. We compared the incremental prognostic value of CCTA for major adverse cardiovascular events (MACE) over CACS and FRS. Results The prevalence of any plaque and obstructive coronary artery disease (CAD) (stenosis ≥ 50%) were 70.7% and 30.2%, respectively. During the median follow-up period of 48 months, 108 patients (7.6%) experienced MACE. Increasing FRS, CACS, and stenosis degree were positively associated with MACE (all p 0.05). Conclusion Assessment of stenosis degree and plaque type using CCTA provided additional prognostic value over CACS and FRS to risk stratify stroke patients without prior history of CAD better.

10 citations


Journal ArticleDOI
TL;DR: Clinical presentation of SAP was a strong predictor for layered plaque at both culprit plaques and non-culprit plaques, and development and biologic significance of layered plaques may be related to a balance between pan-vascular vulnerability and endogenous anti-thrombotic protective mechanism.
Abstract: Healed coronary plaques, morphologically characterized by a layered pattern, are signatures of previous plaque disruption and healing. Recent optical coherence tomography (OCT) studies showed that layered plaque is associated with vascular vulnerability. However, factors associated with layered plaques have not been studied. The aim of this study was to investigate predictors for layered plaque at the culprit plaques and at non-culprit plaques. Patients with coronary artery disease who underwent pre-intervention OCT imaging of the culprit lesion were included. Layered plaques were defined as plaques with one or more layers of different optical density and a clear demarcation from underlying components. Among 313 patients, layered plaque at the culprit lesion was observed in 18.8% of ST-segment elevation myocardial infarction patients, 36.3% of non-ST-segment elevation acute coronary syndrome patients, and 53.4% of stable angina pectoris (SAP) patients (p 70% were independent predictors for layered plaque at the culprit lesion. In addition, 394 non-culprit plaques in 190 patients were assessed to explore predictors for layered plaques at non-culprit lesions. SAP, and thin-cap fibroatheroma and layered plaque at the culprit lesion were independent predictors for layered plaques at non-culprit lesions. In conclusion, clinical presentation of SAP was a strong predictor for layered plaque at both culprit plaques and non-culprit plaques. Development and biologic significance of layered plaques may be related to a balance between pan-vascular vulnerability and endogenous anti-thrombotic protective mechanism.

10 citations


Journal ArticleDOI
TL;DR: Asian and White patients presenting with STEMI and NSTE-ACS showed similar underlying mechanisms of ACS, except for a higher risk of calcified plaque in Whites with NSTE -ACS.
Abstract: Ethnic differences in the pathobiology of acute coronary syndromes (ACS) have not been systematically studied. We compared the underlying mechanisms of ACS between Asians and Whites. ACS patients with the culprit lesion imaged by optical coherence tomography were included. Patients were stratified into ST-elevation myocardial infarction (STEMI) and non-ST-elevation-ACS (NSTE-ACS), and baseline characteristics, underlying mechanisms of ACS, and culprit plaque characteristics were compared between Asians and Whites. Of 1,225 patients, 1,019 were Asian (567 STEMI and 452 NSTE-ACS) and 206 were White (71 STEMI and 135 NSTE-ACS). Asians had more diabetes and hypertension among STEMI patients; among NSTE-ACS patients, Asians had higher prevalence of diabetes and renal insufficiency, and lower prevalence of hyperlipidemia. There were no differences in the incidence of plaque rupture, plaque erosion and calcified plaque between Asians and Whites with STEMI (61.2%, 28.6%, 10.2% vs 46.5%, 38.0%, 15.5%, respectively, p = 0.055). Among NSTE-ACS patients, there was a significant difference between Asians and Whites (40.5%, 47.6%, 11.9% vs 27.4%, 48.9%, 23.7%, respectively, p = 0.001). After adjustment for clinical confounders, the risk of plaque rupture (p = 0.713), plaque erosion (p = 0.636), and calcified plaque (p = 0.986) was similar between the groups with STEMI. In NSTE-ACS patients, the only difference was an increased risk of calcified plaque in Whites (odds ratio: 2.125, 95% confidence interval: 1.213 to 3.723, p = 0.008). In conclusion, after adjustment for clinical confounders, Asian and White patients presenting with STEMI and NSTE-ACS showed similar underlying mechanisms of ACS, except for a higher risk of calcified plaque in Whites with NSTE-ACS.

Journal ArticleDOI
TL;DR: When LDL-C level is elevated, early and aggressive treatment with statin may help to prevent PR by stabilizing plaques through calcification, and the patients with naturally low cholesterol have the lowest risk of PR.
Abstract: Statin therapy reduces low-density lipoprotein cholesterol (LDL-C), inflammation, and atherosclerotic cardiovascular disease. We investigated the association between LDL-C and statin therapy on the prevalence of plaque rupture (PR). Patients with acute coronary syndromes who underwent optical coherence tomography imaging of the culprit lesion were divided into 4 groups based on LDL-C level and statin use (Group 1: LDL-C ≤ 100 without statin; Group 2; LDL-C ≤ 100 with statin; Group 3: LDL-C > 100 with statin; Group 4: LDL-C > 100 without statin), and the prevalence of PR was compared between the groups. Among 896 patients, PR was diagnosed in 444 (49.6%) patients. The prevalence of PR was significantly different among the 4 groups (p = 0.007): it was highest in the high LDL-C without statin group and lowest in the low LDL-C without statin group (53.9% and 39.2%, respectively). Compared with the high LDL-C without statin group, the low LDL-C without statin and low LDL-C with statin groups had a significantly lower prevalence of PR (p = 0.001, p = 0.040, respectively), and the low LDL-C with statin group had a significantly higher prevalence of calcification (p = 0.037). The patients with naturally low LDL-C have the lowest risk of PR. The patients with low LDL-C achieved by statin therapy had a higher prevalence of calcification. When LDL-C level is elevated, early and aggressive treatment with statin may help to prevent PR by stabilizing plaques through calcification.

Journal ArticleDOI
TL;DR: Recently, three subtypes of calcified plaques at the culprit lesion were reported in patients with acute coronary syndrome: eruptive calcified nodule, superficial calcific sheet, and calcified protrusion.

Book ChapterDOI
01 Jan 2020
TL;DR: Current data suggest that rather than focusing on individual coronary plaques, a more comprehensive, integrative approach focusing on the “vulnerable patients” may be more appropriate.
Abstract: The use of optical coherence tomography (OCT) imaging in research and clinical practice has provided useful insights into the pathobiology of the “vulnerable plaque” and acute coronary syndromes (ACS). Although thin-cap fibroatheroma (TCFA), defined as a lipid-rich plaque covered by a thin (i.e., <65 μm) fibrous cap, has historically be considered the prototype of the “vulnerable plaque”, this term should be reserved for plaques that are precursors of all three causes of luminal thrombosis, which include not only plaque rupture but also plaque erosion and calcified plaque. In addition, cardiovascular risk profile and demographics of patients with ACS are actively changing worldwide, partly due to the widespread use of statins and other preventive measures, so that plaque rupture is declining as a cause of ACS, whereas plaque erosion seems to be on the rise. Therefore, a redefinition of the concept of “vulnerable plaque” is probably needed in order to better identify patients at risk for future adverse events and to adopt tailored effective preventive strategies. Current data suggest that rather than focusing on individual coronary plaques, a more comprehensive, integrative approach focusing on the “vulnerable patients” may be more appropriate.


Journal ArticleDOI
TL;DR: Early initiation of ticagrelor at the time of presentation in patients with NSTE-ACS appears to be safe with a greater level of platelet inhibition, however, post-PCI residual thrombus burden did not differ between early and delayed administration of tiagrarelor.
Abstract: OBJECTIVE The level of inhibition of platelet aggregation immediately before percutaneous coronary intervention (PCI) is known to be related to early periprocedural outcomes. Ticagrelor is a reversible P2Y12 inhibitor that provides faster and more effective platelet inhibition compared to clopidogrel. This study sought to compare the antiplatelet effect on residual thrombus between early vs. delayed administration of ticagrelor following PCI in patients presenting with non-ST-elevation acute coronary syndromes (NSTE-ACS). METHODS AND RESULTS Patients presenting with NSTE-ACS were screened in eight Korean centers, and randomized to receive ticagrelor either on presentation (early treatment) or immediately before PCI (delayed treatment). The primary end point was intracoronary thrombus burden after PCI assessed by optical coherence tomography (OCT). Among 100 patients enrolled in the study, post-PCI OCT was performed in 68 patients and the data from 57 patients were included in the final analysis. Although platelet inhibition was greater in the early treatment group than in the delayed treatment group (P2Y12 reaction units, 70.6 ± 62.1 vs. 227.2 ± 76.6, P < 0.001), thrombus burden did not differ between the two groups (1.64 ± 1.10% vs. 1.24 ± 0.92%, P = 0.143). CONCLUSION Early initiation of ticagrelor at the time of presentation in patients with NSTE-ACS appears to be safe with a greater level of platelet inhibition. However, post-PCI residual thrombus burden did not differ between early and delayed administration of ticagrelor.