Language：English   Publishing type：Research paper (scientific journal)  

OBJECTIVE: To determine if prediabetes is associated with atherosclerosis of coronary arteries, we evaluated the degree of coronary atherosclerosis in nondiabetic, prediabetic, and diabetic patients by using coronary angioscopy to identify plaque vulnerability based on yellow color intensity. RESEARCH DESIGN AND METHODS: Sixty-seven patients with coronary artery disease (CAD) underwent angioscopic observation of multiple main-trunk coronary arteries. According to the American Diabetes Association guidelines, patients were divided into nondiabetic (n = 16), prediabetic (n = 28), and diabetic (n = 23) groups. Plaque color grade was defined as 1 (light yellow), 2 (yellow), or 3 (intense yellow) based on angioscopic findings. The number of yellow plaques (NYPs) per vessel and maximum yellow grade (MYG) were compared among the groups. RESULTS: Mean NYP and MYG differed significantly between the groups (P = 0.01 and P = 0.047, respectively). These indexes were higher in prediabetic than in nondiabetic patients (P = 0.02 and P = 0.04, respectively), but similar in prediabetic and diabetic patients (P = 0.44 and P = 0.21, respectively). Diabetes and prediabetes were independent predictors of multiple yellow plaques (NYPs ≥2) in multivariate logistic regression analysis (odds ratio [OR] 10.8 [95% CI 2.09-55.6], P = 0.005; and OR 4.13 [95% CI 1.01-17.0], P = 0.049, respectively). CONCLUSIONS: Coronary atherosclerosis and plaque vulnerability were more advanced in prediabetic than in nondiabetic patients and comparable between prediabetic and diabetic patients. Slight or mild disorders in glucose metabolism, such as prediabetes, could be a risk factor for CAD, as is diabetes itself.

DOI： 10.2337/dc12-1635

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Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press (OUP)  

DOI： 10.1093/eurheartj/ehae902

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Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press (OUP)  

DOI： 10.1093/ehjimp/qyae087

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Language：English  

DOI： 10.1038/s41569-023-00982-z

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Publishing type：Research paper (scientific journal)   Publisher：Japanese Circulation Society  

DOI： 10.1253/circrep.cr-24-0003

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Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Febuxostat is recommended for treatment of severe hyperuricemia in chronic kidney disease (CKD). We previously reported a significant positive correlation between fractional excretion of uric acid (FEUA) and estimated excretion of uric acid (eEUA) in patients receiving febuxostat and proposed that the addition of uricosuric agents could further decrease serum uric acid (sUA) levels by enhancing FEUA and eEUA in patients treated with febuxostat. METHODS: This retrospective study included 34 patients with CKD who were categorized into three groups (G3-G5) according to their estimated glomerular filtration rate (eGFR). The effects on sUA, FEUA, and eEUA of adding dotinurad (0.5 mg/day) to febuxostat (10 mg/day) were evaluated in these patients. Specifically, we examined changes in sUA, FEUA, and eEUA in each group after the addition of dotinurad. RESULTS: Dotinurad significantly increased FEUA in all groups and notably decreased sUA in groups G3 and G4 but not in group G5. There was no significant change in eEUA in any group. Dotinurad maintained the significant positive correlation between FEUA and eEUA in patients receiving febuxostat. CONCLUSIONS: This study is the first to show the effect of combining dotinurad with febuxostat in lowering sUA levels in G3 and G4 patients. Additional research is required in order to clarify the pharmacological mechanisms of dotinurad in patients with CKD.

DOI： 10.1272/jnms.JNMS.2024_91-403

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Publishing type：Research paper (scientific journal)   Publisher：Japanese Association of Cardioangioscopy  

DOI： 10.15791/angioscopy.is.24.001

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Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.amjcard.2023.08.152

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Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Although hyperuricemia is associated with the progression of chronic kidney disease (CKD), a reduction in CKD progression by uric acid (UA)-lowering therapy has been controversial. Recently, dotinurad, a uricosuric drug with selective urate reabsorption inhibitory properties, has been developed. However, its efficacy in lowering serum UA levels and its effects on renal function in patients with severe renal dysfunction are unclear. Thus, this study aimed to determine the effects of dotinurad on renal function in patients with severe renal dysfunction. METHODS: Data from 53 outpatients with hyperuricemia who newly received dotinurad between December 2020 and October 2022 were retrospectively analyzed. The mean baseline estimated glomerular filtration rate (eGFR) was 38.7 ± 17.0 mL/min/1.73 m2. The patients were divided into three groups based on their baseline eGFR: eGFR < 30 (n = 17), 30 ≤ eGFR < 45 (n = 17), and eGFR ≥ 45 (n = 19). RESULTS: The mean follow-up period was 9.8 ± 4.5 (range, 3-21) months. Serum UA levels significantly decreased in all groups. Although eGFR did not significantly change in patients with 30 ≤ eGFR < 45 and eGFR ≥ 45 (P = 0.918 and P = 0.535, respectively), it improved significantly in patients with eGFR < 30 (P = 0.032). The proportion of patients with improved eGFR was significantly higher in patients with eGFR < 30 (P = 0.038) than in patients with 30 ≤ eGFR < 45 and eGFR ≥ 45. In the multivariate logistic regression analysis, baseline eGFR < 30 and achieving a serum UA level of ≤ 6.0 mg/dL were significantly associated with improved eGFR (P = 0.033 and P = 0.015, respectively). CONCLUSIONS: Dotinurad may have UA-lowering effects and the potential to improve kidney function in patients with severe renal dysfunction.

DOI： 10.1007/s10157-023-02419-w

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Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press (OUP)  

Abstract

Background

Diagnostic strategies depend on non-standardized workup, and the causes of myocardial infarction with non-obstructive coronary arteries remain unclear for some patients. Intracoronary imaging is recommended for detecting the missed causes by coronary angiography. Myocardial infarction with non-obstructive coronary arteries is a heterogeneous entity; a meta-analysis of myocardial infarction with non-obstructive coronary artery studies demonstrated that all-cause mortality rate at 1 year is 4.7%, and its prognosis is not so favourable.

Case summary

A 62-year-old man without remarkable medical history complained of acute chest pain at rest, which resolved at his arrival. Although echocardiography and electrocardiogram exhibited normal findings, the concentration of high-sensitive cardiac troponin T increased up to 0.384 from 0.04 ng/mL. Coronary angiography was performed, and mild stenosis of the proximal right coronary artery was detected. He was discharged without catheter intervention and medications as he reported no symptoms. He returned 8 days later because of inferoposterior ST-segment elevation myocardial infarction with ventricular fibrillation. Emergent coronary angiography showed that the mild stenosis of the proximal right coronary artery had progressed to total occlusion. Optical coherence tomography after thrombectomy revealed rupture of the thin-cap fibroatheroma and protruding thrombus.

Discussion

Patients presenting with myocardial infarction with non-obstructive coronary arteries and plaque disruption and/or thrombus detected by optical coherence tomography do not show normal coronaries on coronary angiography. Aggressive investigation into plaque disruption using intracoronary imaging is recommended even if coronary angiography demonstrates mild stenosis to prevent a fatal attack for suspicious cases of myocardial infarction with non-obstructive coronary arteries.

DOI： 10.1093/ehjcr/ytad225

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Other Link： https://academic.oup.com/ehjcr/article-pdf/7/5/ytad225/50301314/ytad225.pdf

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcin.2022.10.059

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

DOI： 10.1097/mca.0000000000001170

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Publishing type：Research paper (scientific journal)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

Background:

Despite the significant decline in cardiovascular mortality in women over the past several decades, sex differences in the underlying pathology of acute coronary syndromes remain poorly understood. Previous postmortem studies have demonstrated sex differences in coronary plaque morphology with a higher prevalence of plaque erosion in young women and more plaque rupture in older women after menopause, whereas men showed no increase in prevalence of plaque rupture with age. However, in vivo data are limited.

Methods:

This study included patients who presented with acute coronary syndrome and underwent preintervention optical coherence tomography imaging of the culprit lesion. The culprit plaque was categorized as plaque rupture, plaque erosion or culprit plaque with calcification, and stratified by age. Features of plaque vulnerability at culprit lesion were also analyzed.

Results:

In 1368 patients (women=286), women and men had a similar distribution of culprit plaque morphology (plaque rupture versus plaque erosion). However, significant sex differences were found in the underlying mechanisms of acute coronary syndrome among different age groups: women showed a significant ascending trend with age in plaque rupture ( P &lt;0.001) and the features of plaque vulnerability such as lipid plaque ( P &lt;0.001), thin-cap fibroatheroma ( P =0.005), and microstructures including macrophages, cholesterol crystals, and calcification ( P =0.026). No trend was observed in men.

Conclusions:

Age related sex differences in culprit plaque morphology and vulnerability were identified in patients with acute coronary syndrome: prevalence of plaque rupture and vulnerability increased with age in women but not in men.

Registration:

URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01110538 and NCT03479723.

DOI： 10.1161/circinterventions.121.011612

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Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.ijcard.2022.03.035

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Language：English   Publishing type：Research paper (scientific journal)  

Since optical coherence tomography (OCT) was first performed in humans two decades ago, this imaging modality has been widely adopted in research on coronary atherosclerosis and adopted clinically for the optimization of percutaneous coronary intervention. In the past 10 years, substantial advances have been made in the understanding of in vivo vascular biology using OCT. Identification by OCT of culprit plaque pathology could potentially lead to a major shift in the management of patients with acute coronary syndromes. Detection by OCT of healed coronary plaque has been important in our understanding of the mechanisms involved in plaque destabilization and healing with the rapid progression of atherosclerosis. Accurate detection by OCT of sequelae from percutaneous coronary interventions that might be missed by angiography could improve clinical outcomes. In addition, OCT has become an essential diagnostic modality for myocardial infarction with non-obstructive coronary arteries. Insight into neoatherosclerosis from OCT could improve our understanding of the mechanisms of very late stent thrombosis. The appropriate use of OCT depends on accurate interpretation and understanding of the clinical significance of OCT findings. In this Review, we summarize the state of the art in cardiac OCT and facilitate the uniform use of this modality in coronary atherosclerosis. Contributions have been made by clinicians and investigators worldwide with extensive experience in OCT, with the aim that this document will serve as a standard reference for future research and clinical application.

DOI： 10.1038/s41569-022-00687-9

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Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

DOI： 10.1007/s11239-021-02500-9

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Other Link： https://link.springer.com/article/10.1007/s11239-021-02500-9/fulltext.html

Language：English   Publishing type：Research paper (scientific journal)   Publisher：NLM (Medline)  

DOI： 10.1097/MCA.0000000000001009

Scopus

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Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.ijcard.2021.08.048

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Publishing type：Research paper (scientific journal)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

<sec xml:lang="en">
<title>Background</title>
<p xml:lang="en">A recent study reported that the outcome of patients with plaque erosion treated with stenting is poor when the underlying plaque is lipid rich. However, the detailed phenotype of patients with plaque erosion, particularly as related to different age groups, has not been systematically studied.


</sec>
<sec xml:lang="en">
<title>Methods and Results</title>
<p xml:lang="en">
Patients with acute coronary syndromes caused by plaque erosion were selected from 2 data sets. Demographic, clinical, angiographic, and optical coherence tomography findings of the culprit lesion were compared between 5 age groups. Among 579 erosion patients, male sex and current smoking were less frequent, and hypertension, diabetes, and chronic kidney disease were more frequent in older patients. ST‐segment–elevation myocardial infarction was more frequent in younger patients. Percentage of diameter stenosis on angiogram was greater in older patients. The prevalence of lipid‐rich plaque (27.3% in age &lt;45 years and 49.4% in age ≥75 years,
<italic>P</italic>
&lt;0.001), cholesterol crystal (3.9% in age &lt;45 years and 21.8% in age ≥75 years,
<italic>P</italic>
=0.027), and calcification (5.5% in age &lt;45 years and 54.0% in age ≥75 years,
<italic>P</italic>
&lt;0.001) increased with age. After adjusting risk factors, younger patients were associated with the presence of thrombus, and older patients were associated with greater percentage of diameter stenosis and the presence of lipid‐rich plaque and calcification.



</sec>
<sec xml:lang="en">
<title>Conclusions</title>
<p xml:lang="en">The demographic, clinical, angiographic, and plaque phenotypes of patients with plaque erosion distinctly vary depending on age. This may affect the clinical outcome in these patients.


</sec>
<sec xml:lang="en">
<title>Registration</title>
<p xml:lang="en">
URL:
<ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="https://www.clinicaltrials.gov">https://www.clinicaltrials.gov</ext-link>
. Unique identifiers: NCT03479723, NCT02041650.



</sec>

DOI： 10.1161/jaha.120.020691

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Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.11909/j.issn.1671-5411.2021.10.010

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Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.jacc.2021.07.032

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

The mechanisms behind poorer cardiac outcomes in underweight patients with acute coronary syndrome (ACS) are not understood and features of coronary culprit lesions in underweight ACS patients have not been fully examined. A total of 1,683 patients with ACS were divided into 4 groups according to body mass index (BMI): <18.5 (n = 73), 18.5 to 24.9 (n = 995), 25 to 29.9 (n = 488), and ≥30 (n = 117). Angiography and optical coherence tomography (OCT) images were analyzed for 1,428 of these patients who had primary percutaneous coronary intervention (PCI) and 838 who had primary PCI with OCT guidance, respectively. Diabetes (p <0.001), hypertension (p <0.001), and dyslipidemia (p <0.001) were less prevalent in BMI <18.5. Statin prescription at discharge was less frequent in the BMI <18.5 group (p <0.001). Quantitative coronary angiography analyses revealed smaller reference vessel (p = 0.001) and minimum lumen diameters after PCI (p = 0.019) and OCT revealed longer lipidic plaque length (p = 0.029) in the BMI <18.5 group. Kaplan-Meier analyses revealed higher rates of cardiac mortality (p <0.001) and major bleeding (p = 0.034) during the 2-year follow-up in the BMI <18.5 group. After adjusting for traditional cardiovascular risk factors, BMI <18.5 independently predicted 2-year cardiac mortality (hazard ratio 1.917 [95% confidence interval [1.082 to 3.397], p = 0.026). In conclusion, being underweight contributed to poorer cardiac outcomes in established ACS population. Smaller minimum lumen diameter after PCI and further progressed atherosclerosis at the culprit lesions despite their lower prevalence of comorbid metabolic risk factors may be related partly to poorer cardiac outcomes.

DOI： 10.1016/j.amjcard.2021.07.041

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Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.jcmg.2020.08.014

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Publishing type：Research paper (scientific journal)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

<sec xml:lang="en">
<title>Background</title>
<p xml:lang="en">The role of coronary calcification in cardiovascular events and plaque stabilization is still being debated, and factors involved in the progression of coronary calcification are not fully understood. This study aimed to identify the predictors for rapid progression of coronary calcification.


</sec>
<sec xml:lang="en">
<title>Methods and Results</title>
<p xml:lang="en">
Patients with serial optical coherence tomography imaging at baseline and at 6 months were selected. Changes in the calcification index and predictors for progression of calcification were studied. Calcification index was defined as the product of the mean calcification arc and calcification length. Rapid progression of calcification was defined as an increase in the calcification index above the median value. Among 187 patients who had serial optical coherence tomography imaging, 235 calcified plaques were identified in 105 patients (56.1%) at baseline. After 6 months, the calcification index increased in 95.3% of calcified plaques from 132.0 to 178.2 (
<italic>P</italic>
&lt;0.001). In multivariable analysis, diabetes mellitus (odds ratio [OR], 3.911;
<italic>P</italic>
&lt;0.001), chronic kidney disease (OR, 2.432;
<italic>P</italic>
=0.037), lipid‐rich plaque (OR, 2.698;
<italic>P</italic>
=0.034), and macrophages (OR, 6.782;
<italic>P</italic>
&lt;0.001) were found to be independent predictors for rapid progression of coronary calcification. Interestingly, rapid progression of calcification was associated with a significant reduction of inflammatory features (thin‐cap fibroatheroma; from 21.2% to 11.9%,
<italic>P</italic>
=0.003; macrophages; from 74.6% to 61.0%,
<italic>P</italic>
=0.001).



</sec>
<sec xml:lang="en">
<title>Conclusions</title>
<p xml:lang="en">Diabetes mellitus, chronic kidney disease, lipid‐rich plaque, and macrophages were independent predictors for rapid progression of coronary calcification. Baseline vascular inflammation and subsequent stabilization may be related to rapid progression of calcification.


</sec>
<sec xml:lang="en">
<title>Registration</title>
<p xml:lang="en">
URL:
<ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="https://www.clinicaltrials.gov">https://www.clinicaltrials.gov</ext-link>
; Unique identifier: NCT01110538.



</sec>

DOI： 10.1161/jaha.120.019235

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Publishing type：Research paper (scientific journal)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

<sec xml:lang="en">
<title>Background</title>
<p xml:lang="en">Specific plaque phenotypes that predict a favorable response to statin therapy have not been systematically studied. This study aimed to identify optical coherence tomography predictors for a favorable vascular response to statin therapy.


</sec>
<sec xml:lang="en">
<title>Methods and Results</title>
<p xml:lang="en">
Patients who had serial optical coherence tomography imaging at baseline and at 6 months were included. Thin‐cap area (defined as an area with fibrous cap thickness &lt;200 μm) was measured using a 3‐dimensional computer‐aided algorithm, and changes in the thin‐cap area at 6 months were calculated. A favorable vascular response was defined as the highest tertile in the degree of reduction of the thin‐cap area. Macrophage index was defined as the product of the average macrophage arc and length of the lesion with macrophage infiltration. Layered plaque was defined as a plaque with 1 or more layers of different optical density. In 84 patients, 140 nonculprit lipid plaques were identified. In
<italic>multivariable</italic>
analysis, baseline thin‐cap area (odds ratio [OR] 1.442; 95% CI, 1.024–2.031,
<italic>P</italic>
=0.036), macrophage index (OR, 1.031; 95% CI, 1.002–1.061,
<italic>P</italic>
=0.036), and layered plaque (OR, 2.767; 95% CI, 1.024–7.479,
<italic>P</italic>
=0.045) were identified as the significant predictors for a favorable vascular response. Favorable vascular response was associated with a decrease in the macrophage index.



</sec>
<sec xml:lang="en">
<title>Conclusions</title>
<p xml:lang="en">Three optical coherence tomography predictors for a favorable vascular response to statin therapy have been identified: large thin‐cap area, high macrophage index, and layered plaque. Favorable vascular response to statin was correlated with signs of decreased inflammation.


</sec>
<sec xml:lang="en">
<title>Registration</title>
<p xml:lang="en">
URL:
<ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="https://www.clinicaltrials.gov">https://www.clinicaltrials.gov</ext-link>
; Unique identifier: NCT01110538.



</sec>

DOI： 10.1161/jaha.120.018205

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Language：English   Publishing type：Research paper (scientific journal)  

Antiplatelet agents and statin therapies are widely used in patients with known cardiovascular disease. Plaque rupture (PR) and plaque erosion (PE) are the most frequent underlying mechanisms of acute coronary syndromes (ACS). The conditions and medications that are associated with ST-segment elevation myocardial infarction (STEMI) following PR or PE have not been systematically studied. A total of 838 ACS patients (494 with STEMI, 344 with NSTE-ACS) who were diagnosed with PR or PE by optical coherence tomography were included. The patients were categorized into two groups based on underlying pathology, and the baseline characteristics and culprit plaque morphology associated with STEMI were investigated within each group. Among 838 patients, 467 (55.7%) had PR, and 371 (44.3%) were diagnosed with PE. Among patients with PR, older age, hyperlipidemia, no antiplatelet therapy, higher level of low-density lipoprotein cholesterol, and greater lipid burden and macrophage infiltration were associated with increased probability of STEMI. Among patients with PE, no dual antiplatelet therapy and no statin therapy were associated with increased probability of STEMI. The incidence of STEMI caused by PR was significantly lower on antiplatelet therapy (P < 0.001), and the incidence of STEMI caused by PE was significantly lower on antiplatelet therapy (P < 0.001) or on statin therapy (P < 0.001). Antiplatelet therapy is associated with lower probability of STEMI, regardless of underlying pathology, and statin therapy is associated with lower probability of STEMI in PE as clinical presentation of ACS. Statin therapy prior to the onset of acute coronary syndromes (ACS) may reduce the probability of plaque rupture. Antiplatelet therapy prior to the onset of ACS is associated with reduced probability of ST-segment elevation myocardial infarction (STEMI) following both plaque rupture and plaque erosion, and dual antiplatelet therapy offers additional protection compared to a single antiplatelet agent in plaque erosion. The combination of statin and antiplatelet therapy may have an additive effect on reducing the probability of STEMI caused by plaque erosion. Yellow: lipid pool(necrotic core); red: fibrin-rich thrombus; gray; platelet-rich thrombus.

DOI： 10.1007/s11239-020-02281-7

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OBJECTIVES: The authors performed a comprehensive analysis on the distribution of coronary plaques with different phenotypes from our 3-vessel optical coherence tomography (OCT) database. 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. 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% were fibrocalcific plaques, 40.8% were thick-cap fibroatheromas, and 18.9% were TCFAs. TCFAs showed clustering in the proximal segment, particularly in the left anterior descending 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 left anterior descending, 2 clustering peaks in the right coronary artery, and 1 clustering peak in the circumflex artery. The pattern of TCFA distribution was less obvious in patients without ACS. The prevalence of TCFA was higher in the highest %AS tertile, compared with the lowest %AS tertile (30% vs. 9%; p < 0.001). CONCLUSIONS: The present 3-vessel OCT study showed that TCFAs cluster at specific locations in the epicardial coronary arteries, especially in patients with ACS. TCFA was more prevalent in segments with tight stenosis. (The Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538).

DOI： 10.1016/j.jcmg.2020.01.013

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Language：English  

DOI： 10.1161/ATVBAHA.120.314971

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AIMS: To investigate local haemodynamics in the setting of acute coronary plaque rupture and erosion. METHODS AND RESULTS: Intracoronary optical coherence tomography performed in 37 patients with acute coronary syndromes caused by plaque rupture (n = 19) or plaque erosion (n = 18) was used for 3D reconstruction and computational fluid dynamic simulation. Endothelial shear stress (ESS), spatial ESS gradient (ESSG), and oscillatory shear index (OSI) were compared between plaque rupture and erosion through mixed-effects logistic regression. Lipid, calcium, macrophages, layered plaque, and cholesterol crystals were also analysed. By multivariable analysis, only high ESSG (odds ratio [OR] 5.29, 95% confidence interval [CI] 2.57-10.89, p < 0.001), lipid (OR 12.98, 95% CI 6.57-25.67 p < 0.001), and layered plaque (OR 3.17, 95% CI 1.82-5.50, p < 0.001) were independently associated with plaque rupture. High ESSG (OR 13.28, 95% CI 6.88-25.64, p < 0.001), ESS (OR 2.70, 95% CI 1.34-5.42, p = 0.005) and OSI (OR 2.18, 95% CI 1.33-3.54, p = 0.002) independently associated with plaque erosion. ESSG was higher at rupture sites than erosion sites (median (interquartile range): 5.78 (2.47, 21.15) versus 2.62 (1.44, 6.18) Pa/mm, p = 0.009), OSI was higher at erosion sites than rupture sites (1.04x10-2 (2.3x10-3, 4.74x10-2) versus 1.29x10-3 (9.39x10-5, 3.0x10-2), p < 0.001), but ESS was similar (p = 0.29). CONCLUSIONS: High ESSG is independently associated with plaque rupture while high ESSG, ESS, and OSI associate with plaque erosion. While ESSG is higher at rupture sites than erosion sites, OSI is higher at erosion sites and ESS was similar. These results suggest that ESSG and OSI may play critical roles in acute plaque rupture and erosion, respectively. TRANSLATIONAL PERSPECTIVE: Plaque rupture and erosion are distinct pathological and clinical entities with possibly different optimal treatments. This study demonstrates that high endothelial shear stress gradient is independently associated with site of both rupture and erosion, and is significantly higher in rupture. High oscillatory shear index is independently associated with the site of erosion only, and is higher in erosion than rupture. Larger studies are necessary to determine whether these indices may detect and distinguish plaque rupture and erosion in a clinical setting or to assess overall risk for acute coronary syndromes.

DOI： 10.1093/cvr/cvaa251

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Previous studies have reported a circadian variation in the onset of ST-segment elevation myocardial infarction (STEMI). However, underlying mechanisms for the circadian variation have not been fully elucidated. We investigated the relationship between onset of STEMI and the underlying pathology using optical coherence tomography (OCT). Patients with a diagnosis of STEMI were selected from a multicenter OCT registry. Patients were divided into 4 groups based on the estimated time of onset (00:00-05:59, 06:00-11:59, 12:00-17:59, or 18:00-23:59). Underlying pathologies of MI (plaque rupture, plaque erosion, and calcified plaque) were compared among the 4 groups. Among 648 patients, plaque rupture was diagnosed in 386 patients (59.6%), plaque erosion in 197 patients (30.4%), and calcified plaque in 65 patients (10.0%). A marked circadian variation was detected in the incidence of plaque rupture with a peak at 09:00, whereas it was not evident in plaque erosion or calcified plaque. The probability of plaque rupture significantly increased in the periods of 06:00-11:59 [odds ratio (OR) 2.13, 95% confidence interval (CI) 1.30-3.49, p = 0.002] and 12:00-17:59 (OR 2.10, 95% CI 1.23-3.58, p = 0.005), compared to the period of 00:00-05:59. This circadian pattern was observed only during weekdays (p = 0.010) and it was not evident during the weekend (p = 0.742). Plaque rupture occurred most frequently in the morning and this circadian variation was evident only during weekdays. Acute MI caused by plaque rupture may be related to catecholamine surge.

DOI： 10.1007/s11239-020-02220-6

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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.

DOI： 10.1016/j.amjcard.2020.03.017

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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 prevalence, angiographic, and optical coherence tomography features of healed plaques in patients with stable angina pectoris. Approach and Results: Patients with stable angina pectoris who had undergone optical coherence tomography imaging were included. Healed plaques were defined as plaques with one or more signal-rich layers of different optical density. Patients were divided into 2 groups based on layered or nonlayered phenotype at the culprit lesion. Among 163 patients, 87 (53.4%) had layered culprit plaque. Patients with layered culprit plaque had more multivessel disease (62.1% versus 44.7%, P=0.027) and more angiographically complex culprit lesions (64.4% versus 35.5%, P<0.001). Layered culprit plaques had higher prevalence of lipid plaque (83.9% versus 64.5%, P=0.004), macrophage infiltration (58.6% versus 35.5%, P=0.003), calcifications (78.2% versus 63.2%, P=0.035), and thrombus (28.7% versus 14.5%, P=0.029). Lipid index (P=0.001) and percent area stenosis (P=0.015) were greater in the layered group. The number of nonculprit plaques, evaluated using coronary angiograms, tended to be greater in patients with layered culprit plaque (4.2±2.5 versus 3.5±2.1, P=0.053). Nonculprit plaques in patients with layered culprit lesion had higher prevalence of layered pattern (P=0.002) and lipid phenotype (P=0.005). Lipid index (P=0.013) and percent area stenosis (P=0.002) were also greater in this group. CONCLUSIONS: 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.

DOI： 10.1161/ATVBAHA.120.314298

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As the degree of luminal narrowing increases, shear stress increases, and high shear stress is known to activate platelets. However, the relationship between the degree of luminal narrowing and the composition of thrombus in patients with plaque erosion has not been studied. A total of 148 patients with plaque erosion and thrombus detected by optical coherence tomography were divided into tertiles based on the minimum lumen area (MLA) at the culprit lesion. Thrombus was categorized as platelet-rich or fibrin-rich. Among 148 patients, 50 (34%) were in the mild stenosis group, 49 (33%) were in the moderate stenosis group, and 49 (33%) were in the severe stenosis group. The composition of thrombus was significantly different among the 3 groups (prevalence of platelet-rich thrombus was 60% in the mild stenosis group; 78% in the moderate stenosis group; and 84% in the severe stenosis group; P = 0.021). The pattern of fibrin-rich thrombus showed the opposite: 40%, 22%, and 16%, respectively. In the multivariate analysis, current smoking was independently associated with fibrin-rich thrombus (odds ratio [OR] 2.364 [95% CI 1.004-5.567], P = 0.049). This study demonstrated that platelet-rich thrombus was the predominant type of thrombus in plaque erosion. The prevalence of fibrin-rich thrombus was highest in the mild stenosis group.

DOI： 10.1007/s11239-020-02159-8

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OBJECTIVES: To investigate the non-culprit plaques (NCPs) characteristics in acute coronary syndrome (ACS) patients with calcified plaques (CP). BACKGROUND: Recently, a new in vivo classification of calcified culprit plaques in patients with ACS was proposed. Characteristics of NCPs in this group of patients are unknown. METHODS: A total of 692 NCPs from 492 ACS patients were retrospectively compared based on the culprit plaque phenotype: 71 from CP patients, 383 from plaque rupture (PR) patients, 238 from plaque erosion (PE) patients. RESULTS: NCPs of CP patients had greater maximal calcium thickness, wider calcium arc, longer calcium length, and greater calcium index, compared to PR or PE patients (CP vs. PR: all p < .001, CP vs. PE: all p < .001). Thin-cap fibroatheroma was less prevalent (p = .023), fibrous cap was thicker (p = .035), and mean lipid arc was narrower in CP than in PR (p < .001). CONCLUSIONS: In conclusion, NCPs of CP patients had greater calcium burden and less vulnerability. This information may help to better understand the underlying mechanisms of ACS and to develop strategy for tailored management.

DOI： 10.1002/ccd.29005

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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.

DOI： 10.1007/s11239-020-02076-w

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OBJECTIVES: This study aimed to investigate the vascular response of lesions with a layered phenotype. BACKGROUND: Recent studies have shown that layered plaques at culprit lesions detected by optical coherence tomography (OCT) have greater plaque burden and more inflammatory features than non-layered plaques. METHODS: This is a retrospective observational study. A total of 193 target lesions from 193 patients [100 patients with acute coronary syndromes (ACS) and 93 with stable angina pectoris (SAP)] who had undergone OCT imaging of the culprit lesion both before and after stenting were included. Layered plaques were identified by OCT as plaques with layers of different optical density. Patients were divided into two groups based on the presence or absence of a layered phenotype at the culprit lesion, and pre- and post-procedure OCT findings were compared. RESULTS: Among 193 patients, 36 (36.0%) lesions in ACS patients and 56 (60.2%) lesions in SAP patients were found to have a layered phenotype at the culprit lesion. At baseline, percent area stenosis was greater in layered plaque than in non-layered plaque (p = .019). Following stent implantation, the stent expansion ratio and mean stent eccentricity index were significantly lower in layered plaques than in non-layered plaques (p = .041, p = .017, respectively), mainly derived from ACS patients. CONCLUSION: Following stent implantation, plaques with a layered phenotype had less stent expansion and more eccentric lumens. Aggressive balloon dilation may be required to obtain optimal stent outcomes in patients with a layered plaque phenotype at the culprit lesion.

DOI： 10.1002/ccd.28940

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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 < 0.001). In the multivariable model, SAP, multivessel disease, type B2/C lesion, and diameter stenosis > 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.

DOI： 10.1007/s11239-020-02116-5

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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.

DOI： 10.1007/s11239-019-01969-9

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OBJECTIVES: To compare the postprocedural optical coherence tomography (OCT) findings and in-hospital outcomes among the three subtypes of calcified plaques: eruptive calcified nodules, superficial calcific sheet, and calcified protrusion. BACKGROUND: Recently, three subtypes of calcified culprit plaques were reported in patients with acute coronary syndrome (ACS). How these subtypes respond to stenting is unknown. METHODS: ACS patients with calcified plaque at the culprit lesion were selected from our database. OCT findings at baseline and after stent implantation were compared. RESULTS: In the final analysis, 87 cases were included. Preprocedural OCT showed eruptive calcified nodules in 19 (21.8%) cases, superficial calcific sheet in 63 (72.4%), and calcified protrusion in 5 (5.7%). Stent edge dissection (SED) and incomplete stent apposition (ISA) were frequently observed in the eruptive calcified nodules group compared to superficial calcific sheet or calcified protrusion (SED; 47.4% vs. 17.5% vs. 20.0%; p = .032, ISA; 94.7% vs. 58.7% vs. 0.0%; p < .001). The superficial calcific sheet group had the smallest minimal stent area (MSA) among the three groups (eruptive calcified nodules vs. superficial calcific sheet vs. calcified protrusion: 6.29 ± 2.41 vs. 4.72 ± 1.37 vs. 6.56 ± 1.13; p = .007). The superficial calcific sheet group had a higher rate of periprocedural myocardial infarction compared to the eruptive calcified nodules group (60.3% vs. 31.6%; p = .028). CONCLUSIONS: This study demonstrated eruptive calcified nodules are associated with higher incidence of SED and ISA, whereas superficial calcific sheets are associated with small MSA and higher periprocedural myocardial infarction.

DOI： 10.1002/ccd.28847

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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.

DOI： 10.1093/ehjci/jez308

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Background Plaque erosion is responsible for 25% to 40% of patients with acute coronary syndromes (ACS). Recent studies suggest that anti-thrombotic therapy without stenting may be an option for this subset of patients. Currently, however, an invasive procedure is required to make a diagnosis of plaque erosion. The aim of this study was to identify clinical or laboratory predictors of plaque erosion in patients with ACS to enable a diagnosis of erosion without additional invasive procedures. Methods and Results Patients with ACS who underwent optical coherence tomography imaging were selected from 11 institutions in 6 countries. The patients were classified into plaque rupture, plaque erosion, or calcified plaque, and predictors were identified using multivariable logistic modeling. Among 1241 patients with ACS, 477 (38.4%) patients were found to have plaque erosion. Plaque erosion was more frequent in non-ST-segment elevation-ACS than in ST-segment-elevation myocardial infarction (47.9% versus 29.8%, P=0.0002). Multivariable logistic regression models showed 5 independent parameters associated with plaque erosion: age <68 years, anterior ischemia, no diabetes mellitus, hemoglobin >15.0 g/dL, and normal renal function. When all 5 parameters are present in a patient with non-ST-segment elevation-ACS, the probability of plaque erosion increased to 73.1%. Conclusions Clinical and laboratory parameters associated with plaque erosion are explored in this retrospective registry study. These parameters may be useful to identify the subset of ACS patients with plaque erosion and guide them to conservative management without invasive procedures. The results of this exploratory analysis need to be confirmed in large scale prospective clinical studies. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT03479723.

DOI： 10.1161/JAHA.119.012322

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BACKGROUND: Although an in vivo diagnosis of coronary plaque erosion has become possible by optical coherence tomography (OCT), angiographic characteristics of erosion have not been studied. The aim of this study was to investigate the angiographic features of plaque erosion in patients with non-ST elevation acute coronary syndromes (NSTE-ACS). METHODS: Patients with NSTE-ACS who underwent OCT of the culprit lesion were collected at 11 institutions from 6 countries. Patients were classified as erosion or non-erosion based on OCT images. Angiographic features of both groups were compared. RESULTS: Among 494 cases with NSTE-ACS, 242 had plaque erosion and 252 had non-erosion. Compared to non-erosion group, erosion patients had less multivessel disease (28.5% vs. 49.6%, p < 0.001), lower Jeopardy score (4.2 vs. 5.0, p < 0.001), lower Gensini score (21.3 vs. 25.6, p = 0.014), and lower Syntax score (8.9 vs. 11.5, p < 0.001). With regard to the culprit lesion morphology, plaque erosion group had smaller reference diameter (2.8 mm vs. 3.0 mm, p = 0.032), less frequent type B2/C lesions (51.2% vs. 71.8%, p < 0.001), and lower prevalence of calcification (4.1% vs. 13.9%, p < 0.001) and thrombus (16.5% vs. 28.2%, p = 0.002). In the mid left anterior descending artery (LAD), erosion was significantly more frequent than non-erosion (30.2% vs. 21.8%, p = 0.034). CONCLUSIONS: Patients with NSTE-ACS caused by plaque erosion have less complex angiographic features both at the 3-vessel level and at the culprit lesion level. Plaque erosion was frequently found in the mid LAD.

DOI： 10.1016/j.ijcard.2019.03.039

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Diabetes mellitus (DM) increases cardiovascular morbidity and mortality. A statin is routinely prescribed to patients with DM. However, whether a statin therapy is equally effective in plaque stabilization in DM patients compared with non-DM patients is unknown. A total of 117 lipid-rich plaques were imaged in 90 patients (54 plaques in 41 DM patients and 63 plaques in 49 non-DM patients) with coronary artery disease, those who were treated with a statin and underwent serial optical coherence tomography imaging were included in this study (mean follow-up period, 362 ± 38 days). The changes in minimum fibrous cap thickness (FCT) and lipid index between baseline and 1-year follow-up were compared between the 2 groups. Minimum FCT increased and lipid index decreased with statin therapy in both groups. No significant differences were observed in percent changes of minimum FCT (p = 0.796) and lipid index (p = 0.336) between DM and non-DM patients. Statin therapy induced a significant increase in FCT and a significant decrease in lipid index in both groups. Vascular response to statin therapy was similar between the 2 groups irrespective of DM status.

DOI： 10.1016/j.amjcard.2019.02.020

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Statins are widely used to lower cholesterol and to reduce cardiovascular events. Whether all statins have similar effects on plaque stabilization is unknown. We aimed to investigate coronary plaque response to treatment with different statins that result in similar lipid reduction using serial multimodality intracoronary imaging. Patients with de novo coronary artery disease requiring intervention were randomized to rosuvastatin 10mg (R10) or atorvastatin 20mg (A20) daily. Optical coherence tomography and intravascular ultrasound were performed at baseline, 6 months, and 12 months. Untreated nonculprit plaques were analyzed by optical coherence tomography for thin-cap fibroatheroma, minimum fibrous cap thickness, lipid arc, and lipid length. Total and percent atheroma volume, respectively were analyzed by intravascular ultrasound. Forty-three patients completed the protocol (R10: 24 patients, 31 plaques; A20: 19 patients, 30 plaques). The decrease in serum lipids was similar. From baseline to 6 months to 12 months, minimum fibrous cap thickness increased in the R10 group (61.4 ± 15.9 µm to 120.9 ± 57.9 µm to 171.5 ± 67.8 µm, p <0.001) and the A20 group (60.8 ± 18.1 µm to 99.2 ± 47.7 µm to 127.0± 66.8 µm, p <0.001). Prevalence of thin-cap fibroatheroma significantly decreased in the R10 and A20 groups (-48% and -53%, respectively, p <0.001 for intragroup comparisons). Only the R10 group had a decrease in macrophage density (-23%, p = 0.04) and microvessels (-12%, p = 0.002). Total atheroma volume decreased in the R10 group (109.2 ± 62.1 mm3 to 101.8 ± 61.1 mm3 to 102.5 ± 62.2 mm3, p = 0.047) but not in the A20 group (83.3 ± 48.5mm3 to 77.6 ± 43.0 mm3 to 77.9 ± 48.6 mm3, p = 0.07). In conclusion, although both statins demonstrated similar reductions in lipid profiles, the rosuvastatin group showed more rapid and robust plaque stabilization, and regression of plaque volume compared to the atorvastatin group.

DOI： 10.1016/j.amjcard.2019.02.019

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DOI： 10.18632/aging.101969

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OBJECTIVES: This study conducted detailed analysis of calcified culprit plaques in patients with acute coronary syndromes (ACS). BACKGROUND: Calcified plaques as an underlying pathology in patients with ACS have not been systematically studied. METHODS: From 1,241 patients presenting with ACS who had undergone pre-intervention optical coherence tomography imaging, 157 (12.7%) patients were found to have a calcified plaque at the culprit lesion. Calcified plaque was defined as a plaque with superficial calcification at the culprit site without evidence of ruptured lipid plaque. RESULTS: Three distinct types were identified: eruptive calcified nodules, superficial calcific sheet, and calcified protrusion (prevalence of 25.5%, 67.4%, and 7.1%, respectively). Eruptive calcified nodules were frequently located in the right coronary arteries (44.4%), whereas superficial calcific sheet was most frequently found in the left anterior descending coronary arteries (68.4%) (p = 0.012). Calcification index (mean calcification arc × calcification length) was greatest in eruptive calcified nodules, followed by superficial calcific sheet, and smallest in calcified protrusion (median 3,284.9 [interquartile range (IQR): 2,113.3 to 5,385.3] vs. 1,644.3 [IQR: 1,012.4 to 3,058.7] vs. 472.5 [IQR: 176.7 to 865.2]; p < 0.001). The superficial calcific sheet group had the highest peak post-intervention creatine kinase values among the groups (eruptive calcified nodules vs. superficial calcific sheet vs. calcified protrusion: 241 [IQR: 116 to 612] IU/l vs. 834 [IQR: 141 to 3,394] IU/l vs. 745 [IQR: 69 to 1,984] IU/l; p = 0.032). CONCLUSIONS: Three distinct types of calcified culprit plaques are identified in patients with ACS. Superficial calcific sheet, which is frequently located in the left anterior descending coronary artery, is the most prevalent type and is also associated with greatest post-intervention myocardial damage. (Identification of Predictors for Coronary Plaque Erosion in Patients With Acute Coronary Syndrome; NCT03479723).

DOI： 10.1016/j.jcin.2018.12.013

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AIMS: Coronary angioscopy (CAS) is a robust imaging methodology for evaluation of vascular healing response after stenting. However, the procedure requires a guiding catheter with a diameter of more than 6 Fr, which is rather invasive at follow-up angiography. Recently, coronary angioscopes of a smaller diameter have been able to pass through a 4 Fr guiding catheter. This study aimed to investigate the feasibility and safety of slender CAS observation using a 4 Fr guiding catheter. METHODS AND RESULTS: Thirty-three consecutive patients who underwent follow-up angiography were evaluated. Following usual angiography via the radial artery, the stent segment was observed by non-occlusive CAS through a 4 Fr guiding catheter. Low molecular weight dextran-L (4 mL/sec) was flushed from a guiding catheter to replace coronary blood. The success rate, anatomical or procedural factors related to the success, and incidence of adverse events were examined. The success rate was 84.8% (n=28/33). The luminal diameter at the orifice of the target vessel was larger in the successful than in the failed group (4.03±0.61 mm vs. 3.39±0.61 mm, respectively; p=0.009). The presence of deep engagement of the guiding catheter into the target vessel was a key factor for sufficient observation (100% in the successful group vs. 0% in the failed group; p<0.0001). No adverse events, such as dissection or acute coronary syndrome, were reported. CONCLUSIONS: The new method of CAS through a 4 Fr guiding catheter demonstrated high feasibility and safety. This less invasive observation via CAS may be useful for stent follow-up.

DOI： 10.4244/AIJ-D-18-00003

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DOI： 10.1016/j.atherosclerosissup.2018.04.121

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Language：English   Publisher：日本心臓血管内視鏡学会  

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複数血管の血管内視鏡検査により、BMIと冠動脈硬化度との関連性について検討した。2000年9月〜2007年7月に複数血管の血管内視鏡検査を施行した冠動脈疾患患者89例を、BMIに基づいて過小体重(<20kg/m2)群7例、正常体重(20〜25kg/m2)群40例、過体重(25〜28kg/m2)群27例、肥満(≧28kg/m2)群15例に分けた。観察した冠動脈で認められた黄色プラーク数(NYP)を数え、各プラークの色をグレード1(淡黄色)、グレード2(黄色)、グレード3(濃い黄色)と定義した。1血管あたりのNYPと最大黄色グレード(MYG)を4群間で比較した。その結果、冠動脈硬化度の重症度(NYP、MYG)は有意に異なっていた。多変量回帰分析により、BMIは1血管あたりのNYPと独立して相関していることが明らかになった。過小体重患者の冠動脈硬化は正常および過体重患者よりも進行しており、低BMIは進行性冠動脈硬化と独立して関連していることが示された。

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症例は85歳女性で、脂質異常症、高血圧症、慢性腎臓病に罹患しており、労作時胸痛を訴え当院に入院となった。患者は2年前に安定狭心症のためステント植込み術を行っており、左前下行枝中部の責任病変をコバルトクロムエベロリムス溶出ステントで治療していた。冠状動脈造影でステント遠位部にステント内再狭窄が認められた。冠動脈内視鏡検査では、再狭窄病変の黄色プラークがステントを完全に覆っているのが確認された。そのため、non-slip element balloonによる治療を行い、stent-in-stentを避けるため薬剤被覆バルーンによる補助的血管形成術を施行した。胸痛は完全に消失し、臨床経過は良好であった。

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Contrast media are considered to cause acute kidney injury by activating various factors that induce renal vasoconstriction. We analysed the renal microvascular haemodynamic response using the Doppler flow wire method. Then changes in urinary liver-type fatty acid-binding protein levels following contrast medium administration were compared between groups with or without a micro-injury of the kidney. In the group without renal micro-injury, the average peak velocity (APV) decreased significantly, whereas the renal artery resistance index (RI) increased significantly following contrast medium administration. In contrast, there was no significant change in either the APV or RI in the group with a renal micro-injury. A blunted microvascular response was found in the micro-injury group, whereas microvascular resistance increased in the non-micro-injury group.

DOI： 10.1111/1440-1681.12653

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This study aimed to examine the association between the non-invasive measurement of the brachial artery volume elastic modulus (V E), an index of arterial stiffness, and the presence of coronary artery stenosis in patients with suspected stable coronary artery disease (CAD). A total of 135 patients with suspected stable CAD (87 men, mean age, 64 ± 12 years) underwent oscillometric measurement of the brachial artery to obtain V E. Coronary angiography was thereafter carried out to diagnose CAD, defined as having ≥75 % stenosis in the epicardial coronary arteries. V E was significantly higher in patients with CAD (1.94 ± 0.34 mmHg/%) than in those without CAD (1.71 ± 0.35 mmHg/%, P < 0.001). In multiple logistic regression analysis, V E was an independent predictor for the presence of CAD (odds ratio 1.19 per 0.1 mmHg/% increase, 95 % CI 1.04-1.51) even after adjusting for multiple potential confounders including the Framingham risk score (FRS). The area under the curve of the receiver operating characteristic curve analysis for discriminating CAD increased significantly after the addition of V E to the FRS (from 0.75 to 0.81, P = 0.034). The category-free net reclassification improvement and the integrated discrimination improvement by adding V E to the FRS were 0.476 (95 % CI 0.146-0.806) and 0.086 (95 % CI 0.041-0.132), respectively. In conclusion, the brachial V E was significantly associated with the presence of coronary artery stenosis. The additional measurement of V E to the FRS improved the ability to identify patients with coronary artery stenosis among those with suspected stable CAD.

DOI： 10.1007/s00380-015-0769-7

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Sleep-disordered breathing (SDB) is known as a cardiovascular risk factor and has high prevalence in hypertension, which is a major risk factor of aortic dissection (AD). However, the impact of SDB on AD has not been fully clarified. The aim of this study is to elucidate the impact of SDB on AD, especially on the type of false lumen in AD. We enrolled twenty-three consecutive patients with acute AD (mean age: 66 ± 13 years). All subjects were evaluated by an ambulatory polygraphic sleep monitoring within 1 month from the onset. AD was evaluated by axial images of computed tomography. We comparatively analyzed SDB and AD. 35 % of the subjects presented severe OSA (apnea-hypopnea index: AHI ≥30). The patent false lumen group showed significantly higher systolic and diastolic blood pressure (BP) on arrival and AHI, and lower percutaneous oxygen saturation (SaO2) compared with those in the thrombosed false lumen group. The prevalence of severe SDB was higher in the patent false lumen group (60 vs 15 %, p = 0.039). Systolic BP on arrival was significantly correlated with AHI (r = 0.457, p = 0.033) and the minimum SaO2 (r = -0.537, p = 0.010). The present study revealed close linkage between SDB and AD, and a high prevalence of SDB among AD patients. Severe SDB was related to the development of AD, especially for the patent false lumen type through highly elevated BP which might be easily evoked in the presence of severe SDB. Repetitive occurrence of intrathoracic negative pressure also might influence the repair or closure of false lumen of AD, although the present analysis did not reach statistical significance.

DOI： 10.1007/s00380-015-0699-4

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This case report describes a patient who underwent implantation of a bare-metal stent (BMS) for the treatment of everolimus-eluting stent (EES) restenosis caused by chronic stent recoil, and the BMS successfully escaped from duplicate restenosis and target lesion revascularization (TLR).

DOI： 10.1007/s00380-014-0588-2

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BACKGROUND: Little is known about the very late-phase morphological vessel characteristics within the sirolimus-eluting stent (SES). METHODS AND RESULTS: We assessed a total of 12 patients with 15 SES implantations who underwent repeat angiographic and angioscopic procedures after 5 and 7 years. The degree of neointimal stent coverage (NSC) was classified as follows: grade 0, uncovered struts; grade 1, visible struts through a thin neointima; or grade 2, invisible struts with complete neointimal coverage. The maximum and minimum NSC grades were evaluated and the existence of in-stent thrombus was also recorded for all patients. The prevalence of a maximum NSC grade of 2 increased and that of a minimum NSC grade of 0 decreased, although there was no significant difference in prevalence between 5 and 7 years. One of four in-stent thrombus identified at 5 years had disappeared from 5 to 7 years and a new thrombus was found in another patient at 7 years. Thus, the incidence of in-stent thrombus did not change from 5 to 7 years. In one case, a thrombus was observed inside the angiographic aneurysmal change, but none of the thrombi were related to adverse events. CONCLUSION: This angioscopic study reported gradual arterial repair and continuous delayed healing associated with subclinical thrombus formation 7 years after SES deployment.

DOI： 10.1097/MCA.0000000000000315

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Contrast-induced nephropathy (CIN) is considered to result from intrarenal vasoconstriction, and occurs more frequently in impaired than in normal kidneys. It was hypothesized that iodinated contrast media would markedly change renal blood flow and vascular resistance in functionally impaired kidneys. Thirty-six patients were enrolled (32 men; mean age, 75.3 ± 7.6 years) undergoing diagnostic coronary angiography and were divided into two groups based on the presence of chronic kidney disease (CKD), defined as an estimated glomerular filtration rate (eGFR) of < 60 mL/min per 1.73 m(2) (CKD and non-CKD groups, n = 18 in both). Average peak velocity (APV) and renal artery resistance index (RI) were measured by Doppler flow wire before and after administration of the iodinated contrast media. The APV and the RI were positively and inversely correlated with the eGFR at baseline, respectively (APV, R = 0.545, P = 0.001; RI, R = -0.627, P < 0.001). Mean RI was significantly higher (P = 0.015) and APV was significantly lower (P = 0.026) in the CKD than in the non-CKD group. Both APV (P < 0.001) and RI (P = 0.002) were significantly changed following contrast media administration in the non-CKD group, but not in the CKD group (APV, P = 0.258; RI, P = 0.707). Although renal arterial resistance was higher in patients with CKD, it was not affected by contrast media administration, suggesting that patients with CKD could have an attenuated response to contrast media.

DOI： 10.1111/1440-1681.12479

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Language：English   Publisher：日本心臓血管内視鏡学会  

74歳女。動脈硬化性閉塞症が疑われ、左大腿動脈よりクロスオーバーアプローチにて血管造影を行った。カテーテルインターベンションにて右総大腿動脈と外腸骨動脈の狭窄部は改善した。左大腿動脈の刺入部をAngio-Sealにて閉鎖したが止血できず、用手圧迫にて止血した。その直後は左膝窩動脈と足背は触知可能であった。翌日、間欠跛行を認め、足関節-上腕血圧指数が低下していた。膝窩動脈と足背動脈にて脈拍を認めず、大動脈-大腿動脈造影にて、浅大腿動脈(SFA)の閉塞を認め、大腿深動脈から側副血行路が生じていた。バルーンカテーテルにてSFAの拡張を行い、血管内視鏡にて赤色・白色血栓の残存と白色の集塊を認めた。カテーテルによる血栓除去を行い、左足の疼痛が残存したため、伏在静脈パッチと大腿大腿動脈バイパスグラフト移植を行い、症状は改善した。

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Language：English   Publisher：日本心臓血管内視鏡学会  

Pre-diabetic患者におけるスタチン療法の効果を、冠動脈内視鏡を用いてアテローム性動脈硬化の程度を比較することにより評価した。pre-diabetic患者28名を対象に後向き研究を行った。黄色プラークの色等級は、血管内視鏡所見の半定量的分析に基づいて1度(淡黄色)、2度(黄色)、3度(濃黄色)に分類した。血管あたりの黄色プラーク数(NYP)と最大黄色度(MYG)を、スタチン治療群と非スタチン治療群の患者間で比較した。LDL-コレステロールの血清中濃度を含む基本的な特徴は、2群間で類似していた。平均NYPおよびMYGは非スタチン群よりスタチン群で有意に低く、それぞれ2.03±0.59対1.12±0.73および2.50±0.71対1.72±0.83であった。スタチン療法は、pre-diabetic患者におけるアテローム性動脈硬化の進行を抑制するのに重要な役割を果たしていると考えられた。

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Diabetes mellitus is a powerful risk factor of coronary artery disease (CAD), leading to death and disability. In recent years, given the accumulating evidence that prediabetes is also related to increasing risk of CAD including cardiovascular events, a new guideline has been proposed for the treatment of blood cholesterol for primary prevention of cardiovascular events. This guideline recommends aggressive lipid-lowering statin therapy for primary prevention in diabetes and other patients. The ultimate goal of patient management is to inhibit progression of systemic atherosclerosis and prevent fatal cardiovascular events such as acute coronary syndrome (ACS). Because disruption of atherosclerotic coronary plaques is a trigger of ACS, the high-risk atheroma is called a vulnerable plaque. Several types of novel diagnostic imaging technologies have been developed for identifying the characteristics of coronary atherosclerosis before the onset of ACS, especially vulnerable plaques. According to coronary angioscopic evaluation, atherosclerosis severity and plaque vulnerability were more advanced in prediabetic than in nondiabetic patients and comparable to that in diabetic patients. In addition, pharmacological intervention by statin therapy changed plaque color and complexity, and the dynamic changes in plaque features are considered plaque stabilization. In this article, we review the findings of atherosclerosis in prediabetes, detected by intravascular imaging modalities, and the therapeutic implications.

DOI： 10.4239/wjd.v6.i1.184

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DOI： 10.1016/j.ijcard.2013.03.134

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A 67-year-old male was admitted because of acute myocardial infarction (AMI). An emergent coronary angiography showed a total occlusion in the left anterior descending artery, and a stent was deployed. Moderate lesion stenosis was found in the right coronary artery (RCA). Fractional flow reserve indicated 0.96, and percutaneous coronary intervention was not performed. Six months later, the patient visited an emergency room due to AMI. Angiograms showed a patency of the previous stent and progressed stenosis with filling delay of the RCA. Protruding red thrombi and plaque disruption of thin-cap fibroatheroma (TCFA) were identified by optical coherence tomography. Mild to moderate lesions are physiologically benign but morphologically malignant in cases of TCFA. <Learning objective: Severe stenosis is a malignant index of plaque vulnerability on the basis of physiological and morphological evaluation. However, mild to moderate lesions are physiologically benign but morphologically malignant in cases of thin-cap fibroatheroma. Although fractional flow reserve can estimate the extent of severe stenosis, one of the elements of vulnerable plaques, it cannot always predict future events related to morphologically vulnerable plaques>.

DOI： 10.1016/j.jccase.2013.03.001

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BACKGROUND: Although several clinical trials have shown the superior efficacy and safety of second-generation everolimus-eluting stents (EES) in comparison with first-generation paclitaxel-eluting stents (PES), the differences in the vascular healing process between EES and PES in a human coronary artery during an early stage are unknown. METHODS: A prospective optical coherence tomography (OCT) observation was performed for 25 EES in 21 patients and 27 PES in 21 patients at 6 months after implantation. Cross-sections within single-stent segments were analyzed at intervals of 1mm. The neointimal (NI) thickness on each strut was measured. Uncovered struts (NI thickness=0 μm), malapposed struts, NI area (%), uncovered strut ratio >0.3 (UCSR; number of uncovered struts/number of total struts) per cross-section, and in-stent thrombus were evaluated. RESULTS: A total of 5198 EES struts in 514 cross-sections and 4243 PES struts in 469 cross-sections were identified. NI thickness and its area were smaller for EES than PES (80.0 ± 84.8 μm vs. 117.9 ± 140.0 μm and 19.1 ± 8.9% vs. 23.7 ± 11.5%, respectively; P<0.001). The frequencies of uncovered struts and malapposed struts were lower in EES compared to PES (2.3% vs. 5.2% and 2.1% vs. 5.7%, respectively; P<0.001). Patients who had cross-sections of UCSR >0.3 and thrombi were identified less frequently in EES than in PES group (5% vs. 57%; P<0.001, and 19% vs. 48%; P=0.05, respectively). CONCLUSIONS: Six-month OCT examination showed a favorable vessel healing response after the implantation of EES, demonstrating less in-stent late loss as well as fewer uncovered struts and better stent apposition to the vessel wall in comparison with PES.

DOI： 10.1016/j.ijcard.2011.10.102

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Although helicopters have been used in an air ambulance system for the past decade in Japan, the appropriate selection of patients for this transport mode has not been investigated. The present study investigates which patients could potentially benefit the most from helicopter emergency medical service (HEMS). We investigated the extent of circulatory and respiratory support required in the intensive care unit (ICU) and ultimate outcomes of 2340 patients with cardiovascular disease admitted to 1 institution between October 2001 and December 2009. Two hundred and seventy were transported by HEMS (HEMS group), and 2070 were transported by other means (non-HEMS group). Temporary cardiac pacing, ventilator management, intra-aortic balloon pumping, percutaneous cardiopulmonary support, electrical defibrillation, and therapeutic hypothermia were more frequently required by patients in the HEMS group vs. the non-HEMS group (10.4, 28.1, 17.0, 5.2, 10.0 and 3.4 vs. 8, 17.9, 10.9, 2.3, 4.5 and 0.4, respectively). The mortality rate was higher in the HEMS group than in the non-HEMS group in the ICU (9.6 vs. 5.3). Disease was more clinically severe and the outcome was poorer among patients with cardiovascular diseases transported by HEMS than by other means. © 2011 Air Medical Journal Associates.

DOI： 10.1016/j.amj.2011.05.004

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Very late stent thrombosis (VLST) after implantation of a drug-eluting stent (DES) is a rare but catastrophic complication and the mechanisms are not completely understood. We describe a 76-year-old patient with recurrent VLST of DES that developed at 13 and 23 months after the initial catheter procedure of DES implantation under the cessation of dual antiplatelet therapy. Optical coherence tomography (OCT) observation revealed small stent area of a DES. Based on the OCT findings, balloon angioplasty for expansion of the DES was performed and angiographic Thrombolysis In Myocardial Infarction grade 3 flow was subsequently obtained. Small stent area is considered a significant factor in acute or subacute stent thrombosis according to previous reports. The present report shows that small stent area of DES may be regarded as a key factor in recurrent VLST as well as cessation of dual antiplatelet therapy.

DOI： 10.1016/j.jccase.2010.07.002

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AIMS: The clinical course including the outcome of acute decompensated heart failure (ADHF) correlates with renal dysfunction, but the evaluation of renal function has not yet been standardized. We therefore investigated the relationship between the prognosis of ADHF and acute kidney injury (AKI) evaluated using the risk, injury, failure, loss, end stage (RIFLE) criteria. METHODS AND RESULTS: This study assessed 376 consecutive patients with ADHF admitted to the intensive care unit (ICU) (mean age 71.6 years; 238 male). The underlying aetiology was ischaemic heart disease, hypertensive heart disease, cardiomyopathy, valvular diseases, and 'other' in 124, 70, 60, 107, and 15 patients, respectively. We defined AKI according to the RIFLE criteria, and the most severe RIFLE classifications during hospitalization were adopted to assess patient outcomes. The in-hospital mortality was significantly higher among patients with AKI (29 of 275; 10.5%) than in those without AKI (1 of 101; 1.0%, P = 0.0010). Both ICU and hospital stays were longer for patients with AKI (8.8 +/- 15.4 vs. 48.6 +/- 47.6 days), than for patients without (5.0 +/- 2.8 vs. 25.7 +/- 16.8 days, P < 0.05 and P < 0.001). CONCLUSION: Acute kidney injury evaluated by the RIFLE criteria was associated with a poorer outcome for patients with ADHF.

DOI： 10.1093/eurjhf/hfp169

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