Association between abdominal fat distribution and coronary plaque instability in patients with acute coronary syndrome

Abstract Background The relationship between eicosapentaenoic acid (EPA) therapy and coronary plaque stability assessed by optical frequency domain imaging (OFDI) has not been thoroughly described. Hypothesis EPA therapy is associated with decreased plaque instability in patients undergoing percutaneous coronary intervention (PCI) using OFDI. Methods Data on coronary artery plaques from 121 patients presenting with acute coronary syndrome or stable angina who consecutively underwent PCI between October 2015 and July 2018 were retrospectively analyzed. Of these patients, 109 were untreated (no-EPA group), whereas 12 were treated with EPA (EPA group). Each plaque's morphological characteristics were analyzed using OFDI. Results We used 1:4 propensity score matching for patients who received or did not receive EPA therapy before PCI. Baseline characteristics were balanced between both groups (age, sex, body mass index, diabetes mellitus, hypertension, dyslipidemia, chronic kidney disease, smoking, previous PCI or coronary artery bypass grafting, previous myocardial infarction, prior statin use, acute coronary syndrome, hemoglobin A1c level, low-density lipoprotein cholesterol concentration, triglyceride concentration, and high-density lipoprotein cholesterol concentration). The EPA group had significantly lower mean lipid index (818±806 vs. 1,574±891) and macrophage grade (13.5±5.9 vs. 19.3±7.4) but higher mean minimum fibrous cap thickness (109.2±55.7 vs. 81.6±36.4 μm) than the no-EPA group (P=0.010, 0.019, and 0.040, respectively). Multiple logistic regression analyses showed that prior EPA use was independently associated with lower lipid index and macrophage grade (P=0.043 and 0.024, respectively). Conclusion This OFDI analysis suggests that EPA therapy is associated with decreased plaque instability in patients undergoing PCI. Acknowledgement/Funding None

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Impact of Total Risk Management on Coronary Plaque Regression in Diabetic Patients with Acute Coronary Syndrome

Journal of Atherosclerosis and Thrombosis ◽

10.5551/jat.31948 ◽

2016 ◽

Vol 23 (8) ◽

pp. 922-931 ◽

Cited By ~ 7

Author(s):

Ryo Naito ◽

Katsumi Miyauchi ◽

Hiroyuki Daida ◽

Takeshi Morimoto ◽

Takafumi Hiro ◽

...

Keyword(s):

Risk Management ◽

Acute Coronary Syndrome ◽

Coronary Plaque ◽

Diabetic Patients ◽

Total Risk ◽

Coronary Syndrome ◽

Plaque Regression

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TCT-320: Gender Differences in Coronary Plaque Components in Patients with Acute Coronary Syndrome: Virtual Histology-Intravascular Ultrasound Analysis

Journal of the American College of Cardiology ◽

10.1016/j.jacc.2010.08.347 ◽

2010 ◽

Vol 56 (13) ◽

pp. B74

Keyword(s):

Gender Differences ◽

Acute Coronary Syndrome ◽

Intravascular Ultrasound ◽

Coronary Plaque ◽

Virtual Histology ◽

Virtual Histology Intravascular Ultrasound ◽

Coronary Syndrome

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Effects of 4 Statins on Regression of Coronary Plaque in Acute Coronary Syndrome

Circulation Journal ◽

10.1253/circj.cj-15-1379 ◽

2016 ◽

Vol 80 (7) ◽

pp. 1634-1643 ◽

Cited By ~ 10

Author(s):

Kensuke Matsushita ◽

Kiyoshi Hibi ◽

Naohiro Komura ◽

Eiichi Akiyama ◽

Nobuhiko Maejima ◽

...

Keyword(s):

Acute Coronary Syndrome ◽

Coronary Plaque ◽

Coronary Syndrome

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Renal Allograft-Related Inflammation and Accelerated Coronary-Artery Disease: A Case Report

10.20944/preprints202104.0337.v1 ◽

2021 ◽

Author(s):

Rainer Ullrich Pliquett ◽

Andrea Tannapfel ◽

Sait Sebastian Daneschnejad

Keyword(s):

Kidney Transplant ◽

Systemic Inflammation ◽

Renal Allograft ◽

Active Role ◽

Coronary Plaque ◽

Plaque Instability ◽

Reactive Protein ◽

Coronary Syndrome ◽

Coronary Syndromes ◽

Artery Disease

Background: Although persistent systemic inflammation is considered to be predictive for future cardiovascular events, it remains unclear whether or not C-reactive protein (CrP) plays an active role in coronary-plaque instability. Here, we report a case of a patient with failed and super-infected renal allograft as a source for systemic inflammation presenting with repeat acute coronary syndromes. Case presentation: A 52-years-old male type-2 diabetic with a failed kidney transplant who was hospitalized for acute urinary-tract infection. In the presence of other, classic cardiovascular risk factors, peak values of CrP coincided with episodes of unstable angina treated by cardiologic interventions. Besides pyelonephritis, the histological examination of the kidney transplant revealed signs of chronic rejection and the presence of a renal cell carcinoma in situ. Once the renal allograft has been removed, systemic inflammation was attenuated, the patient was not rehospitalized for acute-coronary syndrome within the next 12 months. Conclusion: In this case, systemic inflammation was paralleled by instability of coronary plaques as documented by repeat coronary angiograms.

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Abstract 4008: PSGL-1-Expressing CD4 T Cells are Enriched in Culprit Coronary Artery Lesion of Acute Coronary Syndrome

Circulation ◽

10.1161/circ.118.suppl_18.s_817-b ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Keiko Gomita ◽

Kayoko Sato ◽

Kazutaka Kitamura ◽

Nobuhisa Hagiwara

Keyword(s):

T Cells ◽

Acute Coronary Syndrome ◽

Coronary Artery ◽

Adhesion Molecules ◽

Peripheral Blood ◽

Cd4 T Cells ◽

Coronary Artery Lesion ◽

Plaque Instability ◽

Coronary Syndrome

Background: Recently, several evidences on the crucial role of adhesion molecules in the development of atherosclerosis and plaque instability have been reported. While expression of VCAM-1, ICAM-1 and L-selectin has been consistently observed in atherosclerotic plaques it is still uncertain how adhesion molecules on T cells contribute to the incidence of acute coronary syndrome (ACS). In this study, we examined whether adhesion molecules on T cells in ACS have a significant role in the plaque stability and prone to cause ACS. Methods and Results: Fresh CD4 T cells were isolated from the peripheral blood of 76 ACS patients (AMI=35, UAP=41) and 74 age-matched controls (NC). CD69, an activation marker of T cells, was strongly expressed on CD4 T cells from ACS than from NC by FACS (P<0.0001). CD4 T cells from ACS highly expressed p-selectin glycoprotein ligand-1 (PSGL-1) and integrin β (CD18), but not L-selectin by FACS (P < 0.03, P < 0.01, n.s., respectively). Soluble PSGL-1 (sPSGL-1) levels in plasma were lower in ACS patients than in NC (P=0.0001), which correlated negatively with the PSGL-1 expression on CD4 T cells (R=0.405, P<0.02). We further investigated the thrombus-aspirating device samples (n=14) and fresh CD4 T cells derived from both the coronary artery and peripheral blood from the each same patient with ACS. CD4 T cells from the coronary artery strongly expressed PSGL-1 (P<0.002), but not integrin β (CD18) and L-selectin by FACS. Finally, PSGL-1 was expressed on T cells, but not on CD68 positive macrophage, MPO positive neutrophil, or CD41 positive platelets in the thrombus-aspirating device samples. Conclusions: From these results, we demonstrated that PSGL-1-expressing CD4 T cells are enriched in the culprit coronary artery lesion of ACS, contributing to the acceleration of plaque instability and occurrence of ACS.

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Abstract 14134: Effects of Statin Plus Ezetimibe versus Statin Alone on Coronary Atherosclerosis in Acute Coronary Syndrome

Circulation ◽

10.1161/circ.132.suppl_3.14134 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Kiyoshi Hibi ◽

Kazuo Kimura ◽

Shinjo Sonoda ◽

Yutaka Otsuji ◽

Toyoaki Murohara ◽

...

Keyword(s):

Acute Coronary Syndrome ◽

Combination Therapy ◽

Therapy Group ◽

Combined Therapy ◽

Coronary Plaque ◽

Statin Treatment ◽

Combination Therapy Group ◽

Plaque Volume ◽

Coronary Syndrome ◽

Percent Change

Introduction: IMPROVE-IT trial showed that ezetimibe plus statin treatment, as compared with statin alone, decreased cardiovascular events in patients with acute coronary syndrome (ACS). However, proir studies have failed to show a beneficial effect of ezetimibe on carotid plaque progression when added to statin treatment. Hypothesis: The addition of ezetimibe to statin therapy affects coronary plaque behavior in the non-culprit vessel. Methods: We conducted a prospective, randomized open-label parallel group study with blind endpoint evaluation conducted at 10 centers in Japan. A total of 128 statin naïve patients with ACS undergoing intravascular ultrasound (IVUS) guided percutaneous coronary intervention were randomized and nonculprit coronary lesions associated with mild-to-moderate stenosis in 103 patients had evaluable IVUS examinations at baseline and at 8 to 12 months follow-up. Conventional IVUS and integrated backscatter (IB)-IVUS measurements at 1-mm intervals were calculated. Patients were randomly assigned to receive either 2mg/day of pitavastatin plus 10mg/day ezetimibe or 2mg/day of pitavastatin. Primary endpoints were the percentage change in non-culprit coronary plaque volume and percent change in lipid plaque volume. Results: Mean low density lipoprotein cholesterol was reduced from 125mg/dl to 65mg/dl in the combination therapy group receiving statin plus ezetimibe (n=50) and 126mg/dl to 87 mg/dl in the statin alone group (n=53)(between group difference of 16.9%, P<0.0001). Length of analyzed segment did not differ between the groups (median 38.0 vs. 41.2 mm, p=0.40). The primary endpoint, percent change in plaque volume, was -5.1% in the combination therapy group and -6.2% in the statin alone group (P=0.66), although both groups resulted in reduction of plaque volume compared with baseline (both p=0.001). The percent change in lipid plaque volume did not differ between the groups (4.3 vs. -3.0%, P=0.37). Conclusions: Among patients with acute coronary syndrome, combined therapy with ezetimibe and statin did not result in a significant change in coronary plaque regression or tissue component compared with statin alone.

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