Impact of Accumulated Serum Uric Acid on Coronary Culprit Lesion Morphology Determined by Optical Coherence Tomography and Cardiac Outcomes in Patients with Acute Coronary Syndrome

Kobayashi, Nobuaki; Asai, Kuniya; Tsurumi, Masafumi; Shibata, Yusaku; Okazaki, Hirotake; Shirakabe, Akihiro; Goda, Hiroki; Uchiyama, Saori; Tani, Kazuhide; Takano, Masamichi; Shimizu, Wataru

doi:10.1159/000496053

Cited by 10 publications

(5 citation statements)

References 31 publications

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“…Plaque morphology, endothelial dysfunction, oxidative stress, and inflammation play a critical role in the development and progression of atherosclerosis, leading to serious cardiovascular events (Prasad et al, 2017). Optical coherence tomography showed a significant increase in plaque rupture in patients with sUA > 8.0 mg/dl (Kobayashi et al, 2018). Recently, Kimura et al demonstrated that UA promotes the secretion of IL-1b mediated by NLRP3 inflammasomes via regulating the AMPK-mTOR mROS and HIF-1a pathway in human peripheral blood mononuclear cells (Kimura et al, 2020).…”

Section: Ua and Chdmentioning

confidence: 99%

Uric Acid and Cardiovascular Disease: An Update From Molecular Mechanism to Clinical Perspective

2020

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Uric acid (UA) is the end product of purine nucleotide metabolism in the human body. Hyperuricemia is an abnormally high level of UA in the blood and may result in arthritis and gout. The prevalence of hyperuricemia has been increasing globally. Epidemiological studies have shown that UA levels are positively correlated with cardiovascular diseases, including hypertension, atherosclerosis, atrial fibrillation (AF), and heart failure (HF). Hyperuricemia promotes the occurrence and development of cardiovascular diseases by regulating molecular signals, such as inflammatory response, oxidative stress, insulin resistance/diabetes, endoplasmic reticulum stress, and endothelial dysfunction. Despite extensive research, the underlying molecular mechanisms are still unclear. Allopurinol, a xanthine oxidase (XO) inhibitor, has been shown to improve cardiovascular outcomes in patients with HF, coronary heart disease (CHD), type 2 diabetes (T2D), and left ventricular hypertrophy (LVH). Whether febuxostat, another XO inhibitor, can improve cardiovascular outcomes as well as allopurinol remains controversial. Furthermore, it is also not clear whether UA-lowering treatment (ULT) can benefit patients with asymptomatic hyperuricemia. In this review, we focus on the latest cellular and molecular findings of cardiovascular disease associated with hyperuricemia and clinical data about the efficacy of ULT in patients with cardiovascular disease.

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Section: Ua and Chdmentioning

confidence: 99%

Uric Acid and Cardiovascular Disease: An Update From Molecular Mechanism to Clinical Perspective

2020

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“…Some studies identify UA as a determinant of a more severe coronary artery involvement, a larger infarct size [ 37 ], a greater risk of acute plaque complications (such as the formation of a completely obstructing thrombus) [ 38 ] and a higher prevalence of challenging revascularization procedures, which could remain incomplete [ 39 ]. It is also possible that the UA increase in HF is merely an epiphenomenon of the cardiac damage, and is not the triggering cause, as it could secondarily rise due to increased purine metabolism caused by hypoxia and tissue catabolism [ 40 ], enhanced purine release from ischemic cells (both from the heart and from peripheral hypoperfused tissue) and the reduced clearance deriving from ACS-related impaired renal function.…”

Section: Uric Acid and Acute Coronary Syndromementioning

confidence: 99%

The Role of Uric Acid in Acute and Chronic Coronary Syndromes

Maloberti

Biolcati

Ruzzenenti

et al. 2021

JCM

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Uric acid (UA) is the final product of the catabolism of endogenous and exogenous purine nucleotides. While its association with articular gout and kidney disease has been known for a long time, new data have demonstrated that UA is also related to cardiovascular (CV) diseases. UA has been identified as a significant determinant of many different outcomes, such as all-cause and CV mortality, and also of CV events (mainly Acute Coronary Syndromes (ACS) and even strokes). Furthermore, UA has been related to the development of Heart Failure, and to a higher mortality in decompensated patients, as well as to the onset of atrial fibrillation. After a brief introduction on the general role of UA in CV disorders, this review will be focused on UA’s relationship with CV outcomes, as well as on the specific features of patients with ACS and Chronic Coronary Syndrome. Finally, two issues which remain open will be discussed: the first is about the identification of a CV UA cut-off value, while the second concerns the possibility that the pharmacological reduction of UA is able to lower the incidence of CV events.

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“…22) There is also evidence from another study that very high-sUA levels, such as >8.0 mg/dL, are a major predictor of 2-year cardiac mortality and could be partly caused by the negative ef- fect of accumulated sUA on plaque vulnerability in patients with acute coronary syndrome. 23) However, there are no studies comparing the effects of different sUA levels on ISNA progression and ISR plaque vulnerability characteristics using OCT. Our study showed that the incidence of ISNA was significantly higher in the high-sUA group than in the normal-sUA group, as observed using OCT, while the vulnerability of ISR plaques was greater in the high-sUA group than in the normal-sUA group, mainly reflected in lipid plaques and TCFA. We speculated that this might be related to the effect of sUA on the progression of ISNA.…”

Section: Discussionmentioning

confidence: 99%

Association Between Serum Uric Acid Levels and Neoatherosclerosis

Gu,

Liu,

Wang

et al. 2024

Int. Heart J.

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Neoatherosclerosis is a major cause of stent failure after percutaneous coronary intervention. Metabolism such as hyperuricemia is associated with in-stent restenosis (ISR). However, the association between serum uric acid (sUA) levels and in-stent neoatherosclerosis (ISNA) has never been validated.A total of 216 patients with 220 ISR lesions who had undergone optical coherence tomography (OCT) of culprit stents were included in this study. According to their sUA levels, eligible patients were divided into two groups [normal-sUA group: sUA < 7 mg/dL, n = 126, and high-sUA group: sUA !7 mg/dL, n = 90]. OCT findings were analyzed and compared between the normal-and high-sUA groups.The incidence of ISNA (63.0% versus 43.0%, P = 0.004) was significantly higher in the high-sUA group than in the normal-sUA group. Lipid plaques (66.3% versus 43.0%, P < 0.001) and thin-cap fibroatheroma (38.0% versus 18.0%, P = 0.001) were observed more frequently in the restenotic tissue structure in patients in the high-sUA group than in those in the normal-sUA group. Meanwhile, univariate (OR: 1.208, 95% CI: 1.037-1.407; P = 0.015) and multivariate (OR: 1.254, 95% CI: 1.048-1.501; P = 0.013) logistic regression analyses indicated that sUA levels were an independent risk factor for ISNA after adjusting for relevant risk factors.The high-sUA levels were an independent risk factor for the occurrence of neoatherosclerosis in patients with ISR via OCT.

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Impact of Accumulated Serum Uric Acid on Coronary Culprit Lesion Morphology Determined by Optical Coherence Tomography and Cardiac Outcomes in Patients with Acute Coronary Syndrome

Cited by 10 publications

References 31 publications

Uric Acid and Cardiovascular Disease: An Update From Molecular Mechanism to Clinical Perspective

Uric Acid and Cardiovascular Disease: An Update From Molecular Mechanism to Clinical Perspective

The Role of Uric Acid in Acute and Chronic Coronary Syndromes

Association Between Serum Uric Acid Levels and Neoatherosclerosis

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