Impact of Remnant Lipoprotein on Coronary Plaque Components

Matsuo, Norio; Matsuoka, Tetsuro; Onishi, Sumire; Yamamoto, Hiroyasu; Kato, Akinobu; Makino, Yasunaka; Kihara, Shinji

doi:10.5551/jat.26328

Cited by 18 publications

(16 citation statements)

References 41 publications

(45 reference statements)

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“…We have shown that adiponectin can switch macrophage polarization towards an anti-inflammatory phenotype 43) . Macronant lipoprotein levels, which are linked with coronary plaque vulnerability 13,14) . It has also been shown that high plasma adiponectin levels are associated with a reduced risk of myocardial infarction in healthy men 15) and CAD in diabetic men 16) .…”

Section: Introductionmentioning

confidence: 99%

Adipocytokines in Cardiovascular and Metabolic Diseases

Ouchi

2016

JAT

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Obesity, particularly excess visceral fat accumulation, is highly associated with the development of metabolic syndrome and atherosclerotic cardiovascular disease. Adipose tissue produces a variety of secreted proteins, referred to as adipocytokines, which directly affect nearby or remote organs. Dysregulation of adipocytokines caused by obese conditions contributes to the pathogenesis of various metabolic and cardiovascular disorders. This review focuses on the significance of several adipocytokines that potentially exert beneficial actions on obesity-related diseases, including atherosclerosis and ischemic heart disease.J Atheroscler Thromb, 2016; 23: 645-654.

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Section: Introductionmentioning

confidence: 99%

Adipocytokines in Cardiovascular and Metabolic Diseases

Ouchi

2016

JAT

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“…Only 8 months of follow-up and relatively low dose of statin therapy did not decrease the necrotic-core and fibro-fatty components in the present study. As reported by a previous study 31) , the amount of necrotic-core or fibro-fatty components may be associated with remnant lipoprotein or with lipoproteins other than LDL-C and HDL-C. It may be another explanation that cholesterol-lowering therapy with statin did not decrease necrotic-core and fibro-fatty components.…”

Section: Discussionmentioning

confidence: 50%

Efficacy of Statin Therapy in Inducing Coronary Plaque Regression in Patients with Low Baseline Cholesterol Levels

Wakabayashi

Nozue

Yamamoto

et al. 2016

J Atheroscler Thromb

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Aim: The efficacy of statin therapy in inducing coronary plaque regression may depend on baseline cholesterol levels. We aimed to determine the efficacy of statin therapy in inducing coronary plaque regression in statin-naïve patients with low cholesterol levels using serial intravascular ultrasound (IVUS) data from the treatment with statin on atheroma regression evaluated by virtual histology IVUS (TRUTH) study.Methods: The TRUTH study is a prospective, multicenter trial, comparing the efficacies of pitavastatin and pravastatin in coronary plaque regression in 164 patients. All patients were statin-naïve and received statin therapy only after study enrollment. The primary endpoint was the observation of coronary plaque progression, despite statin therapy.Results: Serial IVUS data, at baseline and after an 8-month follow-up, were available for 119 patients. The patients were divided into three groups based on non-high-density lipoprotein cholesterol (HDL-C) levels—low: ≤ 140 mg/dl, n = 38; moderate: 141–169 mg/dl, n = 42; and high: ≥ 170 mg/dl, n = 39. Coronary plaque progression was noted in the low cholesterol group, whereas plaque regression was noted in the moderate and high cholesterol groups [%Δplaque volume: 2.3 ± 7.4 vs. − 2.7 ± 10.7 vs. − 3.2 ± 7.5, p = 0.004 (analysis of variance)]. After adjusting for all variables, a low non-HDLC level (≤ 140 mg/dl) was identified as an independent predictor of coronary plaque progression [odds ratio, 3.7; 95% confidence interval, 1.5–9.1, p = 0.004].Conclusion: Serial IVUS data analysis indicated that statin therapy was less effective in inducing coronary plaque regression in patients with low cholesterol levels but more effective in those with high cholesterol levels at baseline.University Hospital Medical Information Network (UMIN) (UMIN ID: C000000311).

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“…RemL-C is a quantitative marker for the accumulation of remnant lipoproteins, and considered useful for analyzing cardiovascular risk in patients with accumulation of remnant lipoproteins [27,28]. In addition, elevated serum RemL-C levels are associated with coronary plaque vulnerability in patients with stable angina [29], and are useful predictors of postprandial dyslipidemia in young healthy individuals [30]. The administration of Omega-3 may therefore help reduce these residual cardiovascular risk factors in patients with dyslipidemia.…”

Section: Discussionmentioning

confidence: 99%