Dataset Information

Case report: a potential modulation of coronary atheroma by lowering triglyceride-rich lipoproteins with pemafibrate: insights from serial near-infrared spectroscopy imaging.

ABSTRACT:

Background

Pemafibrate is a potent selective peroxisome proliferator-activated receptor α modulator. Whether this agent favorable modulates atherosclerosis in vivo remains unknown. This is the first case report to evaluate serial changes of coronary atherosclerosis under pemafirate use in type 2 diabetic patients already taking a high-intensity statin.

Case description

A 75-year-old gentleman was hospitalized due to peripheral artery disease, which was treated by endovascular treatment. One year later, non-ST-elevation myocardial infarction (NSTEMI) occurred and severe stenosis at his proximal segment of right coronary artery received primary percutaneous coronary intervention (PCI). Due to his suboptimal control of low-density lipoprotein cholesterol (LDL-C) level with moderate intensity statin, high-intensity one (20 mg atorvastatin) and 10 mg ezetimibe were commenced, which enabled to achieve very low LDL-C level (50 mg/dL). However, he required additional PCI due to progression of left circumflex artery one year after NSTEMI. Despite his optimally controlled LDL-C level (46 mg/dL), near-infrared spectroscopy and intravascular (NIRS/IVUS) imaging after PCI visualized the presence of lipid-rich plaque [maximum 4-mm lipid-core burden index (LCBI_4mm) =482] at non-culprit segment in his right coronary artery. Given his continuing residual hypertriglyceridemia (triglyceride =248 mg/dL), 0.2 mg pemafibrate was commenced, which lowered triglyceride to 106 mg/dL. One-year follow-up NIRS/IVUS imaging was conducted to evaluate coronary atheroma. A reduction of attenuated ultrasonic signals was observed, accompanied by plaque calcification. In addition, the amount of yellow signal was lowered, and its MaxLCBI_4mm was 358. Since then, this case does not experience any cardiovascular events. His LDL-C and triglyceride-rich lipoprotein levels are favourably controlled.

Conclusions

A delipidation of coronary atheroma, accompanied by greater plaque calcification was observed after the commencement of pemafibrate. This finding highlights potential anti-atherosclerotic benefit of pemafibrate use in patients receiving a statin.

SUBMITTER: Murata Y

PROVIDER: S-EPMC9971301 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature

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Publications

Case report: a potential modulation of coronary atheroma by lowering triglyceride-rich lipoproteins with pemafibrate: insights from serial near-infrared spectroscopy imaging.

Murata Yu Y Kataoka Yu Y Asaumi Yasuhide Y Noguchi Teruo T

Cardiovascular diagnosis and therapy 20230203 1

<h4>Background</h4>Pemafibrate is a potent selective peroxisome proliferator-activated receptor α modulator. Whether this agent favorable modulates atherosclerosis <i>in vivo</i> remains unknown. This is the first case report to evaluate serial changes of coronary atherosclerosis under pemafirate use in type 2 diabetic patients already taking a high-intensity statin.<h4>Case description</h4>A 75-year-old gentleman was hospitalized due to peripheral artery disease, which was treated by endovascul ...[more]

PMID: 36864976

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Project description:Approximately 25% of US adults are estimated to have hypertriglyceridemia (triglyceride [TG] level ≥150 mg/dL [≥1.7 mmol/L]). Elevated TG levels are associated with increased cardiovascular disease (CVD) risk, and severe hypertriglyceridemia (TG levels ≥500 mg/dL [≥5.6 mmol/L]) is a well-established risk factor for acute pancreatitis. Plasma TG levels correspond to the sum of the TG content in TG-rich lipoproteins (TRLs; ie, very low-density lipoproteins plus chylomicrons) and their remnants. There remains some uncertainty regarding the direct causal role of TRLs in the progression of atherosclerosis and CVD, with cardiovascular outcome studies of TG-lowering agents, to date, having produced inconsistent results. Although low-density lipoprotein cholesterol (LDL-C) remains the primary treatment target to reduce CVD risk, a number of large-scale epidemiological studies have shown that elevated TG levels are independently associated with increased incidence of cardiovascular events, even in patients treated effectively with statins. Genetic studies have further clarified the causal association between TRLs and CVD. Variants in several key genes involved in TRL metabolism are strongly associated with CVD risk, with the strength of a variant's effect on TG levels correlating with the magnitude of the variant's effect on CVD. TRLs are thought to contribute to the progression of atherosclerosis and CVD via a number of direct and indirect mechanisms. They directly contribute to intimal cholesterol deposition and are also involved in the activation and enhancement of several proinflammatory, proapoptotic, and procoagulant pathways. Evidence suggests that non-high-density lipoprotein cholesterol, the sum of the total cholesterol carried by atherogenic lipoproteins (including LDL, TRL, and TRL remnants), provides a better indication of CVD risk than LDL-C, particularly in patients with hypertriglyceridemia. This article aims to provide an overview of the available epidemiological, clinical, and genetic evidence relating to the atherogenicity of TRLs and their role in the progression of CVD.

Dataset Information

Case report: a potential modulation of coronary atheroma by lowering triglyceride-rich lipoproteins with pemafibrate: insights from serial near-infrared spectroscopy imaging.

Background

Case description

Conclusions

Publications

Case report: a potential modulation of coronary atheroma by lowering triglyceride-rich lipoproteins with pemafibrate: insights from serial near-infrared spectroscopy imaging.

Similar Datasets

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