Why the study?
The role of epicardial adipose tissue (EAT) has evolved into a dynamic contributor to cardiovascular risk, warranting examination of its implications and the potential benefits of liraglutide in mitigating its effects.
Does Liraglutide reduce epicardial adipose tissue thickness and residual cardiovascular risk in an obese patient with chronic coronary syndrome?
Does Liraglutide reduce epicardial adipose tissue thickness and residual cardiovascular risk in an obese patient with chronic coronary syndrome?
Liraglutide may be a promising therapeutic option for reducing epicardial adipose tissue and addressing residual cardiovascular risk in obese patients with coronary artery disease.
Hypothesis-generating for liraglutide in obese CCS; prospective trials needed before clinical adoption.
Introduction The role of epicardial adipose tissue (EAT) in cardiovascular health has undergone a paradigm shift in recent years, evolving from a passive reservoir into a dynamic contributor to cardiovascular risk. This case critically examines the multifaceted functions of EAT, explores its implications for cardiovascular risk, and discusses the potential benefits of the GLP-1 receptor agonist Liraglutide in mitigating its effects. Case presentation We present the case of a 62-year-old male patient who is obese, hypertensive, and has a history of chronic coronary syndrome. He was admitted to the emergency room with complaints of palpitations and shortness of breath. The 12-lead ECG revealed atrial fibrillation with a rapid ventricular response and evidence of a new-onset left bundle branch block. The transthoracic echocardiogram showed heart-rate-dependent regional dyskinesias, while both echocardiographic and computed tomographic scan findings indicated the presence of thick EAT. A coronary angiogram showed intrastent restenosis in the left anterior descending artery, which was treated with percutaneous revascularization. To address residual cardiovascular risk, the patient was initiated on Liraglutide during hospitalization. The follow-up revealed reduced low-density lipoprotein-cholesterol and high-sensitivity C-reactive protein levels, along with a decrease in EAT thickness and BMI, accompanied by improved echocardiographic parameters. Discussion Targeted interventions aimed at reducing EAT are imperative given its active role in cardiovascular risk. GLP-1 receptor agonists, such as Liraglutide, hold promise in mitigating the effects of EAT and represent a potential avenue for therapeutic exploration in addressing residual cardiovascular risk.
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Cacciapuoti et al. (2024) studied this question.
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