There are ample studies exploring the progression of coronary atherosclerosis following pharmacological manipulation. At the time of writing, the use of statins is recognized as an effective treatment; statins can result in decreases in plaque and necrotic core volume, and can also significantly reduce the progression of low attenuation plaque (<30 Hounsfield units) and non-calcified plaque [
8,
9]. Other drugs, such as dipeptidyl-peptidase 4 inhibitors [
10], a PPARγ agonist (pioglitazone) [
11], atorvastatin plus ezetimibe [
12], olmesartan [
13], have also been reported to have antiatherosclerotic effects, although the effects have not been verified by large-scale studies. As studies show that EAT volume is associated with plaque progression and cardiovascular adverse events, treatments aimed at reducing EAT volume may finally achieve an antiatherosclerotic, preventive effect. However, at the time of writing, limited studies have aimed at reducing both EAT and plaque volume to achieve an antiatherosclerotic effect. A serial coronary computed tomography angiography (CCTA) study recently indicated that intensive statin therapy can reduce the EAT volume of Europeans, but the study failed to demonstrate a relationship among EAT volume reduction, coronary atherosclerosis progression and clinical prognosis [
14]; moreover, intensive statin therapy might not be appropriate for Asians. The epidemiological studies and clinical researches show that Asians may have poorer tolerability and safety to intensive statins than white people, owing to genetic differences (variants in structure or polymorphisms) in pharmacokinetics and pharmacodynamics properties [
15‐
17]. It has been claimed that polymorphic variants in cytochrome P450 (CYP450) families that were associated with statin metabolism might result in varying rates of metabolic clearance. CYP450 2C19 slow metabolizer phenotype was reported to be present in approximately 16 % of Asians compared with only about 3 % of white people [
18]. Polymorphic variants in the predominant CYP450 isoform, CYP450 3A4, were reported to be associated with a functional decrease in the enzyme’s activity in dyslipidemic Chinese patients [
19]. The HPS2-THRIVE study recently also indicated that, using same-dose statin treatment, an excess of increased alanine aminotransferase was seen mainly among Chinese patients (more than three consecutive values above the upper limit of normal of 0.24 %/year compared with 0.02 %/year in Europe) [
20]. Moreover, the morbidity of chronic hepatitis B was high in china with nearly 90 million infections. For these reasons, intensive statin therapy may result in higher hepatotoxicity in Asian populations than in white populations, so low- to moderate- dose statin therapy might be more appropriate for Asian populations [
15,
16]. Subjects who undergo weight loss exercise, bariatric surgery, or low-dose aspirin therapy can also reduce EAT volume or inflammation, but the effects are weak and these treatments cannot achieve good results in patients with coronary atherosclerosis progression [
21‐
24]. Our aim is to find a drug that reduces EAT volume while inhibiting the progression of coronary atherosclerosis.
In recent years, studies have confirmed that olmesartan medoxomil can improve endothelial function, resist thrombosis, improve tissue reconstruction, and resist oxidative stress to achieve atherosclerosis resistance [
13,
25‐
28]. The latest research shows that olmesartan medoxomil can better inhibit rat epididymal adipose cell hypertrophy and inflammatory reactions [
29]. Therefore, we hypothesized that olmesartan medoxomil may also reduce EAT volume, finally achieving an anti-atherosclerosis effect.