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Atorvastatin attenuates dyslipidaemia and cardiac dysfunction but it can have undesirable effects including increased risk of diabetes and myalgia. Currently, the proprotein convertase subtilisin\/kexin type 9 (PCSK9) inhibitor efficiently reduces low\u2010density lipoprotein cholesterol (LDL\u2010C) levels more effectively than atorvastatin. We have been suggested that PCSK9 inhibitor attenuated cardiometabolic impairment more effectively than atorvastatin in ovariectomized prediabetic rats. Female Wistar rats (n\u00a0=\u00a048) were fed a normal diet (ND) or high\u2010fat diet (HFD) for 12\u00a0weeks. Then, HFD rats were assigned to a sham\u2010operated (Sham) or ovariectomized (OVX) group. Six weeks after surgery, the OVX group was subdivided into 4 treatment groups: vehicle (HFOV), atorvastatin (HFOA) (40\u00a0mg\/kg\/day; s.c.), PCSK9 inhibitor (HFOP) (4\u00a0mg\/kg\/day; s.c.) and oestrogen (HFOE<jats:sub>2<\/jats:sub>) (50\u00a0\u00b5g\/kg\/day; s.c.) for an additional 3\u00a0weeks. Metabolic parameters, cardiac and mitochondrial function, and [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> transients were evaluated. All HFD rats became obese\u2010insulin resistant. HFS rats had significantly impaired left ventricular (LV) function, cardiac mitochondrial function and [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> transient dysregulation. Oestrogen deprivation (HFOV) aggravated all of these impairments. Our findings indicated that the atorvastatin, PCSK9 inhibitor and oestrogen shared similar efficacy in the attenuation in cardiometabolic impairment in ovariectomized prediabetic rats.<\/jats:p>","DOI":"10.1111\/jcmm.15556","type":"journal-article","created":{"date-parts":[[2020,7,6]],"date-time":"2020-07-06T13:19:17Z","timestamp":1594041557000},"page":"9189-9203","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["PCSK9 inhibitor and atorvastatin reduce cardiac impairment in ovariectomized prediabetic rats via improved mitochondrial function and Ca<sup>2+<\/sup> regulation"],"prefix":"10.1111","volume":"24","author":[{"given":"Patchareeya","family":"Amput","sequence":"first","affiliation":[{"name":"Cardiac Electrophysiology Research and Training Center Faculty of Medicine Chiang Mai University Chiang Mai Thailand"},{"name":"Cardiac Electrophysiology Unit Department of Physiology Faculty of Medicine Chiang Mai 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