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PCSK9 inhibition and cardiovascular outcomes by heart failure status: a pooled analysis of SPIRE-1 and SPIRE-2
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DOI：10.1093/ejhf/xuag166.png)
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Abstract
En 中文
Heart failure (HF) remains a major cause of cardiovascular mortality, developing from diverse risk factors including hypertension, metabolic disease, and ischaemic heart disease, which drive microvascular changes and fibrosis.1 While proprotein convertase subtilisin/kexin type 9 (PCSK9) is well characterized for its hepatic regulation of LDL receptors, it is also expressed in the myocardium, where it modulates fibrosis and inflammation.2
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