Abstract
Statins are effective lipid-lowering drugs with a good safety profile that have become, over the years, the first-line therapy for patients with dyslipidemia and a real cornerstone of cardiovascular (CV) preventive therapy. Thanks to both cholesterol-related and “pleiotropic” effects, statins have a beneficial impact against CV diseases. In particular, by reducing lipids and inflammation statins, they can influence the pathogenesis of both myocardial infarction and diabetic cardiomyopathy. Among inflammatory mediators involved in these diseases, interleukin (IL)-1β is a pro-inflammatory cytokine that recently been shown to be an effective target in secondary prevention of CV events. Statins are largely prescribed to patients with myocardial infarction and diabetes, but their effects on IL-1β synthesis and release remain to be fully characterized. Of interest, preliminary studies even report IL-1β secretion to rise after treatment with statins, with a potential impact on the inflammatory microenvironment and glycemic control. Here, we will summarize evidence of the role of statins in the prevention and treatment of myocardial infarction and diabetic cardiomyopathy. In accordance with the dual lipid-lowering and anti-inflammatory effect of these drugs and in light of the important results achieved by IL-1β inhibition through canakinumab in CV secondary prevention, we will dissect the current evidence linking statins with IL-1β and outline the possible benefits of a potential double treatment with statins and canakinumab.
Highlights
Statin discovery dates back to 1976, when mevastatin was isolated from cultures of Penicillium citrinum and proven to inhibit the production of cholesterol molecules [1]
We aim to summarize evidence of the role of statin treatment in myocardial infarction and prevention of myocardial remodeling in patients with diabetes mellitus
Statins are recommended for prevention of myocardial infarction in patients with dyslipidemia, high, or very high cardiovascular risk
Summary
Statin discovery dates back to 1976, when mevastatin was isolated from cultures of Penicillium citrinum and proven to inhibit the production of cholesterol molecules [1]. The statin-related reduction of circulatory lipoprotein induces the hepatic expression of low-density lipoprotein (LDL) receptor (LDLR) and LDL clearance from the bloodstream, accounting for a further decrease in circulating cholesterol levels [3] Thanks to this dual mechanism of action and a good safety profile, both natural and synthetic statins became, over the years, the first-line therapy for dyslipidemia patients and a real cornerstone of cardiovascular (CV) preventive therapy. Soon after first trials with statins were published, evidence suggested that those compounds might have putative, non-lipid-related effects Both Cholesterol and Recurrent Events (CARE) and Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) trials showed that their overall cardiovascular benefit was disproportionate to the magnitude of lipid reduction [4,5]. In accordance with the dual lipid-lowering and anti-inflammatory effect of these drugs and in light of the important results achieved by CANTOS in CV secondary prevention, we dissect the current evidence linking statins with IL-1β and outline possible benefits of double treatment with canakinumab
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