Abstract
Hyperlipidemia is a major risk factor for cardiovascular morbidity and mortality. Statins are the first-choice therapy for dyslipidemias and are considered the cornerstone of atherosclerotic cardiovascular disease (ASCVD) in both primary and secondary prevention. Despite the statin-therapy-mediated positive effects on cardiovascular events, patient compliance is often poor. Statin-associated muscle symptoms (SAMS) are the most common side effect associated with treatment discontinuation. SAMS, which range from mild-to-moderate muscle pain, weakness, or fatigue to potentially life-threatening rhabdomyolysis, are reported by 10% to 25% of patients receiving statin therapy. There are many risk factors associated with patient features and hypolipidemic agents that seem to increase the risk of developing SAMS. Due to the lack of a “gold standard”, the diagnostic test for SAMS is based on a clinical criteria score, which is independent of creatine kinase (CK) elevation. Mechanisms that underlie the pathogenesis of SAMS remain almost unclear, though a high number of risk factors may increase the probability of myotoxicity induced by statin therapy. Some of these, related to pharmacokinetic properties of statins and to concomitant therapies or patient characteristics, may affect statin bioavailability and increase vulnerability to high-dose statins.
Highlights
Published: 28 October 2021Hyperlipidemia is a major risk factor for cardiovascular morbidity and mortality.Statins [3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA) inhibitors] are the first-choice therapy for dyslipidemias and are considered the cornerstone of Atherosclerotic cardiovascular disease (ASCVD) prevention [1]
This review aims to improve diagnostic and therapeutic Statin-associated muscle symptoms (SAMS) approaches in order to increase statin adherence and reduce cardiovascular events
Inhibition of HMG-CoA reductase induced by statin therapy results in lowering of several pathway intermediates, such as dolychols, prenylated proteins, electron transport chain proteins, and ubiquinone/coenzyme Q10, which is involved in oxidative phosphorylation [88]
Summary
Hyperlipidemia is a major risk factor for cardiovascular morbidity and mortality. Statins [3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA) inhibitors] are the first-choice therapy for dyslipidemias and are considered the cornerstone of Atherosclerotic cardiovascular disease (ASCVD) prevention [1]. Farnesyl pyrophosphate and geranylgeranyl pyrophosphate, other intermediates of the mevalonate pathway, are essential for the prenylation of lamins and guanosine-5’-triphosphate (GTP)binding proteins These proteins, need prenylation in order to control cytoskeleton organization and intracellular vesicular transport, promoting muscles’ cell function, growth, and differentiation [6,7,8,9]. Statins are no longer capable of inducing apoptosis in muscle cells once the protein geranylgeranylation is restored by mevalonate, farnesol, or geranylgeraniol [14]. The purpose of this manuscript is to give an update on SAMS diagnosis and pathophysiological mechanisms, focusing on the most effective strategies for statin intolerance clinical management, including new emerging alternative therapies. This review aims to improve diagnostic and therapeutic SAMS approaches in order to increase statin adherence and reduce cardiovascular events
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