Fig. 26.1
Summary of statin initiation recommendations for the treatment of blood cholesterol to reduce atherosclerotic cardio-cerebrovascular disease (ASCVD) risk in adults [1]. Colors correspond to the classes of recommendation (green, Class I; yellow, Class IIa; orange, Class IIb). Assessment of the potential for benefit and risk from statin therapy for ASCVD prevention provides the framework for clinical decision making incorporating patient preferences. *Percent reduction in LDL-C can be used as an indication of response and adherence to therapy but is not in itself a treatment goal. †The pooled cohort equations can be used to estimate 10-year ASCVD risk in individuals with and without diabetes. The estimator within this application should be used to inform decision making in primary prevention patients not on a statin. ‡Consider moderate-intensity statin as more appropriate in low-risk individuals. §For those in whom a risk assessment is uncertain, consider factors such as primary LDL-C ≥ 160 mg/dL or other evidence of genetic hyperlipidemias, family history of premature ASCVD with onset <55 years of age in a first-degree male relative or <65 years of age in a first-degree female relative, hs-CRP ≥2 mg/L, CAC score ≥ 300 Agatston units, or ≥75th percentile for age, sex, and ethnicity (for additional information, see http://www.mesa-nhlbi.org/CACReference.aspx), ABI <0.9, or lifetime risk of ASCVD. Additional factors that may aid in individual risk assessment may be identified in the future. ‖Potential ASCVD risk reduction benefits. The absolute reduction in ASCVD events from moderate- or high-intensity statin therapy can be approximated by multiplying the estimated 10-year ASCVD risk by the anticipated relative risk reduction from the intensity of statin initiated (~30% for moderate-intensity statin or ~45% for high-intensity statin therapy). The net ASCVD risk reduction benefit is estimated from the number of potential ASCVD events prevented with a statin, compared to the number of potential excess adverse effects. ¶Potential adverse effects. The excess risk of diabetes is the main consideration in ~0.1 excess cases per 100 individuals treated with a moderate-intensity statin for 1 year and ~0.3 excess cases per 100 individuals treated with a high-intensity statin for 1 year. In RCTs, both statin-treated and placebo-treated participants experienced the same rate of muscle symptoms. The actual rate of statin-related muscle symptoms in the clinical population is unclear. Muscle symptoms attributed to statin therapy should be evaluated. ABI indicates ankle-brachial index, ASCVD atherosclerotic cardiovascular disease, CAC coronary artery calcium, hs-CRP high-sensitivity C-reactive protein, LDL-C low-density lipoprotein cholesterol, MI myocardial infarction, and RCT randomized controlled trial. Reproduced by permission of Circulation [1]
Table 26.1
High-, moderate-, and low-intensity statin therapy
High-intensity statin therapy | Moderate-intensity statin therapy | Low-intensity statin therapy |
---|---|---|
Daily dose lowers LDL-C, on average, by approximately ≥50% | Daily dose lowers LDL-C, on average, by approximately 30% to <50% | Daily dose lowers LDL-C, on average, by <30% |
Atorvastatin (40)–80 mg Rosuvastatin 20 (40) mg | Atorvastatin 10 (20) mg Rosuvastatin (5) 10 mg Simvastatin 40 (80) mg Lovastatin 40 mg Fluvastatin XL 80 mg Fluvastatin 40 mg/bid Pitavastatin 2–4 mg | Simvastatin 10 mg Pravastatin 10–20 mg Lovastatin 20 mg Fluvastatin 20–40 mg Pitavastatin 1 mg |
26.5 Statin, HMG-CoA Reductase Inhibitor, Pharmacologic Characteristics of Statin
Statin has significant LDL-C-lowering effect, and it also has TG-lowering, HDL-C-uprising effect. Its side effects are relatively rare, and with good tolerability, statin is commonly used to treat dyslipidemia nowadays [5]. Currently used statin formulations are as follows (Table 26.2).
Table 26.2
Effect and pharmacological characteristics of currently used statins
Lovastatin | Pravastatin | Simvastatin | Fluvastatin | Atorvastatin | Rosuvastatin | Pitavastatin | |
---|---|---|---|---|---|---|---|
Daily dose, mg | 20–40 | 10–40 | 20–40 | 20–80 | 10–80 | 5–20 | 1–4 |
LDL-C TG HDL-C | |||||||
−24–−28% −8% 4% | 20 | 20 | 40 | 1 | |||
−30–−36% −13–−10% 6% | 40 | 40 | 20 | 80 | 10 | 2 | |
−39–−45% −13–−23% 5–8% | 80 | 40 | 20 | 5 ~ 10 | 4 | ||
−46–−52% −20–−28% 2–10% | 40–80 | 20 | |||||
Metabolism | CYP3A4 | sulfonylation | CYP3A4 | CYP2C9 | CYP3A4 | CYP2C9 | Glucuronidation,CYP2C9 |
Protein binding, %
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