Statins inhibits HMG-CoA reductase (hepatic enzyme responsible for cholesterol synthesis), increases cellular reabsorption of low density lipoprotein cholesterol (LDL) by inducing expression of LDL-receptor and thus, reducing blood levels of LDL-cholesterol, has poor effect increasing serum levels of HDL [20, 21].

It also diminishes the cardiovascular events by reducing endothelial lesion, improving production of nitric oxide and decreasing production of free radicals of oxygen. Statins have anti-inflammatory action and promote atherosclerotic plaque stability, reducing the progression of plaques and diminishing previous lesions [9, 22]. It reduces levels of high-sensitivity C reactive protein, reducing cardiovascular events even though blood cholesterol levels are normal [9, 20, 23, 24].

Most common side effects are myopathy and liver toxicity, in rare cases leading to kidney insufficiency due to rhabdomyolysis [20]. Patients at increased risk for side effects are those at older age, with low body mass index, hypothyroidism, multisystem disease and alcohol abuse, previous renal and hepatic dysfunction, female gender, and in perioperative periods. There are few cases of autoimmune-induced myopathy caused by statins and slight higher rates of diabetes [25]. The risk of side effects is very low especially when compared to impaired risk of cardiovascular event without statin in patients with moderate or high risk [15, 26–28].

The patients should be assessed individually, but in the absence of other risk factors the screening starts at 40 years for man and 50 years (or postmenopausal) for woman [28]. Patients with risk factors, such as current smoking, diabetes, arterial hypertension, obesity (body mass index above 27, waist circumference ≥93 cm for men and ≥90 for women), familial history of premature coronary artery disease or familial hyperlipidemia, rheumatic or inflammatory diseases (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, ankylosing spondylitis, inflammatory bowel diseases), chronic obstructive pulmonary disease, chronic HIV infection and antiretroviral therapy, chronic kidney disease, abdominal aneurysm, genetic dyslipidemias (xanthomas, xanthelasmas, FH), and erectile dysfunction must to be investigated for hyperlipidemia independent of age [16, 28, 29].

Every patient should be evaluated by medical history , physical examination, and blood levels dosage of total cholesterol (TC), LDL, HDL, TG, glucose, and renal function (glomerular filtration rate, GFR). If dosage of LDL isn’t available and triglycerides <400 mg/dL, LDL can be calculated with Friedewald formula LDL = TC − HDL − TG/2.2 (mmol) and LDL = TC − HDL − TG/5 (mg/dL).

Calculating non-HDL cholesterol (total number of atherosclerosis particles) and Apoprotein B promotes better risk evaluation when compared to LDL only in patients with diabetes mellitus or metabolic syndrome. Non-HDL = VLDL + IDL + LDL (VLDL = TC/TG, if TG < 400).

Other markers such as Apoprotein B , Apoprotein A1 , and Lipoprotein(a) may be considered for risk evaluation. Apoprotein B is the most atherogenic of the lipoprotein and has a good correlation with LDL levels. It is considered a second-line marker in risk evaluation and a good predictor of cardiovascular risk [30]. On the other hand, Apoprotein A1, as the major protein of HDL, is correlated with HDL blood levels. Lipoprotein(a) provides complementary information in families with premature cardiovascular disease [15, 16, 28, 29].

Statins are indicated for high blood levels of LDL-cholesterol and for patients with cardiovascular risk ≥7.5 % [31]. For every reduction of 40 mg/dL in LDL-cholesterol, there is a corresponding 24 % reduction in major cardiovascular events [15, 17, 32, 33].

Statins should also be considered for patients with atherosclerosis [9, 31, 34], diabetes mellitus, asymptomatic patients with multiple risk factors (>5 % cardiovascular risk in 10 years), hypertriglyceridemia (TG > 500 mg/dL need statins combined to fibrates), and >21 years with elevated LDL [33]. Low levels of HDL-cholesterol are independent and are an inverse predictor of cardiovascular disease, since for every 1 mg/dL increase in HDL, there is a lowering in 2–3 % for the risk of coronary artery disease .

There is no target LDL-cholesterol to achieve [6, 11, 12, 17]. The main objective of treatment is to decrease LDL level by 50 % or more. For every 1 mmol/L (40 mg/dL) reduction of LDL, cardiovascular morbidity decreases in 22 % [15, 27, 33].

Benefits are seen in reduction:

Regular blood tests, such as cholesterol and fractions , liver function, and non-HDL (includes also apolipoprotein B), should be evaluated to confirm response to treatment and adhesion to treatment [15, 16, 32].

Intensive statin regimens reduce 15 % more cardiovascular events than less intensive therapy and are indicated for patients with peripheral artery disease [8, 9, 38], with 13 % reduction of coronary death and nonfatal myocardial infarction, 19 % reduction of coronary revascularization, and 16 % reduction of ischemic stroke, but with elevation of hepatic enzymes [31, 39]. In more intensive regimens, for each 1 mmol/L (40 mg/dL) reduction in LDL, all-cause mortality and coronary artery disease were reduced in 10 % and 20 %, respectively [15, 17, 18, 27, 29, 40]. Intensive regimen is recommended for patients with >7.5 % CV risk and >75 years without contraindications [33].

High intensive regimen : Atorvastatin 80 mg and rosuvastatin 20–40 mg [33].

Moderate intensive regimen : Atorvastatin 10–20 mg, rosuvastatin 5–10 mg, simvastatin 20–40 mg, pravastatin 40–80 mg, lovastatin 40 mg, fluvastatin 40 mg bid, fluvastatin XL 80 mg, pitavastatin 2–4 mg [33].

Low intensity regimen : Simvastatin 10 mg, pravastatin 10–20 mg, lovastatin 20 mg, fluvastatin 20–40 mg, pitavastatin 1 mg [33].