A Collaborative Approach Statin Use Materials

LOWERING THE RISK: A COLLABORATIVE APPROACH TO STATIN THERAPY

Faculty:

The following continuing medical education team members were involved in the initial planning, development, authoring, and/or reviewing of this activity:

L. Austin Fredrickson, MD, FACP 

L. Austin Fredrickson is an Associate Professor of Internal Medicine at Northeast Ohio Medical University, where he serves as core faculty and teaches diagnostics, therapeutics, clinical skills, and health humanities. He is board-certified in general internal medicine and practices rural primary care. 

Liz Fredrickson, PharmD, BCPS

Liz Fredrickson, PharmD, BCPS, is an Associate Professor of Pharmacy Practice and Pharmaceutical Sciences at the Northeast Ohio Medical University (NEOMED) College of Pharmacy, where she is course director of the Parenteral Products and Basic Pharmaceutics Lab courses.

Pamela Sardo, PharmD, BS

Pamela Sardo, PharmD, BS, is a freelance medical writer and licensed pharmacist. She is the founder and principal at Sardo Solutions in Texas. Pam received her BS from the University of Connecticut and her PharmD from the University of Rhode Island. Pam’s career spans many years in retail, clinics, hospitals, long-term care, Veterans Affairs, and managed health care responsibilities across a broad range of therapeutic classes and disease states.

Topic Overview

Statins remain the cornerstone of atherosclerotic cardiovascular disease (ASCVD) prevention and are among the most commonly prescribed medications worldwide. These medications are generally safe and well-tolerated, with clinical trials consistently demonstrating their ability to lower LDL cholesterol and improve a patient’s long-term prognosis. Beyond lowering cholesterol levels, statins also have important pleiotropic effects, including decreasing systemic inflammation, lowering C-reactive protein and pro-inflammatory cytokines, improving endothelial function, and regulating hepatic LDL-receptor-related protein. Evidence also supports the use of statin therapy in individuals without established ASCVD but with elevated inflammatory markers, underscoring the importance of these markers in disease prevention. This continuing education activity provides learners with a practical, contemporary overview of statin therapy, including evidence-based use, key patient counseling considerations, and common safety concerns. Learners will also explore the roles of the interprofessional healthcare team in managing statin therapy, with an emphasis on communication, patient education, and collaborative care planning.

Accreditation Statements

In support of improving patient care, RxCe.com LLC is jointly accredited by the Accreditation Council^TM for Continuing Medical Education (ACCME^®), the Accreditation Council for Pharmacy Education (ACPE^®), and the American Nurses Credentialing Center (ANCC^®), to provide continuing education for the healthcare team.

This activity was planned by and for the healthcare team, and learners will receive 3 Interprofessional Continuing Education (IPCE) credits for learning and change.

Joint Universal Activity Number: The Joint Accreditation Universal Activity Numbers assigned to this activity are as follows:

Pharmacists: JA4008424-0000-26-003-H01-P

Pharmacy Technicians: JA4008424-0000-26-003-H01-T

Credits: 3 contact hour(s) (0.3 CEU(s)) of continuing education credit.

Credit Types:

IPCE Credits - 3 Credits

AAPA Category 1 Credit™️ - 3 Credits

AMA PRA Category 1 Credit™️ - 3 Credits

Pharmacy - 3 Credits

Type of Activity: Knowledge

Media: Computer-Based Training (i.e., online courses)

Estimated time to complete activity: 3 contact hour(s) (0.3 CEU(s)), including Course Test and course evaluation.

Release Date: January 12, 2026 Expiration Date: January 12, 2029

Target Audience: This educational activity is for Physicians, Physician Assistants, Pharmacists, and Pharmacy Technicians

How to Earn Credit: From January 12, 2026, through January 12, 2029, participants must:

Read the “learning objectives” and “author and planning team disclosures;”

Study the section entitled “educational activity;” and

Complete the Course Test and Evaluation form. The Course Test will be graded automatically. Following successful completion of the Course Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)

CME Credit: Credit for this course will be uploaded to CPE Monitor® for pharmacists. Physicians may receive AMA PRA Category 1 Credit™ and use these credits toward Maintenance of Certification (MOC) requirements. Physician Assistants may earn AAPA Category 1 CME credit, reportable through PA Portfolio. All learners should verify their individual licensing board's specific requirements and eligibility criteria.

Learning Objectives: Upon completion of this educational activity, participants should be able to:

Identify evidence-based recommendations for statin use in primary and secondary prevention of ASCVD

Describe the mechanisms of action and pharmacologic differences among available statin medications

Recognize common adverse effects, drug–drug interactions, and monitoring recommendations for statin therapy

Recall how healthcare team members can collaborate to optimize patient outcomes with statin therapy

Disclosures

The following individuals were involved in planning, developing, and/or authoring this activity: L. Austin Fredrickson, MD, FACP; Liz Fredrickson, PharmD, BCPS; and Pamela Sardo, PharmD, BS. None of the individuals involved in developing this activity has a conflict of interest or financial relationships related to the subject matter. There are no financial relationships or commercial or financial support relevant to this activity to report or disclose by RxCe.com or any of the individuals involved in the development of this activity. 

© RxCe.com LLC 2026: All rights reserved. No reproduction of all or part of any content herein is allowed without the prior, written permission of RxCe.com LLC.

Educational Activity

Lowering the Risk: A Collaborative Approach to Statin Use

Introduction

Statins remain the cornerstone of atherosclerotic cardiovascular disease (ASCVD) prevention and are among the most commonly prescribed medications worldwide. These medications are generally safe and well-tolerated, with clinical trials consistently demonstrating their ability to lower LDL cholesterol and improve a patient’s long-term prognosis. This continuing education activity provides learners with a practical, contemporary overview of statin therapy, including evidence-based use, key patient counseling considerations, and common safety concerns. Learners will also explore the roles of the interprofessional healthcare team in managing statin therapy, with an emphasis on communication, patient education, and collaborative care planning.

Atherosclerotic Cardiovascular Disease (ASCVD)

Heart disease remains the leading cause of death in the United States (US), accounting for nearly one million deaths in 2023.^1,2 Atherosclerotic cardiovascular disease (ASCVD), which includes coronary artery disease (CAD), cerebrovascular disease, and peripheral arterial disease (PAD), is also the leading cause of mortality worldwide.^3,4,5 Numerous studies have established a strong relationship between ASCVD and lipoproteins, with evidence supporting the use of pharmacologic therapies to lower lipoprotein levels.⁶ The 2018 American Heart Association (AHA)/American College of Cardiology (ACC) guidelines recommend that all adults with established ASCVD receive statin therapy.⁷

Statins are generally safe and well-tolerated, with clinical trials consistently demonstrating their ability to lower LDL cholesterol and improve patients’ long-term prognosis.⁷ They also have important pleiotropic effects, including decreasing systemic inflammation, lowering C-reactive protein and pro-inflammatory cytokines, improving endothelial function, and regulating hepatic LDL-receptor-related protein.⁷ Evidence supports statin therapy in individuals without established ASCVD but with elevated inflammatory markers, highlighting their importance in the prevention of disease as well.⁸

Lipoproteins: The Good, The Bad, and the Ugly

Lipoproteins transport cholesterol and triglycerides throughout the body.^5,9 Apolipoproteins are also found on the surface of lipoproteins and aid in lipoprotein transportation, binding, and function.^9,10 Classes of plasma lipoproteins are separated based on size, composition, and apolipoproteins.^9,10 These include very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), high-density lipoprotein (HDL), chylomicron remnants, and lipoprotein(a) (Lp(a)).⁶ Table 1 details the roles of lipoproteins.^7,9

Table 1

Role of Lipoproteins^7,9,10

Lipoprotein	Role	Atherogenicity
LDL-C	Dominant form of atherogenic cholesterol	Atherogenic
VLDL	Chief carrier of triglycerides	Atherogenic
HDL-C	Returns cholesterol to the liver	Not atherogenic
Chylomicrons	Transports dietary fat	Uncertain

Dietary lipids (“cholesterol”) are incorporated into chylomicrons in the intestines and ultimately absorbed in the liver for processing.⁹ Before hepatic processing, chylomicrons are metabolized by lipoprotein lipase in the circulation, which releases triglycerides for muscle and adipose tissues to utilize.⁹ After this, chylomicron remnants are absorbed in the liver.⁵ Dietary glucose is also delivered to the liver and converted to cholesterol via 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase.⁵ Targeting this enzyme stops cholesterol synthesis.⁵

The human body can produce lipoproteins endogenously by forming VLDL in the liver.⁹ In circulation, adipose and muscle tissue utilize lipoprotein lipase to release free fatty acids from VLDL, and VLDL then becomes IDL.⁹ IDL is further metabolized into LDL, which can deposit its cholesterol into peripheral tissues.⁹ This atherogenic property is what leads to endovascular plaque formation.⁹ In contrast, HDL is responsible for recycling deposited lipids from peripheral tissues back into the liver for processing.⁹ HDL is considered non-atherogenic and can be protective against endovascular plaque formation and ASCVD.⁹

In summary, HDL cholesterol (HDL-C) is “good” as it reduces plaque deposition.⁵ Non-HDL cholesterol (namely LDL-C but also VLDL-C) can be atherogenic, so many patients refer to their LDL cholesterol (LDL-C) as “bad” cholesterol.⁵ Although this is simplistic, it can help patients identify the components of their lipid profiles and why each is important. By understanding which therapies target which problematic levels and subsequently tracking progress over time, patients can be more motivated to adhere to recommended therapies. When individual lipoprotein properties are not understood, patients and prescribers may resort to monitoring only ‘total’ cholesterol levels. A more thorough understanding of lipoprotein composition and function can help guide therapeutic interventions.

Lipid Pathophysiology and ASCVD

Over time, excess cholesterol can be deposited by LDL-C particles underneath the tunica intima layer of blood vessels.¹¹ Initially, this forms as a small fatty streak, but over time, the fatty streak can enlarge into a more voluminous plaque (Figure 1).⁷ This plaque can stabilize and form a thick fibrous shell, leading to decreased blood flow through that vessel.¹¹ If the plaque grows too quickly or too large, the core will only be contained by a thin fibrous layer, making it more vulnerable to rupture.^5,11

Figure 1

ASCVD Pathophysiology⁷

When plaque ruptures through the intima (inner) layer of the blood vessel, the body senses the blood vessel damage. It aims to minimize blood loss by initiating fibrinogenic and thrombotic processes aimed at ‘clotting’ the ruptured area.⁵ Unfortunately, the thrombus (clot) that forms can obstruct the vessel, and organ areas that are supplied by blood flow distal to this lesion may lose their oxygenation and die.⁵ This process of ischemia (loss of blood flow/oxygenation) can ultimately lead to organ injury (infarction).⁵ When a thrombus occurs in a coronary blood vessel, this leads to myocardial (heart) infarction, known as an MI, or ‘heart attack’.⁵ When it occurs in cerebral vessels, it is known as cerebral infarction or ‘ischemic stroke.’⁵ This disruption of blood flow can occur in any artery or arteriole, putting the organ that it supplies at risk of injury.⁵

In contrast, if the plaque grows slowly over time and stabilizes with a fibrous shell, it may not rupture and cause thrombosis.⁵ However, the gradual stenosis (narrowing) of these vessels can also cause damage.⁵ If blood flow is diminished enough, this can cause functional ischemia.⁵ This accounts for the phenomenon of angina (chest pain) in patients with chronically tight coronary vessels or claudication in patients with peripheral arterial disease.

ASCVD: Who is at Risk?

Several factors have been associated with the development of ASCVD. These include independent risk factors (Table 2), which individually contribute to risk, and risk-enhancing factors (Table 3).⁵ Of the longstanding known risk factors, several are nonmodifiable patient characteristics: sex (male), age (≥45 in males, ≥55 in females), and a family history of early cardiac disease (≤ 55 for male relatives, ≤ 65 for female relatives).⁷

Table 2

Independent Risk Factors for ASCVD^7,12

Nonmodifiable	Modifiable
Male	Lipid disorders
Age Males ≥ 45 Females ≥ 55	Cigarette smoking
Family history Males < 55 Females < 65	Hypertension
	Diabetes
	Lifestyle -Obesity -Inactivity -Atherogenic diet -Stress

Table 3

Risk-Enhancing Factors of ASCVD^7,12

Family history of premature ASCVD (males, age <55 years old; females, age <65 years old)

Primary hypercholesterolemia (LDL-C, 160–189 mg/dL [4.1–4.8 mmol/L); non–HDL-C 190–219 mg/dL [4.9–5.6 mmol/L])∗

Metabolic syndrome (increased waist circumference, elevated triglycerides [>150 mg/dL], elevated blood pressure, elevated glucose, and low HDL-C [<40 mg/dL in men; <50 mg/dL in women]) is a factor; a tally of 3 makes the diagnosis)

Chronic kidney disease (eGFR 15–59 mL/min/1.73 m2 with or without albuminuria; not treated with dialysis or kidney transplantation)

Chronic inflammatory conditions such as psoriasis, RA, or HIV/AIDS

History of premature menopause (before age 40) and history of pregnancy-associated conditions that increase later ASCVD risk, such as preeclampsia

High-risk race/ethnicities (e.g., South Asian ancestry)

Lipid/biomarkers: Associated with increased ASCVD risk

Persistently∗ elevated, primary hypertriglyceridemia (≥175 mg/dL)

Elevated high-sensitivity C-reactive protein (≥2.0 mg/L)

Elevated Lp(a): A relative indication for its measurement is a family history of premature ASCVD. An Lp(a) ≥50 mg/dL or ≥125 nmol/L constitutes a risk-enhancing factor, especially at higher levels of Lp(a).

While nothing can be done to mitigate non-modifiable factors, noting them can be very helpful in identifying patients at a naturally higher risk of ASCVD.⁷ Importantly, an interprofessional care team—including physicians, nurses, dietitians, behavioral health providers, and care coordinators—can collaborate to support sustainable changes, monitor progress, address barriers, and reinforce consistent messaging for patients. This team-based approach ensures that patients receive comprehensive, coordinated strategies to reduce their overall cardiovascular risk.

Other risk factors can be modified and are the focus of therapeutic efforts in primary (prevention) and secondary (treatment) prophylaxis.⁵ Lipid disorders, cigarette smoking, hypertension, and diabetes all increase that risk, and each can be modified.⁵ Lifestyle factors are also modifiable, including an atherogenic diet, inactivity, obesity, and potentially stress-related factors.⁵ By recognizing the lifestyle components of all the risk factors, the care team can share the job of ASCVD risk reduction with the patient.

ASCVD risk factors can be estimated using risk calculators, including the 10-year ASCVD risk calculator from the American College of Cardiology.¹³ Care teams can input patient demographics and results into this calculator, and a score results to help guide therapy.¹³ In general, higher-scoring patients are most likely to benefit from lipid-lowering interventions and medications.¹³ By combining this level with the other risk-enhancing factors, patients can be better informed during risk-benefit conversations.

The AHA’s new PREVENT equations (for patients ages 30–79) often yield lower 10-year ASCVD risk than the Pooled Cohort Equations, which can shrink statin eligibility at the margins.¹⁴ Numerous validation and comparison studies have shown lower predicted risks and substantial reclassification to lower-risk groups.¹⁴ Until cholesterol guidance updates thresholds, the AHA advises using PREVENT mainly to inform broader CVD discussions (10- and 30-year CVD/ASCVD/HF risk).¹⁴

Patient Case

Mr. J is a 62-year-old man with type 2 diabetes, hypertension, and a family history of premature CAD. His most recent labs reveal LDL-C 148 mg/dL, HDL-C 38 mg/dL, and triglycerides 180 mg/dL. His ASCVD 10-year risk is calculated at 22%. He currently takes metformin, lisinopril, and aspirin.

Statins: First-line Lipid-Lowering Therapy

Statins are competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-controlling step in cholesterol synthesis.⁵ By blocking this enzyme, less endogenous cholesterol is created, which leads to an increased expression of hepatic LDL receptors, which in turn increases the clearance of LDL from circulation.⁵ By increasing the clearance of circulating LDL and decreasing the synthesis of LDL, statins effectively lower LDL-C.⁵ These medications have also been found to have pleiotropic effects and exert anti-inflammatory, antioxidant, antiproliferative, and immunomodulatory effects.¹⁴ Through these actions, they can stabilize plaques and prevent the aggregation of platelets.¹⁴ Within the COSMOS trial, patients taking rosuvastatin had significant decreases in plaque volume that were unrelated to the level of LDL-C reduction they experienced.¹⁵

Numerous randomized controlled trials have demonstrated that statins decrease the risk of ASCVD. A meta-analysis of 14 statin trials found that for each 38.7mg/dL reduction in LDL-C, there was a 21% relative reduction in ASCVD risk.¹⁶ Doubling the dose of statins generally lowers LDL-C levels by about six percent.¹⁶ However, in clinical practice, the absolute responses of LDL-C reduction to statin therapy depend on a patient’s baseline LDL-C concentrations. Patients with higher baseline LDL-C concentrations can benefit more from LDL-C lowering than those who are near their LDL-C baseline goals.⁷ With this in mind, the goal of statin therapy is not only LDL-C reduction but a reduction in ASCVD events (stroke and myocardial infarctions) and ultimately a reduction in patient morbidity and mortality.⁷

Who Needs a Statin: Using the Latest Guidelines

The FDA-approved indications for statins include hyperlipidemia and mixed dyslipidemia, primary dysbetalipoproteinemia, hypertriglyceridemia, atherosclerosis, primary prevention of ASCVD, secondary prevention in patients with clinical ASCVD, familial hypercholesterolemia, and homozygous familial hypercholesterolemia.^17-23

Statin therapy for primary prevention is recommended or should be considered in the following scenarios:⁷

High-intensity statin therapy should be considered for patients with severe primary hypercholesterolemia (LDL-C ≥ 190 mg/dL).

Statin therapy should be considered for young adults between 20 and 39 years who are high-risk (family history of premature CAD and very high LDL-C ≥160 mg/dL).

Moderate-intensity statin therapy is recommended for patients between 40 and 75 years of age with diabetes who are at intermediate or high risk of future ASCVD.

High-intensity statin therapy is recommended for patients between 40 and 75 years of age with diabetes-specific risk factors (≥ 10 years for T2DM or ≥20 years for type 1 DM or albuminuria, retinopathy, neuropathy, eGFR<60 mL/min/1.73 m² or ankle-brachial index <0.9).

High-intensity statin therapy should be considered for patients between 40 and 75 years of age with ASCVD > 20% (high risk) over ten years.⁷

Moderate-intensity statin therapy should be considered for patients between 40 and 75 years of age with ASCVD ≥ 7.5 to < 20% (moderate risk) over ten years.

Moderate-intensity statin therapy should be considered for patients between 40 and 75 years of age with ASCVD 5% to <7 .5% (high risk) over ten years if risk enhancers are present.

Consider statin therapy for patients with a family history of premature CAD and very high LDL-C (≥160 mg/dL) who are between the ages of 20 and 39.⁷

Certain patients with an intermediate risk (≥7.5% to <20%) or at borderline risk (5% to <7.5%) may require statin therapy.⁷ Coronary artery calcium can be measured via a computed tomography (CT) scan.⁷ This lower-dose CT can then be used to dictate statin therapy by the following.⁷

CAC is 0 Agatston units: no statin is required unless there is a history of diabetes mellitus, a family history of premature CHD, or cigarette smoking is present

CAC is 1 to 99 Agatston units: consider statin therapy

CAC is greater than 100 Agatston units: initiate statin therapy

The more calcium found in the coronary arteries, the stronger the recommendation to initiate statin therapy.⁷ It is implied that calcium suggests plaque and that with increasing levels of calcium beyond simply age-related calcification, plaque burden should be treated with lipid-lowering medication in this intermediate population.⁷ For those of higher risk based on their 10-year ASCVD calculation, where lipids are recommended anyway, then it would provide unnecessary radiation and cost, so it is not recommended as a screening parameter in those patients.⁷

For adults 75 years of age or older, the guidelines suggest initiating a moderate-intensity statin may be reasonable when LDL-C levels are between 70 and 189mg/dL.⁷ For patients 76-80 years of age with the same 70-189mg/dL category, measuring CAC may be useful to avoid statin therapy with a CAC score of zero.⁷ In those patients, with a shorter life expectancy and no evidence of current plaque burden, the benefit of statin therapy may be limited; hence, statin therapy is not recommended.⁷ Guidelines further suggest that it may be reasonable to stop statin therapy when functional decline (physical or cognitive), multimorbidity, frailty, or reduced life expectancy limit the potential benefits of statin therapy for ASCVD prevention.⁷

The United States Preventative Service Task Force (USPSTF) generally agrees with primary prevention of ASCVD via statin therapy for adults 40-75 years old who have 1 or more risk factors (i.e., dyslipidemia, diabetes, hypertension, or smoking) and an estimated 10-year risk of a cardiovascular event (grade B), and selectively offer it for those with an estimated 10-year risk of events between 7.5-10% (grade C).²⁴

Secondary Prevention

Secondary prevention of ASCVD aims to prevent worsening or recurrent clinical ASCVD after an event.⁷ Patients who have had clinical ASCVD are subdivided into those at very high risk and those who are not.⁷ Very high-risk patients include those with a history of multiple major ASCVD events or 1 major ASCVD event and multiple high-risk conditions, as depicted in Table 4 below.⁷

Table 4

ASCVD Major Events and High-Risk Conditions⁷

Major ASCVD Events

Recent ACS (within the past 12 mo)

History of MI (other than recent ACS event listed above)

History of ischemic stroke

Symptomatic peripheral arterial disease (history of claudication with ABI <0.85, or previous revascularization or amputation)

High-Risk Conditions

Age ≥65 years

Heterozygous familial hypercholesterolemia

History of prior coronary artery bypass surgery or percutaneous coronary intervention outside of the major ASCVD event(s)

Diabetes mellitus

Hypertension

CKD (eGFR 15-59 mL/min/1.73 m2)

Current smoking

Persistently elevated LDL-C (LDL-C ≥100 mg/dL) despite maximally tolerated statin therapy and ezetimibe

History of congestive heart failure

For patients not at high risk who are 75 years of age or younger, the guidelines recommend initiating high-intensity statin therapy with a goal LDL-C reduction of at least 50%.⁷ Patients who are 75 years of age may start a moderate- or high-intensity statin (or continue a high-intensity statin).⁷ For those at very high risk, the guidelines recommend initiating high-intensity or maximal statin, and if LDL-C is not less than 70mg/dL, consider adding on additional anti-lipid therapies such as ezetimibe or PCSK9 inhibitors.⁷

Special Populations

The American Diabetes Association (ADA) Standards of Care recommend intensive LDL-C lowering for adults with diabetes.²⁵ Suggestions include the use of high-intensity statins for those with diabetes and ASCVD, to target ≥50% LDL-C reduction and treat to <70 mg/dL for primary prevention in most adults 40–75 years and <55 mg/dL for secondary prevention.²⁵

Healthy Lifestyle: Before, During, and After Statins

For decades, guidelines have recommended healthy lifestyles to promote health and reduce disease. The most recent guidelines also support initiating and maintaining a healthy lifestyle as a baseline for all patients, regardless of their ASCVD risk.⁷ The 2018 ACC/AHA guidelines specifically recommend adopting a dietary pattern that prioritizes the consumption of vegetables, fruits, whole grains, and legumes.⁷ In addition, patients are encouraged to choose healthy protein sources such as low-fat dairy products, skinless poultry, fish and other seafood, and nuts.⁷ Benefits of incorporating nontropical vegetable oils as part of a balanced diet aimed at reducing cardiovascular risk have also been noted.⁷

Each patient’s comorbidities, as well as personal and cultural food needs, restrictions, and preferences, should be considered in any recommended diet, and the diet should be adjusted for appropriate caloric requirements.⁷ This caloric requirement ought to be modified to avoid weight gain and metabolic syndrome.⁵ In obese or overweight patients, diets should be recommended that will assist with weight loss.⁷

Beyond diet, lifestyle recommendations should include healthy exercise routines, which are also patient-centered.⁷ As a general rule, adult patients are advised to engage in 3-4 sessions per week of moderate- to vigorous-intensity aerobic physical exercise, lasting on average 40 minutes per session.⁷ Regardless of what medications are recommended, these baseline healthy lifestyle conditions should be encouraged.⁷ However, just as plaque buildup does not occur overnight, these lifestyle habits can take time to become fully implemented into patient routines. Interprofessional care team members play a vital role in educating patients, reinforcing lifestyle strategies, monitoring progress, and providing ongoing support to reduce ASCVD risk over time.

Statin Comparisons

The FDA-approved statins include atorvastatin, simvastatin, rosuvastatin, pitavastatin, lovastatin, pravastatin, and fluvastatin. Statin doses for primary and secondary prevention of ASCVD (in patients without diabetes) are listed in Table 5.^17-23

Table 5

Statin Doses for Primary and

Secondary Prevention of ASCVD^17-23

Brand/Generic	Primary Prevention	Secondary Prevention
Atorvastatin (Lipitor)	ASCVD 10-year risk of 5-<7.5%: 10- 20 mg once daily ASCVD 10-year risk ≥7.5 to <20%: 10-20 mg once daily ASCVD 10-year risk ≥20%: 40-80 mg once daily	High-intensity therapy: 80 mg once daily
Fluvastatin (Lescol XL)	ASCVD 10-year risk of 5-<7.5%: 40 mg twice daily (IR) or 80 mg once daily (ER) ASCVD 10-year risk ≥7.5 to <20%: 40 mg twice daily (IR) or 80 mg once daily (ER) ASCVD 10-year risk ≥20%:* 40 mg twice daily (IR) or 80 mg once daily (ER)	Moderate-intensity therapy:* 40 mg twice daily (IR) or 80 mg once daily (ER)
Lovastatin (Altoprev)	ASCVD 10-year risk of 5-<7.5%: 40-80 mg once daily (IR) or 40-60 mg once daily (ER) ASCVD 10-year risk ≥7.5 to <20%: 40-80 mg once daily (IR) or 40-60 mg once daily (ER) ASCVD 10-year risk ≥20%:* 40-80 mg once daily (IR) or 40-60 mg once daily (ER)	Moderate-intensity therapy:* 40-80 mg once daily (IR) or 40-60 mg once daily (ER)
Pitavastatin (Livalo)	ASCVD 10-year risk of 5-<7.5%: 1-4 mg once daily ASCVD 10-year risk ≥7.5 to <20%: 1-4 mg once daily ASCVD 10-year risk ≥20%:* 1-4 mg once daily	Moderate-intensity therapy:* 1-4 mg once daily
Pravastatin (Pravachol)	ASCVD 10-year risk of 5-<7.5%: 40-80 mg once daily ASCVD 10-year risk ≥7.5 to <20%: 40-80 mg once daily ASCVD 10-year risk ≥20%:* 40-80 mg once daily	Moderate-intensity therapy:* 40-80 mg once daily
Rosuvastatin (Crestor)	ASCVD 10-year risk of 5-<7.5%: 5-10 mg once daily ASCVD 10-year risk ≥7.5 to <20%: 5-10 mg once daily ASCVD 10-year risk ≥20%: 20-40 mg once daily	High-intensity therapy: 20-40 mg once daily
Simvastatin (Zocor)	ASCVD 10-year risk of 5-<7.5%: 20-40 mg once daily ASCVD 10-year risk ≥7.5 to <20%: 20-40 mg once daily ASCVD 10-year risk ≥20%:* 20-40 mg once daily	Moderate-intensity therapy:* 20-40 mg once daily

*For patients unable to tolerate high-intensity statin therapy

Statins differ in many respects, so the choice of statin should be patient-oriented. Important attributes to consider when recommending which statin to use include cost (to the patient and any applicable insurers), intensity (the efficacy or strength with which it has been shown to lower LDL-C in populations), medication interactions, and adverse event potential (including if the patient has had a history of adverse events to statins previously). Statin intensity is shown in Table 6 below, which presents the expected decrease in LDL-C concentrations for high-intensity (LDL-C reduction of at least half the original value), moderate (LDL-C reduction of 30-49%), and low (LDL-C reduction of less than 30%).^7,17-23

Table 6

High- Moderate- and Low-Intensity Statin Therapy^7,17-23

	High	Moderate	Low
LDL-C ↓	≥50%	30%–49%	<30%
Statins	Atorvastatin 40-80 mg Rosuvastatin 20-40 mg	Atorvastatin 10-20 mg Rosuvastatin 5-10 mg Simvastatin 20–40 mg Pravastatin 40-80 mg Lovastatin 40-80 mg Fluvastatin XL 80 mg Fluvastatin 40 mg BID Pitavastatin 1–4 mg	Simvastatin 10 mg Pravastatin 10–20 mg Lovastatin 20 mg Fluvastatin 20–40 mg

The pharmacokinetic properties of statins can also be compared.^18-24 Lipophilic statins include atorvastatin, simvastatin, fluvastatin, pitavastatin, and lovastatin.^17-23 These agents are absorbed faster than their hydrophilic counterparts (rosuvastatin and pravastatin).^17-23 Lipophilic statins can also enter cells by passive diffusion and are widely distributed across various tissues.⁵

Table 7

Pharmacokinetic Properties of Statins^17-23

Statin	Half-life (hrs)	Bioavailability (%)	Protein binding (%)	CYP P450 metabolism
Atorvastatin	14-30	14	>98	3A4
Fluvastatin	3-10.5	24-29	98	2C9/3A4
Lovastatin	1.1-1.7	Increased with ER tablets	>95	3A4
Pitavastatin	12	51	>99	---
Pravastatin	2-3	17	50	---
Rosuvastatin	19	20	88	---
Simvastatin	---	<5	95	Hepatic via CYP3A4

Protein binding will affect statin distribution and the efficacy of these drugs because only free “unbound” drugs can cause therapeutic effects. Except for pravastatin, all statins are highly protein-bound.⁵ CYP metabolism is an important consideration for statins, with CYP3A4 metabolizing atorvastatin, lovastatin, and simvastatin.⁵ CYP2C9 metabolizes fluvastatin and rosuvastatin to a lesser degree.⁵ In terms of excretion, most statins are extensively metabolized, and only a small amount is excreted unchanged via renal elimination.^17-23 Rosuvastatin is eliminated unchanged via urine and feces.²²

Administration of Statins

Statins are taken orally with or without food.^17-23,26 Because fluvastatin, lovastatin, pravastatin, and simvastatin have short half-lives, they should be taken at night to provide maximum therapeutic benefit.^17-23 Atorvastatin and rosuvastatin can be taken at any time of day, but should be taken at the same time of day.^17-23 Statins metabolized by CYP3A4 should not be taken with grapefruit juice, as this could enhance statin serum levels by inhibiting CYP3A4.⁵ This effect is dose-dependent.⁵

Cost

The initial cost of a statin varies by type or brand, and these price variations can also be influenced by a patient’s location, insurance status, insurance formulary, and dispensing pharmacy. This cost can vary widely. In general, older statins and generic versions are more likely to be priced lower than newer, brand-name statins. By being familiar with the current pricing of statins in the local and mail-order pharmacies, low-cost generic drug programs, and insurance formularies, pharmacists can improve patient adherence by lowering the financial cost of these medications.

Statin Adverse Events

While statins are efficacious and generally well-tolerated, they may not be an appropriate therapeutic choice in some cases. For some patients, statins can cause unwanted side effects, which could lead to poor adherence or discontinuation of the medication.⁵ Care teams should be aware of the following side effects and strategies to mitigate them.^17-23

Allergy or hypersensitivity to statins: Some patients may be allergic to statins or develop a hypersensitivity reaction, including anaphylaxis and angioedema.

 

Muscle symptoms: Muscle symptoms are the most common side effect of statin use.^17-23 Statin-induced muscle disorders include myalgia, myopathy, myositis, rhabdomyolysis, and myonecrosis.¹⁷ Risk factors for these disorders include age (with older individuals at higher risk), female sex, low BMI, and heavy exercise.^17-23 Risks are lower with the hydrophilic statins, pravastatin and rosuvastatin.⁵

 

Statin-induced hepatotoxicity: Statin use can lead to elevated hepatic transaminases, though this risk is generally low.^17-23 This may be transient and resolve after therapy is briefly discontinued.^17-23

 

Statin-associated cognitive dysfunction: This is a rare side effect, and several randomized trials have not found an increased risk with statin use.^17-23

 

New-onset diabetes: Patient-level and trial-level analyses in 2024 clarify that statins cause a modest, dose-dependent increase in new-onset diabetes, mainly among people already near diagnostic thresholds for diabetes.²⁷ The absolute glycemic shifts are small, and the CV benefits typically outweigh this risk.²⁷ Care teams should use this information in shared decision-making and consider early A1c/fasting glucose checks in at-risk patients, without withholding an indicated statin.²⁷

Statin Contraindications

Statins are contraindicated or should be used with caution in certain patient populations, diseases, and with certain other medications.^17-23

Pregnancy: Statins are relatively contraindicated during pregnancy, due to the risk of harm to the developing fetus because of effects on fetal cholesterol synthesis, which is needed for organogenesis of the central nervous system and other tissues.^17-23

Active or chronic muscle disorders: Statins can cause muscle damage in rare cases, so they should be avoided in patients with active or chronic muscle disorders who are at higher risk of Statin-Associated Muscle Symptoms (SAMS).⁵ Interestingly, recent literature has found that many SAMS cases involve nocebo effects, i.e., effects caused by a patient’s negative expectations.^28,29 If a patient stops taking a statin or the primary care physician discontinues statins due to suspected SAMS, the best practice is to rechallenge (i.e., restart) statins, adjust the dose/frequency, and aim for partial tolerance rather than abandoning statins for these patients.^28,29 This may involve changing to a hydrophilic statin that is less likely to cause SAMS. The ACC Statin Intolerance Tool provides a practical, stepwise workflow to evaluate symptoms, secondary causes, and drug interactions.³⁰ This allows a clinician to attempt alternate statin or low or intermittent dosing before moving to nonstatin therapies.^28,31

Drug-drug interactions: Statins have the potential to interact with numerous medications at various levels of severity. Three statins—atorvastatin, lovastatin, and simvastatin—are primarily metabolized by CYP3A4.17-23 When these medications are coadministered with CYP3A4 inhibitors such as amiodarone, amlodipine, ciprofloxacin, and diltiazem, patients need to be closely monitored.⁵ CYP2C9 metabolizes Fluvastatin and rosuvastatin, and drug interactions can occur with medications such as amiodarone, fluconazole, and metronidazole.⁵ Diltiazem may be concomitantly prescribed with statin therapy, but should be avoided with simvastatin and lovastatin, given the risk of increased statin levels. Table 8 details some important drug-drug interactions.⁵

Table 8

Statin Drug-Drug Interactions^17-23

Drug-Drug Interactions	Effect	Recommendation
Gemfibrozil-simvastatin	Increased levels of simvastatin leading to myopathy	Avoid combination (Risk Rating X)
Gemfibrozil-pravastatin	Increase levels of pravastatin, leading to an increased risk of myopathy	Avoid combination   (Risk Rating X)
Amlodipine-lovastatin	Increased levels of lovastatin	Limit the dose of lovastatin to 20 mg/day  (Risk Rating C)
Amiodarone-simvastatin	Increased levels of simvastatin	Limit the dose of simvastatin to 20 mg/day  (Risk Rating D)
Conivaptan-simvastatin	Increased levels of simvastatin leading to myopathy	Monitor therapy and limit the dose of simvastatin  (Risk Rating C)
Cyclosporine-lovastatin	Increased levels of lovastatin	Avoid combination   (Risk Rating X)

Some patients may experience suboptimal outcomes despite adherence to statin therapy. For patients with clinical ASCVD whose LDL-C levels remain ≥70 mg/mL on maximally tolerated statin therapy, add-on therapy may be required.⁷ Patients who are considered very high-risk will require medications such as ezetimibe alongside maximally tolerated statin therapy to lower LDL-C levels even further.⁷ There is also a subset of patients with non-LDL-C dyslipidemias, including hypertriglyceridemia, low HDL-C, and apolipoprotein disorders, who may require non-statin therapies for their individual lipoprotein imbalances.⁷

Monitoring Statin Therapy

According to the 2018 ACC/AHA guidelines, statin therapy requires routine monitoring of several parameters.⁷ A lipid panel, which includes total cholesterol, HDL-C, LDL-C, and triglycerides, should be checked prior to starting statin therapy and then rechecked 4 to 12 weeks later to evaluate therapeutic response.^5,7 Lipid panels should be completed every 3-12 months to check for adherence and ensure the maintenance of LDL-C levels.^5,7 A non-fasting lipid panel is usually acceptable except in the case of patients with hypertriglyceridemia.⁵

Patients should also have baseline AST and ALT levels measured, and AST, ALT, total bilirubin, and alkaline phosphatase may be measured if the patient demonstrates signs of hepatotoxicity, such as loss of appetite, abdominal pain, or dark-colored urine.^17-23 While CPK levels do not need to be routinely monitored, they may be checked in cases where patients have a family history of statin intolerance, present with clinical signs of myopathy or rhabdomyolysis, or are taking concomitant drug therapy that can increase the risk of myopathy.^18-24 Furthermore, patients presenting with signs and symptoms of myopathy should have their CPK level measured.^17-23

Patients can be evaluated with new-onset diabetes throughout the course of statin therapy.^17-23 If diabetes does develop, patients may continue statin therapy with a focus on a healthy diet, physical activity, healthy body weight, and smoking cessation.^17-23 If patients develop memory impairment or become confused, they should be evaluated for non-statin causes, and the possibility of adverse effects associated with statin therapy may be considered in this context.^17-23

Finally, the interprofessional care team plays a critical role in supporting patient adherence to therapy and addressing causes of non-adherence. When adverse events occur, the team can collaboratively assess severity, determine appropriate management, and consider alternative dosing or medication options for potential rechallenge. By working together, physicians, pharmacists, nurses, and other healthcare professionals can help ensure that patients utilize statin therapy safely, effectively, and in a manner that supports long-term cardiovascular health.

Return to Patient Case

Based on his high ASCVD risk (>20%) and history of diabetes, Mr. J should be initiated on high-intensity statin therapy such as atorvastatin 40–80 mg or rosuvastatin 20–40 mg. His care can be optimized through a collaborative, interprofessional approach. The care team can play a vital role in screening for potential drug interactions, counseling Mr. J on possible adverse effects, and following up to assess adherence. The nurse contributes by checking blood pressure, reinforcing medication instructions, and coordinating follow-up appointments to ensure continuity of care. Additionally, the dietitian can support Mr. J in adopting a heart-healthy dietary pattern such as the Mediterranean or DASH diet, with a focus on weight management and lipid improvement. A follow-up lipid panel should be obtained within 4–12 weeks to confirm that LDL-C has been lowered by at least 50%, and therapy should be adjusted if treatment goals are not achieved.

Addressing Patient Concerns

Research has identified what is common knowledge to most clinicians who work directly with patients: despite ample evidence of their safety and efficacy, many patients distrust statins or believe that they are harmful.³² Specific patient concerns generally focus on side effect profiles more than efficacy.³² Some common concerns among patients who either decline to take statins or are not adherent to prescribed statin regimens are the cost of taking the medication, whether or not the medication is truly necessary or working (especially in primary prevention), and the potential for side adverse events (or recurrence of adverse events in patients who had symptoms with another statin or dosage).³²

Studies have also found that although patients who discontinued statins were more likely to worry about heart disease than patients who remain on statin therapy, they are also less likely to believe that statins were effective or that high cholesterol leads to heart attack and stroke.³² These patients consequently believed that statins were less safe than those patients who maintained therapy.³¹ Because the patients fear statins and do not necessarily have a lack of fear toward ASCVD, the care team can empathize with patients by explaining in clear language the complex relationship between LDL-C, plaque, and ASCVD that is detailed above.⁷ By sharing the mechanism of action of statin therapy, in a way that patients can understand, team members can help achieve some “buy-in” from patients who distrust these medications, especially when these pieces of information echo that of the prescribing clinician.

Summary

Statins are the foundation of ASCVD prevention and management, demonstrating consistent reductions in LDL-C and cardiovascular events across diverse populations. Their benefits extend beyond cholesterol lowering, with pleiotropic effects such as improved endothelial function and reduced vascular inflammation. Current guidelines strongly recommend statin therapy for both primary and secondary prevention, with therapy intensity guided by ASCVD risk, comorbidities, and lipid levels. While generally safe and well tolerated, statins may be associated with adverse events, including muscle symptoms, hepatotoxicity, or new-onset diabetes, which require careful monitoring and interprofessional management.

Course Test

Which of the following represents a secondary prevention scenario for atherosclerotic cardiovascular disease (ASCVD)?

60-year-old woman with diabetes but no ASCVD

52-year-old man with prior myocardial infarction

30-year-old man with LDL-C 190 mg/dL and family history of premature CAD

75-year-old woman with a CAC score of 50 and no ASCVD history

A 60-year-old patient suffers from an ischemic stroke. Guidelines call for initiating a statin that lowers LDL by at least 50%. Which of the following is an appropriate “high-intensity” statin?

Simvastatin 10mg

Pravastatin 40mg

Pitavastatin 4mg

Atorvastatin 80mg

A 48-year-old male taking a moderate-intensity dose of atorvastatin complains of myalgias. He requests to try another statin medication. Which of the following statins are hydrophilic, without active metabolites, and therefore may be less likely to cause statin-associated muscle symptoms (SAMS)?

Pravastatin, rosuvastatin

Simvastatin, pitavastatin 

Lovastatin, fluvastatin 

Atorvastatin, simvastatin

A 53-year-old male is initiated on pravastatin for an elevated LDL level. Three months later, he returns without any new symptoms. Which of the following tests would be most appropriate to monitor in this patient to assess response and safety?

CK level

Lipid panel

AST levels 

Hemoglobin level

Which statins are metabolized mainly by CYP3A4 and thus prone to significant drug–drug interactions?

Rosuvastatin and pravastatin

Simvastatin, lovastatin, atorvastatin

Fluvastatin and pitavastatin

Pravastatin and pitavastatin

Which statement correctly matches statin intensity with LDL-C reduction?

Low-intensity = ≥50% reduction

Moderate-intensity = 30–49% reduction

High-intensity = <30% reduction

Moderate-intensity = ≥50% reduction

Which adverse effect is most frequently reported with statin therapy?

Hepatocellular carcinoma

Severe rash

Acute renal failure

Muscle symptoms, e.g., myalgia

A patient taking simvastatin develops elevated levels when prescribed amiodarone. What adjustment is recommended?

Increase simvastatin to 80 mg

Switch to pravastatin

Continue current dose, no change

Discontinue amiodarone immediately

If a patient stops taking a statin or the primary care physician discontinues statins due to suspected statin-associated muscle symptoms (SAMS), the best practice is to

permanently terminate statin therapy altogether.

counsel the patient that the muscle symptoms are caused by the placebo effect.

rechallenge (restart statins), adjust dose/frequency, and aim for partial tolerance.

remeasure the patient’s coronary calcium scores.

A patient is hesitant to start a statin due to fear of side effects. Which team-based approach is most appropriate?

The pharmacist explains statin safety while the physician discusses ASCVD risk, reinforcing consistent messages

The nurse tells the patient to ignore the side effects because they are rare

A dietitian initiates statin therapy independently

A physician prescribes with no additional education

References

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