hypercholesterolemia – Real Life Pharmacology

February 19, 2026February 6, 2026

Miscellanous Cholesterol Agents – Test Prep and Practice Pearls

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In this episode, we explore several important non-statin cholesterol-lowering therapies, focusing on their mechanisms, clinical uses, and practical considerations for patient care.

We start with bile acid sequestrants, also known as resins, including cholestyramine, colestipol, and colesevelam. These medications lower LDL cholesterol by binding bile acids in the gut, prompting the liver to use more cholesterol to make new bile acids. They are effective for LDL reduction but may cause gastrointestinal side effects and have drug interaction considerations.

Next, we cover niacin (vitamin B3), which can lower LDL and triglycerides while raising HDL cholesterol. While niacin was historically widely used, its role has declined due to flushing, gastrointestinal symptoms, and potential liver toxicity.

Omega-3 fatty acids, including icosapent ethyl (EPA), primarily lower triglycerides and are used in patients with severe hypertriglyceridemia to reduce the risk of pancreatitis. Icosapent ethyl is a purified EPA formulation with evidence of cardiovascular benefit in select high-risk patients.

Finally, we discuss bempedoic acid, a newer oral agent that inhibits ATP-citrate lyase in the liver. Because it is activated only in the liver, bempedoic acid may be useful for patients with statin-associated muscle symptoms. Common adverse effects include elevated uric acid and mild increases in liver enzymes.

This episode highlights how these non-statin agents can be strategically used alone or in combination with other therapies to help patients reach their lipid goals and reduce cardiovascular risk.

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February 5, 2026February 5, 2026

Fibrates – Test Prep and Practice Pearls

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Fibrate derivatives are lipid-lowering medications that primarily target triglycerides rather than LDL cholesterol. Common agents include gemfibrozil, fenofibrate, and fenofibric acid. While their use has declined with the widespread adoption of statins, fibrates remain an important option for patients with severe hypertriglyceridemia, particularly to reduce the risk of acute pancreatitis rather than for routine cardiovascular risk reduction.

Fibrates work by activating PPAR-alpha, which increases lipoprotein lipase activity and enhances the clearance of triglyceride-rich lipoproteins. This leads to significant reductions in triglycerides, modest increases in HDL cholesterol, and variable effects on LDL cholesterol. Because they are not strong LDL-lowering agents, fibrates should not replace statins in patients who require LDL reduction, but they can be effective in select clinical scenarios when triglycerides are the primary concern.

From a safety standpoint, fibrates are generally well tolerated but require careful monitoring. Common concerns include gastrointestinal side effects, liver enzyme elevations, gallstone risk, and muscle toxicity, especially when combined with statins. Gemfibrozil carries a higher risk of drug interactions, while fenofibrate is usually preferred if combination therapy is necessary. Appropriate patient selection, lab monitoring, and lifestyle counseling are essential to maximize benefit and minimize harm when using fibrate derivatives.

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January 29, 2026January 27, 2026

Statin Test Prep and Practice Pearls

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On this podcast episode, I discuss important practice pearls and important test prep information about statins. Statins are cornerstone agents for ASCVD risk reduction, so test questions often focus on indication, intensity, and monitoring. Health care professionals should quickly identify statin intensity: high-intensity therapy (atorvastatin 40–80 mg, rosuvastatin 20–40 mg) lowers LDL by ~50% and is indicated for patients with clinical ASCVD, LDL ≥190 mg/dL, or high-risk diabetes patients age 40–75. Moderate-intensity statins (e.g., atorvastatin 10–20 mg, simvastatin 20–40 mg) are commonly tested for primary prevention.

Statin-associated muscle symptoms range from myalgias (most common, normal CK) to rare but serious rhabdomyolysis (marked CK elevation and AKI). Risk factors include high doses, advanced age, hypothyroidism, drug interactions, and renal impairment. If muscle symptoms occur, stopping the statin, ruling out secondary causes (like hypothyroidism), and rechallenging with a lower dose or different statin is often the correct clinical approach.

Drug interactions and statin selection frequently separate good from great test-takers. Lipophilic statins (simvastatin, atorvastatin, lovastatin) are more prone to muscle effects and CYP3A4 interactions, while hydrophilic statins (pravastatin, rosuvastatin) are preferred in patients with prior intolerance or complex drug regimens. Grapefruit juice, strong CYP3A4 inhibitors, and certain calcium channel blockers raise simvastatin levels—often prompting dose limits or avoidance on exams. If LDL goals aren’t met, adding ezetimibe or a PCSK9 inhibitor is the next evidence-based step.

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