1. How do you determine whether a long-term statin user should continue therapy, particularly in older adults or those with multiple comorbidities? 2. What clinical indicators or risk thresholds guide your decision to deprescribe or adjust statin therapy? 3. How do you balance the long-term benefits of statins with concerns about polypharmacy, side effects, or patient fatigue? 4. Do current guidelines provide enough clarity on when to stop statins, or is this primarily an individualized judgment? 5. Is there anything you’d like to add about this topic that you think clinicians should consider or that isn’t often discussed? Requirements for participation: • Must be US-based • Must have verified physician credentials (MD or DO) • Responses are considered permission to quote with attribution • Conflict of interest disclosure required if relevant

As a physician who sees the long-term vascular effects of chronic disease, I think the real question with statins in older adults isn't "do they work," it's "what's the marginal benefit now." Once patients are in their 80s, often with several comorbidities and 8 or 10 medications, the balance shifts. Polypharmacy fatigue becomes real. I tend to look at overall vascular health, lifestyle, and remaining life expectancy more than absolute LDL targets. If the medication burden outweighs the projected gain, it's time to talk about stopping or tapering. Guidelines help, but this decision is always individual and should happen face-to-face, not as an automatic continuation.

Q1. When determining whether an older adult should continue treatment, the central consideration is whether the balance of cardiovascular benefit versus potential harm remains favorable. In younger or middle-aged adults, statins are well supported for both primary and secondary prevention of cardiovascular disease, but in older adults with multiple comorbidities, frailty, or limited life expectancy, the calculus often shifts. If the patient is taking a statin for secondary prevention, such as a history of myocardial infarction, stroke, or established atherosclerotic disease, there is generally strong evidence to continue therapy if tolerated. In primary prevention, especially after the age of 75, evidence becomes less robust, and individualized assessment is more important. Q2. Clinical indicators that guide deprescribing or dose adjustment include diminishing cardiovascular risk reduction relative to life expectancy, increasing frailty, functional decline, or competing comorbidities that make long-term prevention less meaningful. Worsening liver function, new-onset muscle symptoms, persistent fatigue, cognitive changes, or polypharmacy interactions are also key signals to reevaluate. Risk estimation tools such as pooled cohort equations are less reliable in very elderly patients, so the clinical picture often carries more weight than formal risk scores. Q3. Balancing long-term benefits against polypharmacy and side effects requires careful discussion with patients and caregivers. Statins can be extremely beneficial in the right context, but their benefit takes years to fully accrue, which matters when life expectancy is limited. In patients already managing multiple medications, simplifying regimens can improve adherence and quality of life, especially when the expected marginal benefit of a statin is low. Q4. Most guidelines emphasize continuation for secondary prevention and suggest individualized decisions for primary prevention in older adults. There is no universally accepted age or risk threshold at which statins should be stopped, so clinical judgment remains central. Q5. A point worth emphasizing is that discontinuing statins in the right clinical context is not a failure of care but often a thoughtful, patient-centered decision. Regularly reassessing the indication for chronic preventive medications, especially in older adults, is just as important as starting them in the first place.