What is the problem you’re referring to David? Is it the problem of accurately estimating 10 year MI risk in a primary prevention setting (i.e, are you highlighting the suboptimal nature of existing CV risk estimators/calculators in common use)? Or are you questioning whether it’s valid to extrapolate the relative benefits of statins from secondary prevention trials to a primary prevention context? Or are you questioning whether the relative efficacy of statins might decrease as a patient’s baseline LDL decreases?
From a purely practical standpoint, I don’t really perceive a major problem, provided that we consider that the primary role of statins is to reduce CV risk rather than just LDL.
I know none of the MDs on this site need to hear this, but non MDs might be interested in how primary care physicians and cardiologists usually approach discussions around statin treatment:
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Everyone agrees that patients with clinical evidence of CAD (e.g., angina or a history of MI) need statins- these patients have already proven that they have vascular lipid plaque. This treatment context is called “secondary” prevention;
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For those without symptoms (e.g., no angina or past history of MI), we use risk calculators derived from large, longterm observational cohort studies (as imperfect as they may be) to estimate 10 year MI risk. Examples of risk factors included in these calculators include: age, smoking status, lipid levels, presence/absence of diabetes and hypertension, etc…We share the 10 year absolute risk estimate with patients and we then usually quote the relative statin effect, as derived from large historical statin RCTs (which were conducted in a secondary prevention context). We apply this relative statin effect to each patient’s estimated absolute baseline risk, thereby providing them with an estimate of the absolute risk reduction they might expect over a given period of time if they were to start a statin;
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A third group of patients has arisen in the past few years and the size of this group is expanding rapidly as our imaging techniques improve. These are patients who have imaging done for reasons unrelated to their vascular health, whose CT scans and ultrasounds (chest, abdomen) incidentally show evidence of atherosclerosis. There are no guidelines for how to manage these asymptomatic patients who nonetheless have anatomical evidence of atherosclerosis. My informal observation is that cardiologists tend to recommend statins (usually high intensity) for them (and this has been my own practice as well). These patients fall somewhere “between” the primary and secondary prevention context, not really fitting into either category.
Was there a better way to design the original large statin trials? If so, what would they have looked like? Is there a better way for us to be managing statin discussions than the method we’re using now?