Cholesterol Levels Should Play a More Important Role in Identifying Statin Recipients.
نویسندگان
چکیده
Recent recommendations for statin treatment 1,2 have departed from earlier clinical guidelines for cholesterol lowering.3 According to the authors of these new recommendations, the reason for their approach is that it is closest to the randomized clinical trial evidence. However, that opinion lacks circumspection. Greater recognition should have been given to the absolute decrease in low-density lipoprotein cholesterol (LDL-C) as a major determinant of the achievable reduction in cardiovascular disease (CVD) risk.4,5 We do not dispute that the new recommendations are a great advance in statin treatment for people with high absolute CVD risk but whose cholesterol is below average. Many patients, however, encountered in practice with higher LDL-C are badly served by the new guidance, which ironically favors people with low LDL-C above those with higher levels. The 26 statin randomized clinical trials used drugs of differing potencies in various doses and thus each trial produced a different degree of lowering of absolute LDL-C concentration, such that in meta-analysis it is clear that the decrease in CVD incidence relative to control (placebo or in a few trials vs less intensive statin therapy) is related to the mean LDL-C differences between active treatment and control achieved.4 Overall for each 1 mg/dL reduction in LDL-C, the CVD risk decreases to 0.9936 of that of the controls. Thus, a 1 mg/dL decrease in LDL-C will reduce CVD to 0.9936 of its untreated incidence, a 2 mg/dL decrease to 0.99362, a 3 mg/dL decrease to 0.99363, and so on.5 Multiplying this relative risk reduction by the pretreatment absolute CVD risk (which clinicians routinely estimate by methods advocated in the guidelines1,2) gives the number of events prevented. For example a 60 mg/dL decrease in LDL-C in people at 20% 10-year absolute CVD risk prevents (1-0.993660) x 20=6.4 events prevented per 100 people treated for 10 years. In this example, dividing 100 by 6.4 gives 16, the number of people who need to be treated (NNT) for 10 years to prevent 1 CVD event. We have used this approach to calculate NNTs to test the effectiveness of the new guidance in commonly met clinical scenarios.5 Our method based directly on randomized clinical trial data can be summarized in the formula NNT = 100/([1-0.9936LDL-C decrease] x CVD risk) when LDL-C is in mg/dL or NNT = 100/([1-0.78LDL-C decrease] x CVD risk) in mmol/l. For illustration, consider primary prevention treatment decisions in 2 hypothetical patients with similar 20% 10-year CVD risk but different initial LDL-C levels (Table). One (A) has LDL-C 100 mg/dL and the other (B) 200 mg/dL. Moderate intensity statin is recommended, such as atorvastatin 20 mg daily, typically lowering LDL-C by 43%.2 Thus, on this treatment, LDL-C in A is expected to be 57 mg/dL and in B 114 mg/dL. The NNT for the A is 100/([10.9936 100x0.43] x 20) = 21, and for B it is 100/([1-0.9936200x0.43] x 20=12. The lower the NNT, the more effective the statin. So, treatment is more beneficial in the case of the patient with the higher LDL-C. However, treatment could provide even more Cholesterol Levels Should Play a More Important Role in Identifying Statin Recipients
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ورودعنوان ژورنال:
- Circulation
دوره 135 7 شماره
صفحات -
تاریخ انتشار 2017