The currently reported association between lipid levels under
statin treatment and CHD risk corroborates those recently obtained
in middle-aged subjects in post hoc analyses of randomized
controlled trials of primary and secondary prevention [21–23].
Conversely, they are in contrast to the results of a post hoc analysis
from the PROSPER trial that included elderly participants of
70–82 years of age. In this analysis, neither standard lipids nor
apoA1 or ApoB levels after 3 months of statin therapy predicted
CHD over 3.2 years [24]. This trial, however, consisted of elderly
individuals with a history of vascular disease or who were at high
risk for CHD, contrary to our study population. Moreover, the current
study indicates that the pattern of association between lipids
and CHD is different between those under statins and those under
fibrates. In the latter, triglycerides were the sole lipids to be predictive
of CHD once non-lipid risk factors and LDL and non-HDL
cholesterol were adjusted for. This heterogeneity might reflect differences
in the baseline characteristics between statin and fibrate
users. Fibrate users were less educated and more diabetic while
statin users exercised more and drank less compared to those who
were free of LLT. However, adjustment for these differences did
not eliminate such heterogeneity in the current study. It may also
reflect the indication for which the respective agent was given, usually
hypercholesterolemia for statins and hypertriglyceridemia for
fibrates. It should be remembered however that treatment indication
was not reported in the current study. Further studies not only
in the elderly but also in the middle-aged population are therefore
needed to confirm and explore the mechanisms of this heterogeneity
The currently reported association between lipid levels understatin treatment and CHD risk corroborates those recently obtainedin middle-aged subjects in post hoc analyses of randomizedcontrolled trials of primary and secondary prevention [21–23].Conversely, they are in contrast to the results of a post hoc analysisfrom the PROSPER trial that included elderly participants of70–82 years of age. In this analysis, neither standard lipids norapoA1 or ApoB levels after 3 months of statin therapy predictedCHD over 3.2 years [24]. This trial, however, consisted of elderlyindividuals with a history of vascular disease or who were at highrisk for CHD, contrary to our study population. Moreover, the currentstudy indicates that the pattern of association between lipidsand CHD is different between those under statins and those underfibrates. In the latter, triglycerides were the sole lipids to be predictiveof CHD once non-lipid risk factors and LDL and non-HDLcholesterol were adjusted for. This heterogeneity might reflect differencesin the baseline characteristics between statin and fibrateusers. Fibrate users were less educated and more diabetic whilestatin users exercised more and drank less compared to those whowere free of LLT. However, adjustment for these differences didnot eliminate such heterogeneity in the current study. It may alsoreflect the indication for which the respective agent was given, usuallyhypercholesterolemia for statins and hypertriglyceridemia forfibrates. It should be remembered however that treatment indicationwas not reported in the current study. Further studies not onlyin the elderly but also in the middle-aged population are thereforeneeded to confirm and explore the mechanisms of this heterogeneity
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