To the Editor: Dr Kamstrup and colleagues1 assessed the association between elevated lipoprotein(a) and risk of myocardial infarction using data from the Copenhagen General Population Study (CGPS), the Copenhagen City Heart Study, and the Copenhagen Ischemic Heart Disease Study. We believe that several limitations were not adequately addressed in their article.
Measurement of lipoprotein(a) levels in the CGPS began before the IFCC/WHO consensus on lipoprotein(a) and the SRM-2B reference reagent study2 leading to adoption of lipoprotein(a) measurement as a molar particle concentration (lipoprotein[a]-P), independent of apolipoprotein(a) kringle IV type 2 repeat isoform. The values of lipoprotein(a) in the CGPS are based on an assay determining lipoprotein(a) mass and are subject to bias by apolipoprotein(a) molecular weight. Comparison with current isoform-independent molar assays confirms substantial bias with the older methods.2 The generalizability of the CGPS lipoprotein(a) serum level and lipoprotein(a) population percentile data to current lipoprotein(a) molar serum assays may be limited by the differences in measurement methodology.
Furthermore, lipoprotein(a) molar particle concentration alone may incompletely capture the risk associated with lipoprotein(a). Most research has centered on the unique properties of apolipoprotein(a) or risk associated with lipoprotein(a) whole particle measures. In epidemiologic studies, lipoprotein(a) cholesterol levels have similar correlations with risk as lipoprotein(a) by other whole particle–based measures,3 although the 2 measures have not been directly compared in a single cohort. It is not known whether lipoprotein(a) cholesterol or measures of core particle size add predictive value when used together with lipoprotein(a)-P.
There are few outcome data to support treatment decisions in patients with increased levels of lipoprotein(a). The only conventional drug therapy shown to reduce lipoprotein(a) levels is nicotinic acid, but risk reduction may not follow changes in lipoprotein(a) serum levels. Statin therapy resulting in reduction of low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B to well below population mean levels has been the mainstay of treatment for most patients. Statins have little or no effect on lipoprotein(a) levels, but their use has been based on clinical and quantitative coronary angiography data showing loss of incremental risk attributable to lipoprotein(a) at low levels of LDL-C.4 Trials evaluating risk assessment strategies incorporating lipoprotein(a) and treatment strategies aimed at lowering levels of apolipoprotein B and lipoprotein(a) levels in primary and secondary prevention are needed to form the basis for incorporation of lipoprotein(a) into prevention guidelines.
Financial Disclosures: Dr Jones reported receiving research grants from Atherotech and being a consultant for Abbott and AstraZeneca. Dr Blumenthal reported no disclosures.
Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature
Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal
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