To the Editor.
—The article by Ridker et al1 describing similar Lp(a) concentrations in patients with MI and matched controls is very welcome since prospective studies on this subject are sparse.2,3 In the article and in the accompanying Editorial,4 some possible reasons for the discrepant results compared with numerous (retrospective) studies are listed, but we would like to draw the attention to two further aspects.Despite similar apo(a) isoform and phenotype distribution we were able to detect 53% lower Lp(a) concentrations in patients with hypertriglyceridemia (>12.93 mmol/L [500 mg/ dL], n=147) compared with controls (n=404, P<.0001). Concentrations of triglycerides and Lp(a) were negatively correlated in hypertriglyceridemic patients (r=-0.22, P<.01).5 In the study by Ridker et al, triglyceride concentrations are not given, but the cases had markedly lower high-density lipoprotein (HDL) cholesterol values compared with the controls. Because of the known negative correlation, this
Ritter MM, Geiss HC, Richter WO, Schwandt P. Lipoprotein(a) and Risk of Myocardial Infarction. JAMA. 1994;271(14):1077. doi:10.1001/jama.1994.03510380033020