Lipoprotein (a) is composed of one molecule of an LDL particle containing apolipoprotein B-100.1 It contains repeated `Kringle' structures, which are comparable with plasminogen.2 This may confer pro-thrombotic and pro-atherogenic potential.3 Concentrations below 30 mg/dl are thought to be an independent risk factor for myocardial infarction. Luc et al. contend that the possible association between lipoprotein (a) and cardiovascular outcomes may be insignificant.4 There appears to be no clear consensus on the role of lipoprotein (a) as a primary risk factor for myocardial infarction or whether routine measurement is justified in order to conduct risk stratification.

Lipoprotein (a) consists of two essential components, namely LDL-C and apolipoprotein (a). Apolipoprotein B100 (ApoB) is bound to Apolipoprotein (a) via a single disulfide bond.2 Further, in contrast to LDL-C, lipoprotein (a) catabolism is less dependent on LDL-C receipt, and prior studies have shown that statins have only a modest effect on lipoprotein (a) regulation. Nordestgaard et al. (2010) also indicated that apolipoprotein (a) may enhance thrombus formation and promote atherosclerosis.5 The data on the association between serum lipoprotein (a) level and cardiovascular outcomes, including coronary artery stent restenosis post-PCI, in Chinese populations are limited.6 However, the Australian Dubbo study (2023) reported that there was a greater risk of recurrent coronary heart disease in patients with higher concentrations of Lp(a) vs. those with lower concentrations of Lp(a).7

Additionally, patients with diabetes mellitus (DM) are at a two- to four-fold higher risk of cardiovascular disease than those without DM, according to a study by Konishi and colleagues.8 Further, their study indicates that Lp(a) can be considered a risk factor for adverse events. Earlier meta-analyses have reported an association between elevated Lp(a) and coronary heart disease.9, 10, 11 Evidence is now emerging of a relationship between increased Lp(a) and the risk of recurrent CVD or the progression of atherosclerotic disease. One recent meta-analysis evaluating nearly 950,000 participants in 75 studies reported an overall higher risk of all-cause mortality in the general population or patients with advanced CVD with a higher Lp(a).12 Furthermore, the association with mortality, particularly in high-risk patients like diabetics, remains underexplored, as the clinical implications of Lp(a) in patients with DM who underwent PCI are largely unknown.8,13 Further, patients with DM who underwent PCI had worse outcomes compared with those without DM despite using drug-eluting stents.14 As a consequence, it is imperative that for patients with diabetes, there be an investigation of the effect of raised Lp(a) levels on cardiac mortality in diabetics post-PCI.