“…One analysis from the Heinz Nixdorf Recall study suggested Lp(a) to be a causal risk factor for CAC by demonstrating a significant association between a single nucleotide polymorphism at the Lp(a) locus and CAC [30] . However, more recent data from MESA demonstrated that Lp(a) was not associated with baseline CAC volume or density and was only modestly associated with volume progression [31] . Apart from CAC, advanced plaque composition assessment by coronary computed tomography angiography (CCTA) has shown that among patients with advanced stable CAD, Lp(a) is associated with accelerated progression of low-attenuation plaque (a quantitative marker of necrotic core and high risk plaque) [32] .…”