While plasma concentrations of Lp(a) are reported to rise acutely under pathological challenge such as after myocardial infarction and percutaneous coronary intervention [33], it has been demonstrated that prolonged exposure to high circulating apolipoprotein(a) levels would render the vascular smooth muscle cells more contractile via the RhoA/ROCK-mediated mechanism [33]. Here, LPA is linked to myocardial infarction.