Lipoprotein(a) Is Associated with Thrombus Burden in Culprit Arteries of Younger Patients with ST-Segment Elevation Myocardial Infarction

Abstract

Background Lipoprotein(a) [Lp(a)] is a risk factor for cardiovascular disease. The burden of thrombus in ST-segment elevation myocardial infarction (STEMI) has implications on treatment and outcomes. However, the association between Lp(a) and atherothrombosis in STEMI remains unclear. Objectives Determine the association between Lp(a) and culprit artery thrombus burden in younger patients with STEMI. Methods Single-centre study of 83 patients aged <65 years with STEMI between 2016-2018 who underwent percutaneous coronary intervention and measurement of Lp(a); those receiving thrombolytic therapy were excluded. Thrombus burden in the culprit artery was determined angiographically using the Thrombolysis in Myocardial Infarction score and classified as absent-to-small, moderate, or large. Elevated Lp(a) was defined as plasma mass concentration >30 mg/dL. Multivariate analysis was performed adjusting for cardiovascular risk factors. Results The mean age was 48.08.4 years and 78.3% were male. Thirteen (16%), 9 (11%) and 61 (73%) patients had small, moderate, or large thrombus burden, respectively, and 34 (41%) had elevated Lp(a). Elevated Lp(a) was associated with greater thrombus burden compared to normal Lp(a) (large burden 85% versus 65%; P=0.024). Elevated Lp(a) was associated with moderate or large thrombus in univariate [OR 10.70 (95% CI 1.32-86.82); P=0.026] and multivariate analysis [OR 10.33 (95% CI 1.19-89.52); P=0.034]. Lp(a) was not associated with culprit artery or stenosis location according to culprit artery. Conclusions Elevated Lp(a) is associated with greater thrombus burden in younger patients with STEMI. The finding of this observational study accords with the thrombotic and anti-fibrinolytic properties of Lp(a). A causal relationship requires verification.

Spontaneous reperfusion in STEMI: Its mechanisms and possible modulation

“…Lp(a) levels were shown to be significantly higher in patients with persistent occlusion compared with those with spontaneous reperfusion of the IRA in the early phase of ACS [64]. More recently, Sankhesara et al [65] have shown elevated Lp(a) levels to be associated with greater thrombus burden in younger STEMI patients. The findings of these studies accord with the thrombotic and anti-fibrinolytic properties of Lp(a).…”

Lipoprotein(a) and calcific aortic valve disease: current evidence and future directions

“…Lp(a) is prothrombotic, the apo(a) moiety having a high degree of homology with plasminogen [23 ▪ ]. Accordingly, Lp(a) may play a role in arterial thrombosis [24]. By competing with plasminogen for fibrin binding sites, Lp(a) inhibits the action of plasmin in dissolving fibrin clots, which leads to fibrin retention [23 ▪ ].…”

“…After the inception of calcification, the decreased compliance of the cusps leads to further mechanical stress, inducing a cycle whereby ''calcium begets calcium' ' ]. Accordingly, Lp(a) may play a role in arterial thrombosis [24]. By competing with plasminogen for fibrin binding sites, Lp(a) inhibits the action of plasmin in dissolving fibrin clots, which leads to fibrin retention [23 & ].…”