In the treatment of coronary artery disease (CAD), fractional flow reserve (FFR) can be performed during coronary angiography to evaluate the need for percutaneous coronary intervention (PCI).1 Nevertheless, the efficacy of wire-based FFR is constrained by its practical limitations.1,2 Computational

Atherosclerotic cardiovascular disease (ASCVD) continuesto be a leading cause of morbidity and mortality worldwide,with over 17.9 million people dying from cardiovascular (CV)diseases annually.1,2 Given the fact that the recurrent riskis high among patients with established ASCVD, secondarypreventio

Acute myocardial infarction (AMI) is caused by large coronary plaques characterized by a lipid-rich pool covered by a thin fibrous cap, and visualized by intracoronary imaging.¹ Alirocumab, a PCSK9 inhibitor, lowers low-density lipoprotein cholesterol (LDL-C) and reduces the risk of major cardiovascular (CV) events in stabilized acute coronary syndrome (ACS) patients.1 However, these patients remain at an increased risk of recurrent thrombosis due to high-risk plaques.¹

Familial hypercholesterolemia (FH) is a common codominant monogenic dyslipidemia that can result in the lifelong and prominent elevation of plasma low-density lipoprotein cholesterol (LDL-C).^1,2 Whereas homozygous FH is rare with an estimated frequency of 1 in 160,000-320,000 individuals, heterozygo

Patients with familial hypercholesterolemia (FH) have an elevated low-density lipoprotein cholesterol (LDL-C) level, which translates into a higher risk of cardiovascular events.¹ Although maximum standard treatment of statins and ezetimibe in FH patients helps reduce the LDL-C level by at

Patients who have recently experienced a myocardial infarction (MI), with multiple prior MIs or residual multivessel coronary artery disease (CAD) are at higher risk for recurrent MACEs. In these high-risk groups, a substantial relative and

Patients with higher levels of plasma Lp(a) are at an increased risk of atherosclerotic cardiovascular disease (ASCVD) independent of low-density lipoprotein-cholesterol (LDL-C) levels.¹ Recent ESC/EAS guidelines have emphasized the identification of patients with elevated levels of Lp(a) and implementation of treatment with appropriate

Lowering low-density lipoprotein cholesterol (LDL-C) levels is directly correlated with reducing the incidence of cardiovascular (CV) events.¹ Although statins can lower LDL-C levels, a significant number of patients do not reach the recommended LDL-C targets.² Introduction of proprotein