Remnant cholesterol (remnant-C) has emerged as a significant cardiovascular (CV) risk factor, complementing the traditional focus on low-density lipoprotein cholesterol (LDL-C). Recent years have witnessed an increased understanding of remnant-C’s atherogenicity, highlighting its prominent role in the residual risk of cardiovascular events, even after LDL-C reduction (1, 2). Interestingly, the widespread use of LDL-C-lowering drugs has overshadowed the understanding of remnant-C as a causal CV risk factor for over 30 years.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a clinically distinct entity characterized by myocardial infarction without significant epicardial coronary artery stenosis. This heterogeneous syndrome, accounting for 5–15% of myocardial infarction cases, remains diagnostically and therapeutically challenging (1-3). While mechanisms such as microvascular dysfunction, coronary vasospasm, and plaque erosion have been proposed, recent evidence highlights ferroptosis—a regulated, iron-dependent form of cell death driven by lipid peroxidation—as a potential key contributor to cardiomyocyte injury and MINOCA pathophysiology.

Pseudoxanthoma elasticum (PXE) patients have more arterial calcification due to lower levels of inorganic pyrophosphate, caused by mutations in the ABCC6 gene, but the relation with vascular complications is poorly understood. Because of the slow progressing nature of arterial disease in PXE patients, there is a need for a valid and reliable intermediate endpoint to be used in future clinical trials. Arterial calcification measured on computed tomography (CT) is a promising candidate, if associated with future cardiovascular events.

Most tissues have the capacity for endogenous lipid synthesis. A crucial foundational pathway for lipid synthesis is de novo lipid synthesis (DNL), a ubiquitous and complex metabolic process that occurs at high levels in the liver, adipose and brain tissue. Under normal physiological conditions, DNL is vital in converting excess carbohydrates into fatty acids. DNL is linked to other pathways, including the endogenous synthesis of phospholipids and sphingolipids. However, abnormal lipid synthesis can contribute to various pathologies and clinical conditions.