The review focusses on the role of liver transplantation, and rarely combined liver and heart transplantation, in the current management of homozygous familial hypercholesterolaemia (HoFH).

Low-grade systemic inflammation, as determined by high-sensitivity C-Reactive Protein (hsCRP), plays a significant role in the progression and development of atherosclerotic cardiovascular disease (ASCVD) and is recognized as a risk enhancer for increased incidence of major adverse cardiovascular events (MACE). (In 2024, the US Food and Drug Administration approved colchicine, as the first anti-inflammatory agent for secondary cardiovascular prevention. While this step signified a translational milestone, recent neutral colchicine trials such as CLEAR- SYNERGY, have reignited controversy regarding the overall efficacy of colchicine, and the need for alternative anti-inflammatory therapies. As the understanding of inflammation's role in atherosclerosis grows, questions persist about the best management strategies and future therapeutic options. This review aims to provide an updated summary that includes insights from recent key trials, explores investigational anti-inflammatory treatments, and discusses considerations for future trial designs.

Triglyceride-rich lipoproteins (TRLs) and LDL remain major drivers of atherosclerotic cardiovascular disease, and angiopoietin-like protein 3 (ANGPTL3) has emerged as a promising target to lower both triglycerides and LDL cholesterol (LDL-C). This review provides an overview on ANGPTL3 inhibition, including genetic insights and clinical evidence, and examines patient groups in which therapies may be particularly well suited to reduce residual cardiovascular risk.

In 1994, the 4S trial was revolutionary by showing that cholesterol lowering with simvastatin reduced, not only atherosclerotic vascular disease (ASCVD) events, but also all-cause mortality as compared to placebo. During the following 30 years, statins have proved to be well tolerated and effective and also paved way for new innovations in the field of dyslipidaemia therapy.

This review explores the evolving understanding of efferocytosis - the clearance of dead or dying cells by phagocytes - in the context of atherosclerosis. It highlights recent discovers in cell death modalities, impaired clearance mechanisms and emerging therapeutic strategies aimed at restoring efferocytosis to stabilize plaques and resolve inflammation.

Elevated plasma lipoprotein(a) [Lp(a)] is a causal and independent risk factor for atherosclerotic cardiovascular disease and an emerging therapeutic target. Over the past 15 years, many medical bodies from around the world have released scientific statements and clinical guidelines regarding Lp(a). This review tracks how recommendations on Lp(a) have evolved over this timeframe.

The causal role of LDL in atherosclerotic cardiovascular disease (ASCVD) is well established, but the contribution of HDL has proven more complex. CETP inhibitors were originally developed to increase HDL-cholesterol (HDL-C), but the failure of clinical trials and genetic evidence have changed our understanding of CETP biology. With the development of obicetrapib, a next-generation CETP inhibitor, there has been renewed interest in its therapeutic potential. This review summarizes the latest findings on CETP inhibition and highlights the evolving perspectives from lipid modulation to broader clinical applications.

Well conducted, prospective, blood-based biomarker studies on dementia risk are growing, providing valuable insights into disease mechanisms that precede clinical symptoms. These investigations are crucial for advancing our understanding of dementia pathology and identifying early biological changes.

Lipid metabolism and de-novo lipogenesis (DNL) is broadly controlled by the SREBP transcription factors. These transcription factors are matured from membrane-anchored precursor proteins by the proteolytic actions of the proteases S1P and S2P. In this review, we summarize the current understanding of SPRING, a recently identified activator of S1P.

Type 2 diabetes (T2D) is a heterogeneous, progressive metabolic disease and a major contributor to cardiovascular disease worldwide. Current prevention strategies, centred on population-level lifestyle recommendations, have had limited success, highlighting the need for more comprehensive approaches that account for interindividual variation in intervention response.

Cardiovascular diseases (CVDs) are a leading cause of death worldwide. While it is well known that obesity, dyslipidemia and diabetes are major risk factors of CVD, observational clinical studies have shown that variability in body weight, circulating LDL-cholesterol (LDL-C) or glucose levels further increase this risk. The underlying mechanisms, however, leading to increased risk of CVD due to metabolic cycling are not well understood.

Elevated plasma lipoprotein(a) (Lp(a)) is a causal and independent risk factor for atherosclerotic cardiovascular disease; therefore, understanding the fundamental mechanisms underlying Lp(a)-mediated pathogenesis is of significant clinical importance. This review summarizes recent advances in understanding the precise cellular targets of Lp(a) in atherogenesis, uncovering potential therapeutic avenues worth exploring.

Peripheral artery disease (PAD) is a major cause of global health burden, including amputation and impaired quality of life. This review examines the evidence implicating lipoprotein(a) [Lp(a)] in PAD, which is timely as novel therapies lowering Lp(a) are currently being tested in several clinical trials.

Peripheral arterial disease (PAD) is an atherosclerotic and thrombotic disease associated with substantial morbidity and mortality. Although risk factors for PAD are mostly modifiable, prognosis remains poor, and patients are at a high risk of cardiovascular events. This review aims to summarize current evidence surrounding the role of lipoprotein(a) (Lp[a]) in PAD and examines the available data on lipoprotein apheresis as an effective management approach for patients with PAD with elevated Lp(a).

This review integrates recent structural and biochemical insights into apolipoprotein B (apoB) containing lipoproteins to highlight how factors beyond cholesterol levels contribute to atherosclerosis.

A review of recent publications demonstrating the important role of the intestine in the pathogenesis of cardiovascular disease.

To identify the opportunity of targeting patients with elevated lipoprotein(a) [Lp(a)] in patients with peripheral arterial disease (PAD).

Myocardial infarction survivors are at a high risk of a recurrent event despite receiving guideline preventive therapy. There is accumulated evidence that persistent atherosclerotic plaque inflammation contributes to this risk. Oxidized low-density lipoprotein (LDL) is widely recognized as a key factor in plaque inflammation and instability; however, no therapies that directly target oxidized LDL are to date available for clinical use. We will here review recent observations indicating that treatment with the anti-oxidized LDL antibody orticumab specifically inhibits plaque inflammation.

Lipoprotein(a) [Lp(a)] is a significant player in cardiovascular disease (CVD) and type 2 diabetes (T2D). While Lp(a) contributes to residual cardiovascular risk in T2D, lower levels paradoxically increase the risk of developing T2D. This review explores Lp(a)'s dual role in cardiometabolic disease, its association with T2D, and emerging Lp(a)-lowering therapies.