Annals of Medicine

Lipoprotein(a) as an Alarming New Cardiovascular Risk Factor - Consequences on Clinical Practises

Lipoprotein (a) [Lp(a)] is an atherogenic lipoprotein particle structurally similar to low-density lipoprotein (LDL). Thus, its surface contains a single molecule of apolipoprotein B-100 (apo B-100) and phospholipids, and its core is filled with cholesterol. Uniquely, a large glycoprotein, apolipoprotein(a), is linked to the apo B-100, and a fraction of the phospholipids are oxidized (ox-PLs). By entering the arterial wall and carrying cholesterol there, Lp(a) can accelerate the growth of atherosclerotic plaques. In addition, the ox-PLs increase plaque inflammation and susceptibility to rupture and local thrombus formation. By preventing thrombolysis, Lp(a) increases thrombus growth and the likelihood of the development of an occluding thrombus with ensuing acute ischemic event.

Lp(a) levels are genetically determined on both the paternal and maternal sides. Based on genetic studies, case-control studies, and prospective cohort studies, high Lp(a) levels predict coronary artery disease, ischemic stroke, peripheral arterial disease, and aortic valve calcification. The adverse cardiovascular effects of Lp(a) particles are independent and potentiate those of other risk factors. According to the European guidelines for the management of dyslipidemias, Lp(a) measurement should be considered at least once in the lifetime of every adult. Lp(a) levels above 50 mg/dl increase the risk of cardiovascular disease in all adults, and higher levels further increase the risk.

PCSK9 inhibitors reduce Lp(a) by 25–30% while statins have no effect. Since the available lipid-lowering drugs have not been able to significantly reduce Lp(a) levels, drugs have been developed that can block the formation of Lp(a) in the liver. Injectable drugs are based on antisense oligonucleotides (ASOs) or small interfering RNAs (siRNAs) and they target the production of apolipoprotein(a) in liver cells thereby lowering the circulating Lp(a) levels by 80–98%. Also, an oral small molecule inhibitor of Lp(a) formation, muvalaplin, is currently being investigated.

For this Article Collection, we welcome submissions of Original Research, Clinical Trials, Protocols, Case Series and Commentaries to provide our readers with new information about the clinical significance of elevated Lp(a). The focus is on the importance of an elevated Lp(a) as an independent genetically determined risk factor of atherosclerotic cardiovascular disease and aortic stenosis. Presentation and critical analysis of the new drugs in development to lower Lp(a) levels and cardiovascular risk are also welcome.

Guest Advisors

Alpo Vuorio. University of Helsinki, Finland. Section Editor of Cardiology and Cardiovascular Disorders, Annals of Medicine

Alpo Vuorio MD, PhD is adjunct professor of molecular medicine in University of Helsinki, Finland. He is also section editor of the Cardiology and Cardiovascular Disorders section in Annals of Medicine and a member of the Finnish dyslipidaemia guideline group. Over the years his research has been targeted at genetics and treatment of familial hypercholesterolemia (FH). In addition, Lp(a) as a cardiovascular risk factor and its treatment is a part of his research interest.

Petri Kovanen. Wihuri Research Institute, Finland

Petri Kovanen, MD, PhD is adjunct associate professor of Experimental Medicine at the University of Helsinki, Finland. He has served as Scientific Director and Director of Wihuri Research Institute in Helsinki and now serves as Director Emeritus of the Atherosclerosis Research Laboratory of the Institute. His main research interests focus on the pathogenesis and clinical implications of atherosclerotic cardiovascular disease.

All manuscripts submitted to this Article Collection will undergo a full peer-review; the Guest Advisors for this Collection will not be handling the manuscripts (unless they are an Editorial Board member). The Guest Advisors declare the following Conflicts of Interests:

• Alpo Vuorio has received consultancy fees from Amgen and Novartis. AV is a section editor of Cardiology and Cardiovascular Disorders of Annals of Medicine.
• Petri Kovanen has received consultancy fees, lecture honoraria, and/or travel fees from Amgen, Novartis, Raisio Group, and Sanofi.

Please review the journal scope and author submission instructions prior to submitting a manuscript.

The deadline for submitting manuscripts is 31st October 2026.

Please contact Francis Straw at [email protected] for more information and discount codes for this Article Collection.

Please be sure to select theArticle Collection "Lipoprotein(a) as an Alarming New Cardiovascular Risk Factor - Consequences on Clinical Practises" from the drop-down menu in the submission system. Please select Cardiology & Cardiovascular Disorders from the list of available sections during submission. Failure to select the appropriate Article Collection or Section name can result in delays.