February marks heart health month.

This global initiative looks to educate the population on heart disease and what preventative measures can be taken to improve cardiovascular health1. In this blog, we reflect on the prevalence of cardiovascular disease, the problems faced in development of cardiovascular therapeutics and explore the established and emerging treatments available.

Cardiovascular diseases (CVDs) are the leading cause of death globally, taking an estimated 17.9 million lives each year₂. CVDs are a group of disorders of the heart and blood vessels and include coronary heart disease, cerebrovascular disease and rheumatic heart disease.

Due to the high prevalence and considerable healthcare costs associated with CVDs, extensive research efforts have been made to develop effective therapeutic agents. However, there are significant challenges to overcome during development stages, such as current treatment modalities do not exhibit uniform efficacy across all patients, and the emergence of drug resistance poses a significant challenge to further therapeutic efforts₃. Furthermore, chronic administration can result in toxicity₄ – this is a significant issue due to the long-term management required for CVDs. Therefore, prevention is often seen as an effective strategy₅, with modalities such as dietary supplements the preferred line of treatment and risk reduction.

Small molecules such as Prostaglandins (PGs), have been identified as being involved in cardiovascular processes₆. PGs are a group of hormone-like lipids formed in the body of essential fatty acids. More specifically, they activate or inhibit platelet buildup for blood clot formation and cause vasodilation or vasoconstriction₇. PGs and thromboxanes are produced in vivo both from the Omega-6 fatty acid arachidonic acid (AA) and the Omega-3 fatty acid eicosapentaenoic acid (EPA)₆. Certain beneficial effects may result from altered PG metabolism resulting from increases in the EPA/AA ratios of precursor phospholipids₆.

Dietary supplementation of Omega 3 concentrate in ethyl ester form has therefore been widely documented as a treatment and preventative measure against CVD₄. EPA protects against the development of atherosclerosis in atheroprone mice via the metabolites 18-hydroxy-eicosapentaenoic acid and 17,18-epoxy-eicosatetraenoic acid, which reduce endothelial activation₈. Epidemiological studies have also shown that EPAs show similar effects in the human population with significant reduction in the risk of atherosclerotic CVD due to triglyceride (TG) lowering, membrane stabilisation, and antithrombotic, anti-inflammatory, or antiarrhythmic properties₉. The JELIS (the JAPAN EPA Lipid Intervention Study) trial showed a reduction in major coronary events in patients with hypercholesteremia using purified EPA₈.

EPA and DHA differ markedly, with distinct effects on membrane structure, rates of lipid oxidation, inflammatory biomarkers, and endothelial function, as well as tissue distributions₁₀. Ongoing scientific efforts to understand the mechanism of action for EPA will help usher in a new era of cardiovascular therapeutics₁₁.

1. https://www.heartuk.org.uk/get-involved/heart-month-2025
2. https://www.who.int/health-topics/cardiovascular-diseases#tab=tab_1
3. https://www.sciencedirect.com/science/article/abs/pii/S1359644623002465
4. https://www.sciencedirect.com/science/article/pii/S0735109715044630
5. https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(15)60110-6.pdf
6. https://pmc.ncbi.nlm.nih.gov/articles/PMC9962914/#:~:text=Prostanoids%2C%20including%20prostaglandins%20and%20thromboxane,8%2C9%2C10%5D.
7. https://www.ahajournals.org/doi/10.1161/atvbaha.110.207449
8. https://pubmed.ncbi.nlm.nih.gov/17398308/
9. https://pmc.ncbi.nlm.nih.gov/articles/PMC11314407/
10. https://pubmed.ncbi.nlm.nih.gov/32212849/
11. https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bph.14154#bph14154-bib-0008