Researchers Freddy Ganse and Sara Delgado, from the Cardiovascular Diseases Research Group at the Vall d'Hebron Research Institute (VHIR) and members of the CIBER Network for Cardiovascular Diseases (CIBER-CV), were honoured during the International Society for Heart Research (ISHR) 2026 Congress, held this year in Birmingham, United Kingdom.

Specifically, Freddy Ganse received the award for the Best Rapid Fire Presentation, while Sara Delgado was recognised with the award for the Best Scientific Poster. Both studies have been executed in collaboracion with CIBERCV and address some of the main current challenges in cardiovascular research: preventing arrhythmias associated with environmental pollution and identifying new therapeutic targets to combat heart failure.

New strategies to reduce arrhythmias caused by air pollution

The study awarded the prize for the Best Rapid Fire Presentation was led by Freddy Ganse under the supervision of Dr Antonio Rodríguez-Sinovas, principal investigator of the Cardiovascular Diseases Research Group at VHIR and member of the CIBER-CV. The research is based on increasingly strong evidence that exposure to air pollution increases the risk of ventricular arrhythmias and sudden cardiac death. Several epidemiological studies have particularly linked particles emitted by diesel engines with increased inflammation, oxidative stress and electrical alterations in the myocardium, processes that promote the development of severe arrhythmias. Despite this evidence, there are still few strategies specifically aimed at preventing these effects.

To address this challenge, the researchers analysed two different but complementary therapeutic approaches. On the one hand, they evaluated the use of cerium oxide (CeO₂) nanoparticles, known for their high antioxidant capacity and their ability to neutralise the reactive oxygen species responsible for a significant proportion of cellular damage. On the other hand, they investigated heat acclimation, a physiological process that activates the body's natural protective mechanisms and increases tissue resistance to stress.

The study was carried out using an experimental model in which animals were exposed to diesel engine particles for three weeks. Subsequently, the researchers analysed the electrical behaviour of the heart and the ease with which ventricular arrhythmias could be induced, as well as several molecular markers related to inflammation, oxidative stress and cardiac fibrosis.

The results showed that chronic exposure to these particles significantly increased the incidence of sustained ventricular arrhythmias and caused structural and functional alterations in the heart. In contrast, both treatment with cerium oxide nanoparticles and heat acclimation markedly reduced susceptibility to developing these arrhythmias. Both approaches also decreased oxidative stress, the inflammatory response, myocardial fibrosis and electrical conduction abnormalities, although each did so through different mechanisms.

In the case of the nanoparticles, the protective effect is mainly explained by their ability to eliminate free radicals and reduce oxidative damage. By contrast, heat acclimation stimulates the expression of stress proteins, known as heat shock proteins, which activate the body's natural cellular protection mechanisms against adverse conditions. Although they act through different pathways, both strategies converge in reducing the processes that promote the development of arrhythmias.

A new therapeutic target to slow the progression of heart failure

The second award-winning study, recognised as the Best Scientific Poster at the congress, corresponds to the research led by Sara Delgado within Dr Javier Inserte's research line. The project investigates the role of the amino acid transporter LAT1 (SLC7A5) in the development of pathological ventricular hypertrophy and heart failure.

When the heart is subjected to a prolonged workload, as occurs in conditions such as aortic stenosis or arterial hypertension, the cardiac muscle increases in size in an attempt to maintain its function. Although this response is initially adaptive, over time it becomes a pathological process that progressively impairs cardiac function and can ultimately lead to heart failure.

In this context, the researchers sought to determine the role of LAT1, a protein responsible for transporting branched-chain amino acids into cardiomyocytes. These amino acids activate the mTOR signalling pathway, a molecular mechanism involved in cell growth that, when persistently activated, contributes to the development of cardiac hypertrophy.

The study demonstrates that LAT1 expression is increased both in samples from patients with cardiac hypertrophy and in experimental models subjected to haemodynamic stress. Furthermore, the researchers observed that partial reduction of this transporter decreases amino acid uptake into cardiac cells, reduces activation of the mTOR pathway, limits the development of hypertrophy and better preserves cardiac function.

The experiments also show that reducing LAT1 prevents the accumulation of amino acids in both the myocardium and the circulation and reduces cardiomyocyte growth, reinforcing the hypothesis that this transporter plays a key role in disease progression.