Our laboratory focuses on the study of myocardial diseases leading to heart failure (HF) and pulmonary hypertension (PH) from a translational perspective ranging from molecular studies and experimental models to multicenter clinical trials. The main interests of our group are: (1) the development of new diagnostic algorithms and patient phenotyping based on cardiac advanced imaging and multi-omics; (2) the discovery of novel mechanisms involved in the adaptation of the right ventricle (RV) to pressure overload or genetic cardiomyopathies; and (3) the path towards new therapeutic targets. We are a multidisciplinary team that includes cardiologists and cardiac surgeons and closely collaborate with experts in molecular biology, proteomics, metabolomics and genetics.

We have developed and deeply characterized four different models of PH or RV pressure overload in pigs, induced by different mechanisms: pulmonary vein banding, aorto-pulmonary artery shunt, pulmonary artery stenosis and repeated pulmonary embolization with microspheres. These models have been used for the development of new diagnostic algorithms based on cardiac magnetic resonance to quantify and monitor pulmonary vascular resistance in a non-invasive fashion and to identify early RV involvement. In parallel, these models have been used to evaluate the mechanisms underlying the beneficial effects of current treatments and to assess the effect of novel targets, such as the beta-3 adrenoreceptors or pulmonary denervation. Some of these investigations have been carried forward to the clinical arena and evaluated as multicenter clinical trials (i.e. SPHERE-HF trial) with the collaboration of relevant hospitals across the country. In the last years, our efforts are centered on understanding the underlying mechanisms of RV dysfunction in PH through the integration of advanced imaging and omics (proteomics, metabolomics and genomics), from studies in our experimental models and in patients with various types of PH. The heterogeneity in RV involvement in the presence of a genetic cardiomyopathy is currently also a matter of study by our group. A model of left HF due to hibernated myocardium after a surgical casein ameroid implant around the proximal left anterior descending artery has been also recently established. Finally we closely collaborate in major projects, as The Progression of Early Subclinical Atherosclerosis (PESA) and the Bioimage (A Clinical Study of Burden of Atherosclerotic Disease in an At-Risk Population) aimed to assess the factors involved in the progression of atherosclerosis.

In summary, our group seeks to decipher the mechanisms that lead to RV dysfunction in the presence of PH and various cardiomyopathies with a translational vision that moves from basic research to the clinics and vice versa, all with an open and friendly dialogue between professionals with different scientific background.