Ricerc@Sapienza

Heart failure (HF) is a multifaceted syndrome addressing for an high rate of death among general population. The common approach to this disease has been always based on the evaluation of the left ventricular ejection fraction by two-dimensional echocardiography with Simpson¿s method. Mounting evidences have demonstrated the pitfalls of this method and have suggested that the management of heart failure requires a deep knowledge of the pathophysiological insights of the disease and cannot rely only on the evaluation of the left ventricular ejection fraction. Several advanced imaging technologies overwhelm the evaluation of ejection fraction and could provide a better understanding of the myocardial abnormalities underlying heart failure. Morover, cardiovascular imaging alone defines disease. We rarely look at tissue. Almost all heart failure patients fail, wasting billions. Where successful, benefit is modest - we control, not cure disease. We should change this. The present research project plan to use scanning, genetics and molecular analysis to optimally conventionally define heart failure. We aim to study activated pathways and simulate the heart at all scales of disease, enrolling 50 patients with HF due to ischemic etiology and 50 HF patients due to non-ischemic etiology (i.e. myocarditis and cardiomyopathies). By linking these to outcomes that matter (death, heart failure, arrhythmia and response to therapy), we aim to redefine heart failure based commonality, difference, define causal biology,. We aim to identify treatable pathways for personalized therapy, and re-group diseases by both process and imaging aspects, retargeting existing treatments to try to improve outcomes of millions.