His work is based around heart failure and the molecular mechanisms involved in the regulation of signaling through cardiovascular adrenergic receptors, the study of G-protein coupled receptor function and signaling, and heart failure gene therapy. His recent studies are investigating into the use of novel viral-mediated myocardial gene delivery for use in congestive heart failure, with an aim at developing reproducible surgical means of gene therapy. He is also involved in research to understand novel molecular signaling mechanisms responsible for the beneficial effects of exercise training and beta-blocker therapy in animal model of heart failure and aging. He is studying new molecular mechanism responsible of neurohormonal overdrive observed in heart failure. In particular he reported the first demonstration of a molecular mechanism for sympathetic nervous system hyperactivity in heart failure by identifying adrenal GRK2 activity as a new sympatholytic target. He described a new interaction between β-1 adrenergic receptor and sphingosine 1 phosphate receptor 1 that has a relevant role in HF pathogenesis and progression. Inhibition of this GRK2-dependent interaction is therapeutic in HF. More recently, Giuseppe has demonstrated that blood GRK2 levels can independently predict prognosis in HF patients, providing a new prospective for the clinical utility of GRK2 in HF. Finally, he has provided the first evidence of a direct correlation between increased epicardial adipose tissue thickness and cardiac sympathetic denervation, demonstrating that epicardial adipose tissue is a relevant source of catecholamine.