Cardiovascular complications are one of the most prevalent in patients with acromegaly and contribute to the increase of morbidity and mortality associated with the disease. Specifically, cardiomyopathy may be frequent findings. The underlying physiopathology and evolutionary progression has not been fully elucidated, although uncontrolled and prolonged disease, age and coexistence of other cardio-vascular risk factors are significant influencing variables. Nowadays no specific therapies, targeting the main physiopathology mechanisms, exist to arrest this important complication. Our team group perform a pilot study proof-of-concept with 15 patients with acromegaly cardiomyopathy to evaluate the effect of 5 months of phosphodiesterase type 5A (PDE5A) inhibition (Tadalafil 20 mg once daily) on structural and functional cardiac alterations, measured by Cardiac Magnetic Resonance (CMR) and 2D-Echocardiography. The aim of this study is to identify a cluster of circulating cardiovascular (NT-ProBNP, TGFb, MCP1) and oxidative stress (iNOS, COX2, ROS, RANTES) markers. The changes of these markers will be analyzed together with the structural and functional cardiac parameters, analyzed by our team group, to provide an overall overview of acromegaly cardiomyopathy and detect predictive markers for treatment response.
Cardiovascular complications are the main causes of morbidity and mortality in patients with acromegaly. Particularly acromegaly increases cardiovascular risk leading to hypertrophic remodeling and diastolic dysfunction. We will characterize the features of this unexplored model of endocrine cardiomyopathy with circulating biomarkers in correlation with advanced imaging methods. Since to date there are no specific treatments for this condition, we aim to discover a potential cluster of biomarkers that could predict cardiomyopathy stage, disease progression and response to treatment. The identification of a tailored therapy will allow a more rapid and effective clinical response, saving the cost given by prescription of ineffective therapies. Detect a specific biomarker signature for cardiac remodeling and treatment response will improve the diagnosis and follow-up of the disease.