It is commonly known that heart failure (HF) is the main cause of mortality and morbidity which affects about 15 million people in the world and is the primary chronic cause of death. In spite of the development of pharmacological therapies which have led to a good control of the pathology, almost 50% of patients with advanced HF does not survive after the first year. Heart failure consists of a deterioration of the cardiac pump, whose performance become insufficient to satisfy the organism needs. HF can be the consequence of various pathologies, such as ischemia, chronic hypertension, valvulopathies, pericarditis, etc. In conditions of chronic overload, as the one induced by the cited pathologies, the cardiomyocytes reply with hypertrophy and/or death due to necrosis or apoptosis. At the same time, there is a collagen alteration which causes the substitution of the myocardial damaged portion with fibrotic material, increasing in this way cardiac rigidity and reducing contractility. Finally, the onset of inflammation, the activation of the immune system and of the inflammatory mediators affect heart functionality. These phenomena are regulated by a complex interaction between the cellular and molecular mechanisms, which moreover guarantee the homeostasis maintenance in physiological conditions. Nevertheless, their imbalance activates a complex series of events which have recently started to be recognized and studied. In effect, a recent work has underlined the importance of the splenic monocytes in the cardiac response to acute heart ischemia, changing our vision concerning the role of the immune system in heart diseases.Historically, the term "cardiac remodeling" had been introduced to describe the anatomical change of the heart which occurs after myocardial infarction. At a later stage, it has been acknowledged that also other pathological conditions, such as chronic hypertension, can be a cause of the myocardial remodeling. Physiologically, the immune system cells have always been considered for their role of protection from infections. Recently, instead, evidence have been showing that immune system cells might have far more complex functions in the heart. The myocardial remodeling comes from modifications that may be adaptive to the initial insult, but then this structural adjustment may become the activation of structural/metabolic circles which can potentially culminate in the transition to HF.
This observational study will evaluate the immunological profile in relation to cardiac geometry variations in hypertensive patients. Aim of this project is to characterize the profile of immune system activation during the process of cardiac remodeling which is typical of the cardiomyopathy of overload. The main goal will be reached through the characterization of the circulating profile of immune system cells, in order to find a correlation with the clinical phenotype.