Heart rate variability in animal models of psychological-cardiovascular comorbidity

Cardiovascular disease and psychopathologies, including depression and anxiety, represent respectively the first and second leading cause of serious illnesses, reduced quality of life, and mortality among the population of the Western countries. Interestingly, epidemiological and clinical studies highlighted a bidirectional association between cardiovascular dysfunction and psychiatric illnesses. The presence of environmental stressors represents a common factor in the development of both psychopathologies and cardiovascular disease. However, the precise neurobiological mechanisms linking cardiovascular dysfunction and altered mood or anxiety are not completely clarified. The alteration of autonomic neural regulation of the heart has been proposed as one of the most important pathophysiological mechanisms underlying this link. Cardiac autonomic dysfunction includes increased heart rate, decreased vagal tone, sympathetic hyperactivity, reduced heart rate variability, augmented catecholamine release, and reduced sensitivity of the baroreceptor reflex. Reliable animal models that mimic human psychiatric illnesses may provide further insights into the alterations that characterize comorbid depression/anxiety and cardiovascular dysfunction. In this thesis the possible alterations of cardiac autonomic control were investigated via heart rate variability analysis in rat models of psychopathology (depression and anxiety). The findings obtained in these studies clarify and extend the knowledge about the mechanistic links between psychological and cardiovascular pathologies.