Abstract
Neurological disorders including depression, anxiety, post-traumatic stress disorder (PTSD), schizophrenia, autism and epilepsy are associated with an increased incidence of cardiovascular disorders and susceptibility to heart failure. The underlying molecular mechanisms that link neurological disorders and adverse cardiac function are poorly understood. Further, a lack of progress is likely due to a paucity of studies that investigate the relationship between neurological disorders and cardiac electrical activity in health and disease. Therefore, there is an important need to understand the spatiotemporal behavior of neurocardiac mechanisms. This can be advanced through the identification and validation of neurological and cardiac signaling pathways that may be adversely regulated. In this review we highlight how dysfunction of the hypothalamic–pituitary–adrenal (HPA) axis, autonomic nervous system (ANS) activity and inflammation, predispose to psychiatric disorders and cardiac dysfunction. Moreover, antipsychotic and antidepressant medications increase the risk for adverse cardiac events, mostly through the block of the human ether-a-go-go-related gene (hERG), which plays a critical role in cardiac repolarization. Therefore, understanding how neurological disorders lead to adverse cardiac ion channel remodeling is likely to have significant implications for the development of effective therapeutic interventions and helps improve the rational development of targeted therapeutics with significant clinical implications.
Highlights
Psychiatric disorders are widely prevalent globally, affecting about 25–30% of patients in Europe and the United States, with anxiety disorder and depression being the most common conditions (7% and 5% respectively) [1]
Others and we have demonstrated that pathological levels of the saturated free fatty acid, palmitic acid, led to adverse remodeling of major cardiac ion channels in distinct animal models [39,40,41,42]
It is becoming increasingly clear that distinct biological, behavioral and psychosocial factors mediate the physiological link between mental illnesses and the increased risk of Cardiovascular disorders (CVDs)
Summary
Psychiatric disorders are widely prevalent globally, affecting about 25–30% of patients in Europe and the United States, with anxiety disorder and depression being the most common conditions (7% and 5% respectively) [1]. A complex set of behavioral and psychosocial aspects are mediators for increased CVD risk, including smoking, alcohol and substance abuse, poor diet and reduced physical activity that can lead to obesity, non-adherence to medications and sleep disorders, anger and hostility, social isolation and low socioeconomic status [3,4,5]. These CVD risk factors are significantly present among subjects with mental illness, resulting in an additive effect over the disease-related biological risk factors [6] that these patients have for CVD. In this context our goal is to further highlight unacknowledged common and unique molecular mechanisms of neurological channelopathies and cardiomyopathies that merits significant investigation
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