Pathophysiological mechanisms of cardiovascular disorders in Parkinson’s disease

Parkinson’s disease is the second most common progressive neurodegenerative disease after Alzheimer’s disease, characterized by selective loss of dopaminergic neurons in the compact part of the substantia nigra. This leads to striatal dopamine deficiency and motor symptoms. Along with this, non-motor disorders, in particular cardiovascular dysfunctions, play a significant role in the pathogenesis of Parkinson’s disease, which have a significant impact on the quality of life of patients. Neurogenic mechanisms include pathological accumulation and aggregation of alpha-synuclein with the formation of Lewy bodies and neurites, detected in both the central and peripheral autonomic nervous systems, including the heart sympathetic innervation. Additionally, non-neurogenic factors (decreased intravascular volume due to dysphagia and inadequate fluid intake, heart failure, and antiparkinsonian-induced hypotension) contribute to orthostatic hypotension and other cardiovascular events, increasing the risk of stroke and other complications. In addition to autonomic and motor manifestations, mental and cognitive impairment is of paramount importance in Parkinson’s disease. Depression, anxiety, and dementia are found in 40-50% of patients, often in the early stages of the disease, and through activation of the sympathoadrenal system, increased cortisol levels, and baroreflex dysfunction can exacerbate arrhythmias, ischemic episodes, and other cardiac events. In addition, decreased motivation and adherence to therapy with mental symptoms further increases the risk of adverse cardiovascular outcomes in this group of patients.