Abstract
Dysautonomia is a common non-motor symptom in Parkinson’s disease (PD). Most dysautonomic symptoms appear due to alterations in the peripheral nerves of the autonomic nervous system, including both the sympathetic and parasympathetic nervous systems. The degeneration of sympathetic nerve fibers and neurons leads to cardiovascular dysfunction, which is highly prevalent in PD patients. Cardiac alterations such as orthostatic hypotension, heart rate variability, modifications in cardiogram parameters and baroreflex dysfunction can appear in both the early and late stages of PD, worsening as the disease progresses. In PD patients it is generally found that parasympathetic activity is decreased, while sympathetic activity is increased. This situation gives rise to an imbalance of both tonicities which might, in turn, promote a higher risk of cardiac damage through tachycardia and vasoconstriction. Cardiovascular abnormalities can also appear as a side effect of PD treatment: L-DOPA can decrease blood pressure and aggravate orthostatic hypotension as a result of a negative inotropic effect on the heart. This unwanted side effect limits the therapeutic use of L-DOPA in geriatric patients with PD and can contribute to the number of hospital admissions. Therefore, it is essential to define the cardiac features related to PD for the monitorization of the heart condition in parkinsonian individuals. This information can allow the application of intervention strategies to improve the course of the disease and the proposition of new alternatives for its treatment to eliminate or reverse the motor and non-motor symptoms, especially in geriatric patients.
Highlights
Parkinson’s disease (PD) is broadly known to be a movement disorder, originating from the reduction of brain dopamine (DA) content as a consequence of the degeneration of the nigrostriatal system, together with the presence of proteinaceous cytoplasmic inclusions enriched in α-synuclein, named Lewy bodies [1]
We currently know that noradrenergic degeneration in the central nervous system (CNS) is as important as dopaminergic degeneration [24]. This knowledge, together with the appearance of autonomic dysfunction, inspired the thought that noradrenergic innervation could be altered outside the CNS. This relationship is supported by the fact that most of the CNS regions affected in PD are in charge of regulating the activity of the autonomic nervous system, and their degeneration is coupled with the specific reduction of sympathetic terminals in the heart (Figure 1A) [14]
The current methodology to clinically evaluate the loss of noradrenergic innervation in the heart is mainly based on the use of peripheral tracers that bind to catecholaminergic structures [14]: (i) positron emission tomography (PET) with 6-[18 F]fluorodopamine
Summary
Parkinson’s disease (PD) is broadly known to be a movement disorder, originating from the reduction of brain dopamine (DA) content as a consequence of the degeneration of the nigrostriatal system, together with the presence of proteinaceous cytoplasmic inclusions enriched in α-synuclein, named Lewy bodies [1]. PD and cardiovascular diseases have common risk factors: oxidative stress, maintained inflammatory processes, diabetes, obesity and hypertension [10,11,12] Both conditions are comorbidities that appear during aging. The specific concept of “the Parkinsonian Heart” has become more popular during the last decades, since PD patients show unique cardiac features that are different from age-matched control subjects and from other forms of systemic dysfunction [14]. These alterations of the cardiovascular system include sympathetic denervation, functional and structural modifications, and changes at the molecular level [15]. This work reviews the relationship between cardiac alterations and PD, with a special focus on clinical findings (including the effect of antiparkinsonian treatments) and the evidence provided by experimental models used in PD research
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
