Key result
Levodopa reduces elevated central aortic and peripheral blood pressures in Parkinson disease.
Why the study?
Cardiovascular autonomic dysfunction leading to hemodynamic disorders is common in Parkinson's disease, but central aortic pressure and arterial stiffness parameters remained to be compared against controls and evaluated before and after levodopa intake.
Does Parkinson's disease increase central aortic pressure and arterial stiffness, and how does levodopa affect these parameters?
Cross-Sectional (n=158)
No
Does Parkinson's disease increase central aortic pressure and arterial stiffness, and how does levodopa affect these parameters?
Patients with Parkinson's disease exhibit increased central aortic pressure and arterial stiffness compared to healthy controls, suggesting cardiovascular autonomic dysfunction that is partially mitigated by levodopa.
Background: Cardiovascular autonomic dysfunction, which leads to hemodynamic disorders, is commonly observed in patients with Parkinson's disease (PD). Central aortic pressure (CAP) is the systolic blood pressure (SBP) at the root of the aorta. In young people, CAP is lower than peripheral arterial blood pressure. In older people, the difference between CAP and peripheral arterial blood pressure decreases depending on the extent of arterial stiffness (AS). In patients with AS, CAP increases. CAP is thus regarded as an indicator of AS. Objective: To compare CAP and other hemodynamic parameters for AS between patients with Parkinson's disease and control group. We also aimed to evaluate changes in these hemodynamic parameters after the levodopa (LD) intake. Methods: We included 82 patients with PD and 76 healthy controls. Age, sex, disease duration, disease subtype, Hoehn-Yahr stage (H&Y), and nonmotor symptoms (NMS) were documented. TensioMed Software v.3.0.0.1 was used to measure CAP, peripheral arterial blood pressure, pulse pressure (PP), heart rate (HR), mean arterial pressure (MAP), augmentation index (AI), pulse wave velocity, and ejection time. All patients were being treated with LD, and measurements were performed 1 h before and 1 h after LD intake. Results: < 0.001, respectively) after LD intake in the PD group. Disease subtype, duration, and severity did not affect any of the hemodynamic parameters. When NMS were evaluated, patients with psychosis and dementia showed higher baseline parameters. Conclusion: Loss of postganglionic noradrenergic innervation is well-known with PD. Several cardiac hemodynamic parameters were affected, suggesting cardiac autonomic dysfunction in these patients. The data obtained were independent of disease severity, duration, and subtype. After LD intake, most of these parameters decreased, which might have a positive effect on the vascular burden.
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Balal et al. (2022) conducted a cross-sectional in Parkinson's Disease (n=158). Parkinson's Disease vs. Healthy controls was evaluated on Central aortic pressure and hemodynamic parameters (SBP, PP, HR) (p=<0.001). Central aortic pressure and peripheral arterial blood pressure were significantly higher in patients with Parkinson's disease compared to healthy controls, and these parameters decreased significantly following levodopa administration.
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