Abstract
Reduced uptake of 123I-meta-iodobenzylguanidine (123I-MIBG) and orthostatic hypotension (OH) are independently associated with worse clinical outcomes of Parkinson’s disease (PD). However, their interactive influence on PD has not been studied. The role of 123I-MIBG myocardial uptake, as a biomarker of PD severity, was investigated, conditional on the mediating effects of OH. A total of 227 PD patients were enrolled. Their motor and nonmotor aspects were assessed with standardized tools. Global disease burden was estimated by averaging the scaled z-scores of the assessment tools. Every patient went through 123I-MIBG scan, and OH was evaluated with the head-up tilt-test. The mediating role of orthostatic blood pressure changes (ΔBP) on the association between cardiac sympathetic denervation and disease burden was investigated. Low heart-to-mediastinum (H/M) ratio with less than 1.78 was seen in 69.6% of the patient population, and 22.9% of patients had OH. Low H/M ratio was associated with OH, and these patients had worse disease burden than subjects with normal 123I-MIBG uptake (global composite z-score: normal 123I-MIBG vs. abnormal 123I-MIBG; −0.3 ± 0.5 vs. 0.1 ± 0.7; p < 0.001). The mediation models, controlled for age and disease duration, revealed that the delayed H/M ratio and global composite score were negatively associated, irrespective of orthostatic ΔBP. Adverse relationship between cardiac sympathetic denervation and disease burden was shown without any interference from orthostatic blood pressure fluctuations. This result suggested that extracranial cardiac markers might reflect disease burden, regardless of labile blood pressure influence.
Highlights
Cardiovascular dysautonomia is increasingly accepted as a prodromal ‘window’ in which Parkinson’s disease (PD) can be detected[1,2,3,4,5]
We investigated whether a mediating role for orthostatic hypotension (OH) could be disproved in the context of a significant association between cardiac sympathetic denervation and clinical disease burden
Cardiac sympathetic denervation and orthostatic hypotension were encountered in early PD patients
Summary
Cardiovascular dysautonomia is increasingly accepted as a prodromal ‘window’ in which Parkinson’s disease (PD) can be detected[1,2,3,4,5]. These findings have been reported as clinical biomarkers for predicting PD clinical outcomes and consequences[6,7,8,9,10]. Reduced myocardial uptake of 123I-MIBG indicates norepinephrine transporter dysfunction in sympathetic neurons, and may reflect physiological consequences in residual functional cardiac sympathetic axons[7,12]. PD patients with SWEND had mild Hoehn and Yahr (H&Y) stage, short disease duration, slow progression of motor dysfunction, a lower incidence of the wearing-off phenomenon, and a lower prevalence of nonmotor symptoms[7,10,11,12,14,15]
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