Clinical Autonomic Research最新文献

Aim: The study aimed to assess the haemodynamic effects of fludrocortisone and midodrine, alone or combined, in patients with recurrent syncope and/or symptoms due to hypotension and ≥ 1 daytime systolic blood pressure (SBP) drop < 90 mmHg or ≥ 2 daytime SBP drops < 100 mmHg recorded by 24-h ambulatory blood pressure monitoring (ABPM1).

Method: A total of 53 patients (mean age, 40.9 ± 18.5 years, 37 female) were treated with fludrocortisone (0.05-0.2 mg per day) and/or midodrine (2.5-10 mg two or three times per day). A second ABPM (ABPM2) was performed within 6 months and the results of ABPM1 AND ABPM2 were compared to assess the effects of BP-rising drugs.

Results: In 32 patients assigned to fludrocortisone, 24-h SBP increased from 107.1 ± 9.9 mmHg to 116.3 ± 14.9 (p = 0.0001), the number of daily SBP drops < 90 mmHg decreased by 73% (p = 0.0001) and that of drops < 100 mmHg decreased by 41% (p = 0.0005). In 14 patients assigned to midodrine, 24-h SBP increased from 112.7 ± 7.4 mmHg to 115.0 ± 9.1 (p = 0.12), the number of daily SBP drops < 90 mmHg decreased by 52% (p = 0.04) and that of drops < 100 mmHg decreased by 34% (p = 0.007). In the seven patients taking both fludrocortisone and midodrine, 24-h SBP increased from 110.1 ± 11.5 mmHg to 114.0 ± 12.4 (p = 0.002), the number of daily SBP drops < 90 mmHg decreased by 69% (p = 0.22) and that of drops < 100 mmHg decreased by 44% (p = 0.04).

Conclusions: Both fludrocortisone and midodrine effectively increased 24-h SBP and reduced SBP drops on ABPM but fludrocortisone seemed to be more effective than midodrine. Further randomised studies are needed to confirm these observations.

Purpose: The parasympathetic effects of the sphenopalatine ganglion (SPG) on the cerebral vasculature provide a compelling rationale for its therapeutic application in cerebrovascular ischemia. In recent years, attempts have been made to stimulate the SPG to achieve beneficial effects on cerebral circulation.

Methods: This review synthesizes the available publications on SPG stimulation. It critically evaluates the evidence from preclinical studies and clinical trials to assess its potential as a treatment for acute cerebrovascular disorders and outlines aspects that still require more study.

Results: The medical literature provides consistent evidence of the significant effects of stimulating the SPG on cerebrovascular circulation. In addition, considerable evidence supports the therapeutic role of SPG stimulation in patients with cerebral ischemia.

Conclusion: Given the current understanding, future research could explore the potential of SPG stimulation as a non-reperfusion intervention to improve long-term outcomes for individuals with ischemic cerebrovascular conditions.

Purpose: Cardiovascular autonomic neuropathy remains underdiagnosed in type 1 diabetes mellitus, posing a risk for severe complications, particularly in patients with lowered V̇O_2max, compared to controls. This study aimed to determine whether heart rate variability during cardiovascular autonomic reflex tests reveals early signs of cardiovascular autonomic neuropathy in patients with uncomplicated type 1 diabetes mellitus and normal cardiovascular fitness, compared to healthy controls.

Methods: A type 1 diabetes mellitus group (n = 14) with no other diagnosed diseases (diabetes duration 15 ± 7 years) and a control group (n = 31) underwent deep breathing test, passive orthostatic test, and cardiopulmonary exercise test. Participants were assessed for heart rate variability, heart rate, blood pressure, and V̇O_2max (mL/min/kg).

Results: Participant characteristics, including V̇O_2max (mL/min/kg), showed no significant differences. The type 1 diabetes mellitus group had higher systolic blood pressure during the supine phase of the orthostatic test than healthy controls (131.6 ± 14.7 mmHg vs. 122.4 ± 10.8 mmHg, p = 0.022). After 5 mins in the upright position, systolic blood pressure (132.2 ± 20.6 mmHg vs. 118.7 ± 11.7 mmHg, p = 0.036), heart rate (85 (76; 89) bpm vs. 75 (72; 83) bpm, p = 0.013), and the root mean square of successive RR interval differences (20.22 (11.22; 27.42) vs. 27.11 (19.90; 35.52), p = 0.033) were significantly different compared to controls.

Conclusion: Patients with uncomplicated type 1 diabetes mellitus, despite having normal cardiorespiratory fitness, exhibited higher systolic pressure and greater sympathetic activation in orthostatic tests, suggesting subclinically altered cardiovascular autonomic function.

Purpose: For Long COVID autonomic dysfunction, we have summarized published evidence on treatment effectiveness, clinical practice guidelines, and unpublished/ongoing studies.

Methods: We first interviewed 11 stakeholders (clinicians, clinician/researchers, payors, patient advocates) to gain clinical insights and identify key areas of focus. We searched Embase, CINAHL, Medline, PsycINFO, and PubMed databases for relevant English-language articles published between 1 January 2020 and 30 April 2024. We also searched several other resources for additional relevant guidelines (e.g., UpToDate) and unpublished/ongoing studies (e.g., the International Clinical Trials Registry Platform). All information was summarized narratively.

Results: We included 11 effectiveness studies that investigated numerous treatment regimens (fexofenadine + famotidine, maraviroc + pravastatin, selective serotonin reuptake inhibitors, nutraceutical formulations, multicomponent treatments, heart rate variability biofeedback, inspiratory muscle training, or stellate ganglion block). One randomized trial reported benefits of a nutraceutical (SIM01) on fatigue and gastrointestinal upset. The 11 guidelines and position statements addressed numerous aspects of treatment, but primarily exercise/rehabilitation, fluid/salt intake, and the use of compression garments. The 15 unpublished/ongoing studies are testing nine different interventions, most prominently ivabradine and intravenous immunoglobulin.

Conclusion: Existing studies on the treatment of Long COVID autonomic dysfunction are often small and uncontrolled, making it unclear whether the observed pre-post changes were due solely to the administered treatments. Guidelines display some overlap, and we identified no direct contradictions. Unpublished/ongoing studies may shed light on this critical area of patient management.

Background: Autonomic synucleinopathies feature autonomic failure and intracellular deposition of the protein alpha-synuclein. Three such conditions are the Lewy body diseases (LBDs) Parkinson's disease (PD) and pure autonomic failure (PAF) and the non-LBD synucleinopathy multiple system atrophy (MSA). These diseases all entail catecholaminergic abnormalities in the brain, sympathetically innervated organs, or both; however, little is known about renal catecholaminergic functions in autonomic synucleinopathies. We measured urinary excretion rates of the sympathetic neurotransmitter norepinephrine, the hormone epinephrine, the autocrine-paracrine substance dopamine, the catecholamine precursor 3,4-dihydroxyphenylalanine (DOPA), 3,4-dihydroxyphenylglycol (DHPG, the main neuronal metabolite of norepinephrine), and 3,4-dihydroxyphenylacetic acid (DOPAC, a major dopamine metabolite), in PD, PAF, and MSA groups and controls.

Methods: Data were reviewed from all research participants who had urine collections (usually 3.5 h) at the National Institutes of Health (NIH) Clinical Center from 1995 to 2024. The control cohort had neither autonomic failure nor a movement disorder.

Results: Norepinephrine excretion rates were decreased compared with controls in PD (p = 0.0001), PAF (p < 0.0001), and MSA (p < 0.0001). Dopamine excretion was also decreased in the three groups (PD: p = 0.0136, PAF: p = 0.0027, MSA: p = 0.0344). DHPG excretion was decreased in PD (p = 0.0004) and PAF (p = 0.0004) but not in MSA. DOPA and epinephrine excretion did not differ among the study groups.

Conclusions: Autonomic synucleinopathies involve decreased urinary excretion rates of norepinephrine and dopamine. Since virtually all of urinary dopamine in humans is derived from circulating DOPA, the low rates of urinary norepinephrine and dopamine excretion may reflect dysfunctions in the renal sympathetic noradrenergic system, the DOPA-dopamine autocrine-paracrine system, or both systems.

Purpose: Autonomic failure has a major impact on the quality of life of individuals with Parkinson's disease (PD), especially in advanced stages of the disease. Levodopa/carbidopa intestinal gel (LCIG) infusion is a well-established treatment for advanced PD with severe motor fluctuations and provides substantial benefit in managing some non-motor symptoms (NMS), such as sleep, fatigue, and neuropsychiatric issues. The effect of LCIG on autonomic symptoms is by contrast not well known. Here we performed a systematic review on the influence of LCIG therapy on autonomic dysfunction in PD individuals.

Methods: Following the PRISMA guidelines, we systematically searched for studies that included autonomic outcome measures in LCIG-treated PD individuals, limiting the search to articles written in English and published between January 2005 and June 2023. We evaluated improvement, stability, or worsening of gastrointestinal, urinary, and cardiovascular symptoms at six different timepoints according to clinimetric scale changes compared to baseline. Data on autonomic adverse events (AEs) possibly related to LCIG treatment were also collected.

Results: Of the 1476 studies identified in the initial search, 16 ultimately met the inclusion criteria and underwent quality assessment and data extraction, with data from 1361 PD patients (18.3 months mean follow-up). Thirteen studies reported improvement or stability of gastrointestinal, urinary, and cardiovascular symptoms over the interventional period. One study found a worsening of cardiovascular symptoms and two of urological symptoms. Regarding safety, seven studies reported gastrointestinal (8.4%), urinary (0.5%), and cardiovascular (1.1%) autonomic LCIG-related AEs.

Conclusions: LCIG infusion may help to reduce the burden of autonomic symptoms in advanced PD. Prospective studies specifically addressing the effect of LCIG on autonomic function in advanced PD are warranted.