Autonomic Determinants of POTS - Pilot1
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT04050410|
Recruitment Status : Recruiting
First Posted : August 8, 2019
Last Update Posted : September 10, 2019
|Condition or disease||Intervention/treatment||Phase|
|Postural Tachycardia Syndrome||Drug: Moxonidine Drug: Placebo||Early Phase 1|
Postural tachycardia syndrome (POTS) is a relatively common condition affecting mostly otherwise healthy young women. It is the cause of significant disability and an impairment in quality of life of a magnitude comparable to patients with chronic obstructive pulmonary disease or congestive heart failure. It is characterized by sympathetic activation with an exaggerated orthostatic tachycardia that responds to low doses of beta-blockers. The underlying pathophysiology of this disorder and the nature of this sympathetic activation is not clear and is likely heterogeneous. In many patients this sympathetic activation could be an appropriate compensatory response to hypovolemia, deconditioning or partial neuropathy.
The investigators have identified a subset of patients in whom sympathetic activation appears to be a primary phenomenon. These patients are characterized by high central sympathetic outflow, as determined by muscle sympathetic nerve activity (MSNA) above the upper 95% confidence interval for the group. This "hyperadrenergic" phenotype is associated with a paradoxical increase in blood pressure on standing and exaggerated pressor response to the vasoconstrictive phase of the Valsalva maneuver, and clinical observations suggest they improve clinically when treated with central sympatholytics.
The investigators propose to test the hypothesis that there is a subset of POTS patients with a central sympathetic activation as the primary pathophysiology. In an acute double blind, placebo-controlled, randomized study, the investigators propose that administration of the central sympatholytic moxonidine will improve orthostatic symptoms and abnormalities in orthostatic hemodynamics, as well as sympathetic outflow.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||48 participants|
|Intervention Model:||Crossover Assignment|
|Intervention Model Description:||Randomized, double-blind, placebo-controlled crossover|
|Masking:||Double (Participant, Investigator)|
|Masking Description:||Subject and investigator will be blinded. The randomization will be generated by the pharmacy. A staff member of the Autonomic Dysfunction Center who is not involved in the study will keep secretly the randomization blinding table for emergencies. Blinding will be broken for intermediate data analysis and in case of emergencies if necessary. The blinding will be broken at the end of statistical analysis for interpretation of results.|
|Official Title:||Autonomic Determinants of Postural Tachycardia Syndrome (Acute Pilot Study 1)|
|Actual Study Start Date :||August 27, 2019|
|Estimated Primary Completion Date :||July 31, 2024|
|Estimated Study Completion Date :||December 31, 2025|
Patients will receive a single oral dose of moxonidine 0.4 mg.
active drug given as 1 dose
Other Name: Physiotens
Placebo Comparator: Placebo
Patients will receive a single oral dose of placebo.
placebo pill given as 1 dose
Other Name: inactive pill
- Change in Orthostatic Symptom Burden [delta (delta VOSS)] [ Time Frame: after 30 min supine to after 15 min upright (delta VOSS), 2-3 hours after placebo or moxonidine intake [delta (delta VOSS)]. ]VOSS is a validated questionnaire that consists of 9 items: mental clouding, blurred vision, shortness of breath, rapid heartbeat, tremulousness, chest discomfort, headache, lightheadedness, and nausea. Each item is scored on a 0 to 10 scale (with 0 reflecting absence of symptoms), and the change of the total scores (range: 0-90) from supine to upright postures (delta VOSS) will be used as a measure of orthostatic symptom burden. The primary outcome measure will be the difference in orthostatic symptom burden [delta (delta VOSS)] following placebo vs. moxonidine administration.
- Change in Orthostatic Change in Heart Rate [delta (delta HR)] [ Time Frame: after 30 min supine to after 15 min upright (delta HR), 2-3 hours after placebo or moxonidine intake [delta (delta HR)]. ]Difference in heart rate change from supine to upright postures (delta HR) following placebo vs. moxonidine administration.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT04050410
|Contact: Emily C Smith, RN||615 email@example.com|
|United States, Tennessee|
|Vanderbilt University Medical Center||Recruiting|
|Nashville, Tennessee, United States, 37232|
|Contact: Emily C Smith, RN 615-875-1516 firstname.lastname@example.org|
|Principal Investigator: Andre Diedrich, MD|
|Principal Investigator:||André Diedrich, MD||Vanderbilt University Medical Center|