Chronic Kidney Disease and Heart Failure With Preserved Ejection Fraction: The Role of Mitochondrial Dysfunction
|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. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT03960073|
Recruitment Status : Active, not recruiting
First Posted : May 22, 2019
Last Update Posted : March 26, 2020
|Condition or disease||Intervention/treatment||Phase|
|Renal Insufficiency, Chronic Heart Failure With Preserved Ejection Fraction||Dietary Supplement: MitoQ Dietary Supplement: Placebo||Phase 4|
Heart failure is a public health epidemic affecting 6.5 million Americans. Heart failure with preserved ejection fraction (HFpEF) accounts for a large burden of heart failure with the incidence and cost associated with the disease projected to double in the next 20 years. The pathophysiology of HFpEF has not yet been fully elucidated and no proven therapies for improving outcomes in HFpEF currently exist, posing major diagnostic and therapeutic challenges. The addition of chronic kidney disease (CKD) presents a complicated cardio renal syndrome that manifests a distinctly different phenotype and exacerbates the diagnostic and therapeutic challenges of HFpEF. This study aims to address the urgent need to establish treatment targets and therapies by investigating potential underlying biological contributors to HFpEF and its symptoms.
Mitochondrial dysfunction is consistently reported in CKD and heart failure. Mitochondrial dysfunction has been implicated in cardiac, skeletal muscle and vascular dysfunction and is therefore an attractive target for a 'whole systems' therapeutic approach that would encompass exercise intolerance and abnormal blood vessel hemodynamics. A known contributor to and subsequent cyclical result of mitochondrial dysfunction is an abnormally heightened production of mitochondria derived oxidative stress. This study will address the role of mitochondria derived oxidative stress in mitochondrial dysfunction, exercise intolerance and large blood vessel hemodynamics HFpEF patients with and without CKD.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||18 participants|
|Intervention Model:||Crossover Assignment|
|Masking:||Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)|
|Official Title:||Chronic Kidney Disease and Heart Failure With Preserved Ejection Fraction: The Role of Mitochondrial Dysfunction|
|Actual Study Start Date :||July 31, 2019|
|Estimated Primary Completion Date :||October 31, 2021|
|Estimated Study Completion Date :||May 30, 2022|
20mg daily oral dose of MitoQ
Dietary Supplement: MitoQ
4 week 20mg oral daily dose of Mito Q
Placebo Comparator: Placebo
Oral TTP placebo
Dietary Supplement: Placebo
4 week oral daily dose of TTP placebo
- Exercise Capacity [ Time Frame: Change over 4 weeks ]Maximal aerobic capacity (VO2peak) obtained from cardiopulmonary exercise testing
- Reflected Pulse Wave Amplitude [ Time Frame: Change over 4 weeks ]Late systolic pulsatile load on the left ventricle represented by reflected pulse wave amplitude; assessed by echocardiography combined with applanation tonometry.
- Forward Pulse Wave Amplitude [ Time Frame: Change over 4 weeks ]Central hemodynamic assessment of the forward pulse wave amplitude assessed by echocardiography combined with applanation tonometry.
- Mitochondrial Respiration [ Time Frame: Change over 4 weeks ]High resolution mitochondrial respirometry
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT03960073
|United States, Virginia|
|Virginia Commonwealth University|
|Richmond, Virginia, United States, 23298-0256|
|Principal Investigator:||Danielle L Kirkman, PhD||Virginia Commonwealth University|