Chronic Kidney Disease and Heart Failure With Preserved Ejection Fraction: The Role of Mitochondrial Dysfunction

Heart Failure With Preserved Ejection Fraction Clinical Trial

Official title:

Chronic Kidney Disease and Heart Failure With Preserved Ejection Fraction: The Role of Mitochondrial Dysfunction

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT03960073
• Other study ID #: HM20015440
• Status: Completed
• Phase: N/A
• Start date: July 31, 2019
• Est. completion date: September 30, 2022

Study information

• Verified date: December 2022
• Source: Virginia Commonwealth University
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial Summary

The purpose of this study is to investigate the role of mitochondrial derived oxidative stress on exercise capacity and arterial hemodynamics in HFpEF patients with and without chronic kidney disease.

Description:

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 25
• Est. completion date: September 30, 2022
• Est. primary completion date: September 30, 2022
• Accepts healthy volunteers: No
• Gender: All
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

1. above the age of 18 years

2. a clinical diagnosis of stable Stage C Heart Failure with NYHA Class II-III symptoms

3. a left ventricular ejection fraction >50%

Exclusion Criteria:

1. current cancer

2. current pregnancy

3. current antioxidant supplement use and unwilling to have a 7-day antioxidant washout period before the beginning the trial and to continue antioxidant disuse throughout the trial.

4. current antiretroviral medication use

5. absolute contraindications to exercise testing according to the American College of Sports Medicine guidelines

6. fluid overload

7. unable to provide informed consent

Related Conditions & MeSH terms

• Heart Failure
• Heart Failure With Preserved Ejection Fraction
• Kidney Diseases
• Renal Insufficiency
• Renal Insufficiency, Chronic

Intervention

Dietary Supplement:
• MitoQ
4 week 20mg oral daily dose of Mito Q
• Placebo
4 week oral daily dose of TTP placebo

Locations

Country	Name	City	State
United States	Virginia Commonwealth University	Richmond	Virginia

Sponsors (1)

Lead Sponsor	Collaborator
Virginia Commonwealth University

Country where clinical trial is conducted

United States, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Exercise Capacity	Maximal aerobic capacity (VO2peak) obtained from cardiopulmonary exercise testing	Change over 4 weeks
Secondary	Reflected Pulse Wave Amplitude	Late systolic pulsatile load on the left ventricle represented by reflected pulse wave amplitude; assessed by echocardiography combined with applanation tonometry.	Change over 4 weeks
Secondary	Forward Pulse Wave Amplitude	Central hemodynamic assessment of the forward pulse wave amplitude assessed by echocardiography combined with applanation tonometry.	Change over 4 weeks
Secondary	Mitochondrial Respiration	High resolution mitochondrial respirometry	Change over 4 weeks