Using Clonidine to Improve Leg Weakness in People With Heart Failure

Overview

People with heart failure often have weakness in their leg muscles. This study will determine whether the leg weakness is due to very high adrenaline levels and whether the medication clonidine can improve leg weakness.

Full Title of Study: “Clonidine and the Skeletal Myopathy of Heart Failure”

Study Type

  • Study Type: Interventional
  • Study Design
    • Allocation: Randomized
    • Intervention Model: Parallel Assignment
    • Primary Purpose: Basic Science
    • Masking: Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)
  • Study Primary Completion Date: March 2011

Detailed Description

Heart failure is a common condition, affecting approximately 5 million people in the United States. People with heart failure are encouraged to exercise and lose weight. However, many people with heart failure develop weakness in their leg muscles, which can make exercise difficult. Increased sympathetic nerve activity, which involves the nerves that carry adrenaline, also occurs in people with heart failure. It is possible that the increased sympathetic nerve activity may actually cause the leg muscle weakness. Clonidine, a medication used to treat high blood pressure, has been found to decrease sympathetic nerve activity. This study will further examine the connection between leg weakness and sympathetic nerve activity. It will also evaluate the effectiveness of clonidine at decreasing leg weakness in people with heart failure. Results from this study may explain why some people with heart failure are unable to exercise and may help to identify ways in which leg strength can be increased. This study will enroll people with heart failure. Participants will be randomly assigned to wear either a clonidine patch or a placebo patch for 3 months. Participants will wear the patch on their upper arm, and they will replace the patch each week. At study visits at baseline and Month 3, participants will undergo the following procedures: – Sympathetic nerve activity recording, which will record nerve activity in the lower leg, using small electrodes inserted through the skin – Muscle biopsy, in which a small piece of muscle tissue will be obtained from participants' legs – Heart rate and blood pressure measurements – Arterial baroreceptor measurements, in which the nerves in the body that respond to changes in blood pressure will be examined while participants receive different medications to increase and decrease their blood pressure – Echocardiography to obtain images of the heart – Magnetic resonance scan of the leg – Passive exercise procedure, in which study researchers will conduct an arm exercise with participants There will be no follow-up visits.

Interventions

  • Drug: Clonidine Patch
    • A clonidine patch (0.1 mg/week) to be worn for a period of 3 months.
  • Other: Matching Placebo Patch
    • A matching placebo patch to be worn for a period of 3 months.

Arms, Groups and Cohorts

  • Experimental: Clonidine patch
    • Participants assigned to wear a clonidine patch.
  • Placebo Comparator: Placebo
    • Participants assigned to wear a matching placebo patch.

Clinical Trial Outcome Measures

Primary Measures

  • Change in Citrate Synthase Activity as an Estimate of Mitochondrial Activity
    • Time Frame: Baseline, 3 months

Secondary Measures

  • Change in Proportion of Type 1 Fibers
    • Time Frame: Baseline, 3 months
    • Fibers were typed as I or II according to presence of myosin heavy chain.

Participating in This Clinical Trial

Inclusion Criteria

  • Heart failure Exclusion Criteria:

  • Currently on Coumadin therapy – Experienced a heart attack in the 3 months before study entry – Medically unable to receive clonidine – Advanced kidney or liver disease

Gender Eligibility: All

Minimum Age: 21 Years

Maximum Age: 65 Years

Are Healthy Volunteers Accepted: No

Investigator Details

  • Lead Sponsor
    • University of California, Los Angeles
  • Collaborator
    • National Heart, Lung, and Blood Institute (NHLBI)
  • Provider of Information About this Clinical Study
    • Principal Investigator: Holly R Middlekauff, Professor – University of California, Los Angeles
  • Overall Official(s)
    • Holly R. Middlekauff, MD, Principal Investigator, University of California, Los Angeles

Citations Reporting on Results

Middlekauff HR, Verity MA, Horwich TB, Fonarow GC, Hamilton MA, Shieh P. Intact skeletal muscle mitochondrial enzyme activity but diminished exercise capacity in advanced heart failure patients on optimal medical and device therapy. Clin Res Cardiol. 2013 Aug;102(8):547-54. doi: 10.1007/s00392-013-0564-3. Epub 2013 Apr 11.

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