Pathophysiological Mechanisms of Hypertensive LVH:Optimising Regression

This study has been completed.
Sponsor:
Collaborator:
The Leeds Teaching Hospitals NHS Trust
Information provided by (Responsible Party):
Dr JP Greenwood, University of Leeds
ClinicalTrials.gov Identifier:
NCT00518479
First received: August 17, 2007
Last updated: August 15, 2012
Last verified: August 2012

August 17, 2007
August 15, 2012
September 2003
Not Provided
The primary outcome measure is decrease in LV mass as assessed by cardiac MRI compared between the two treatment groups. [ Time Frame: 6 months ] [ Designated as safety issue: No ]
The primary outcome measure is decrease in LV mass as assessed by cardiac MRI compared between the two treatment groups. [ Time Frame: 6 months ]
Complete list of historical versions of study NCT00518479 on ClinicalTrials.gov Archive Site
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Pathophysiological Mechanisms of Hypertensive LVH:Optimising Regression
Pathophysiological Mechanisms of Hypertensive LVH:Optimising Regression

Uncontrolled high blood pressure can cause heart muscle 'thickening', and this increases the likelihood of complications and death. The high blood pressure explains some but not all of this increase in heart size. This study will investigate the other causes, and will measure the heart muscle 'thickness' very accurately using the latest and most accurate technique called cardiac magnetic resonance imaging (MRI). The best way to treat this heart thickening remains to be determined. We hope to be able to show that by specifically targeting the cause of heart muscle thickening we can reduce its occurrence more effectively than by other standard means of blood pressure treatment

Not Provided
Interventional
Not Provided
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Treatment
  • Hypertension
  • Left Ventricular Hypertrophy
  • Drug: Bendroflumethiazide 2.5mg OD; Amlodipine 10mg OD
  • Drug: Valsartan 160mg OD; Moxonidine 400mcg OD
  • Experimental: 1
    Neurohormonal stimulatory arm
    Intervention: Drug: Bendroflumethiazide 2.5mg OD; Amlodipine 10mg OD
  • Experimental: 2
    Neurohormonal inhibitory arm
    Intervention: Drug: Valsartan 160mg OD; Moxonidine 400mcg OD
Burns J, Sivananthan MU, Ball SG, Mackintosh AF, Mary DA, Greenwood JP. Relationship between central sympathetic drive and magnetic resonance imaging-determined left ventricular mass in essential hypertension. Circulation. 2007 Apr 17;115(15):1999-2005. Epub 2007 Mar 26.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
42
April 2004
Not Provided

Inclusion Criteria:

  • Recently diagnosed essential hypertension (within 6 months).
  • Age 25 to 80 years; Weight < 100kg.
  • Sinus rhythm without significant ventricular or atrial ectopy.

Exclusion Criteria:

  • Current angiotensin II receptor antagonist or ACE Inhibitor treatment.
  • Contra-indication to any of the protocol anti-hypertensive agents.
  • Angina requiring treatment with a Beta blocker or calcium antagonist
  • Any disease affecting the autonomic nervous system e.g. congestive cardiac failure, diabetes, neurological disease, malignancy, pregnancy.
  • Contraindication to MRI (pacemaker, intra-orbital debris, intra-auricular implants, intra-cranial clips, history of claustrophobia, inability to lie supine for 15 minutes etc).
Both
25 Years to 80 Years
No
Contact information is only displayed when the study is recruiting subjects
United Kingdom
 
NCT00518479
PG/03/001
No
Dr JP Greenwood, University of Leeds
University of Leeds
The Leeds Teaching Hospitals NHS Trust
Principal Investigator: John P Greenwood, MBChB, PhD Leeds University
University of Leeds
August 2012

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP