Heart FailurePhase 3RECOVER-LVNCT03552575
The Effects of Sacubitril/Valsartan Compared to Valsartan on LV Remodelling in Asymptomatic LV Systolic Dysfunction After MI
A Phase 3 study testing sacubitril/valsartan and Valsartan in people with Heart Failure, run by NHS Greater Glasgow and Clyde at 2 sites in United Kingdom.
Trial summary
Prior to reperfusion therapy, the major therapeutic breakthrough in myocardial infarction was the demonstration that ACE inhibitors or ARBs, given to prevent adverse "remodelling" (progressive dilatation and decline in systolic function) in high risk patients, reduced the likelihood of developing heart failure and the… Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Heart Failure
- What is being tested?
- sacubitril/valsartan and Valsartan
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 93 participants
- Where
- 2 sitesUnited Kingdom
- Study dates
- 1 Jul 2018to 25 Jul 2020
- Phase
- Phase 3
- Are there results?
- Yes, posted in the registrySummary in the doctors' view
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Acute myocardial infarction (AMI) at least 3 months prior to recruitment
- Left ventricular ejection ≤40% as measured by transthoracic echocardiography
- Ability to provide written, informed consent
- Age ≥18 years
- Tolerance of a minimum dose of ACE inhibitor/ARB (ramipril 2.5mg BD or equivalent)
- Treatment with a beta-blocker unless not tolerated or contraindicated.
Who cannot join
- Contraindication to CMR (ferrous prosthesis, implantable cardiac device or severe claustrophobia)
- Clinical and/or radiological heart failure (NYHA≥2)
- Symptomatic hypotension and/or systolic blood pressure <100mmHg
- eGFR < 30 mL/min/1.73m2 and/or serum potassium >5.2mmol/L
- Persistent/permanent atrial fibrillation
- History of AMI within last 3 months
Show all 17Show fewer
- History of hypersensitivity or allergy to ACE-inhibitors/ARB
- History of angioedema
- Known hypersensitivity to the active study drug substances, contrast media or any of the excipients
- Obesity (where body girth exceeds MRI scanner diameter)
- Pregnancy, planning pregnancy, or breast feeding
- Inability to give informed consent or comply with study protocol
- Evidence of hepatic disease as determined by any one of the following: AST or ALT values exceeding 2 x ULN at Visit 1, history of hepatic encephalopathy, history of oesophageal varices, or history of portacaval shunt
- History of biliary cirrhosis and cholestasis
- Active treatment with cholestyramine or colestipol resins
- Active treatment with lithium or direct renin inhibitor
- Participation in another intervention study involving a drug or device within the past 90 days (co-enrolment in observational studies is permitted)
Trial locations and contacts
2 sites in 1 country.
United Kingdom2 sites
Glasgow Cardiovascular Research Centre
Glasgow, Scotland, G12 8TA
Glasgow Clinical Research Facility
Glasgow, Scotland, G51 4TF
About this study
Official title: The Effects of Sacubitril/Valsartan Compared to Valsartan on Left Ventricular Remodelling in Asymptomatic Left Ventricular Systolic Dysfunction After Myocardial Infarction: a Randomised, Double-blinded, Active-comparator, Cardiac-MR Based Trial
Prior to reperfusion therapy, the major therapeutic breakthrough in myocardial infarction was the demonstration that ACE inhibitors or ARBs, given to prevent adverse "remodelling" (progressive dilatation and decline in systolic function) in high risk patients, reduced the likelihood of developing heart failure and the risk of death. The neurohumoral systems which are activated in patients after myocardial infarction (and in heart failure) are not all harmful and some endogenous systems may be protective. The best recognised of these is the natriuretic peptide system.
A- and B-type natriuretic peptides are secreted by the heart when it is stressed and these peptides promote vasodilation (reducing left ventricular wall stress), stimulate renal sodium and water excretion (i.e. antagonising the retention of salt and water characterising heart failure) and inhibit pathological growth i.e. hypertrophy and fibrosis (key components of the adverse left ventricular remodelling that occurs after infarction and in heart failure).The augmentation of plasma levels of endogenous natriuretic peptides can be achieved through inhibition of neutral endopeptidase, also known as neprilysin (NEP), which is responsible for the breakdown of natriuretic peptides. Recently, the addition of neprilysin inhibition to blockade of the RAAS (using sacubitril/valsartan), compared with RAAS blockade alone, reduced the risk of heart failure hospitalisation and death in patients with HF-REF. These exciting findings may lead to a new approach to the treatment of heart failure, with an angiotensin receptor neprilysin inhibitor (ARNI) replacing an ACE inhibitor as one of the fundamental treatments for this condition. We believe that the same approach may be beneficial in highrisk survivors of myocardial infarction. Recently, sacubitril/valsartan was shown to ameliorate adverse left ventricular remodelling in an experimental model of acute myocardial infarction. The objective of the present proposal is to gather "proof-ofconcept", mechanistic, evidence in humans to support adoption of this new approach in patients at high risk after myocardial infarction as a result of residual left ventricular systolic dysfunction.
Read the detailed description
The objective of the present proposal is to obtain information, which is currently not available, on the cardiac effects of sacubitril/valsartan in patients with LVSD, better characterise the neurohumoral actions of sacubitril/valsartan and gather "proof-ofconcept", mechanistic, evidence in humans to support adoption of this new treatment in patients at high risk after myocardial infarction as a result of residual LVSD.
Surprisingly, there is currently limited evidence about how sacubitril/valsartan works in humans. PARADIGM-HF was a large pragmatic mortality/morbidity trial with no mechanistic sub-studies and this is also true of a ongoing trial (PARADISE-MI) in acute myocardial infarction. Moreover, both trials either used or will use an ACE inhibitor (enalapril and ramipril, respectively), rather than an ARB as the active comparator for sacubitril/valsartan; use of valsartan in our study will allow us to precisely define the effects of neprilysin inhibition. A-type (or atrial) natriuretic peptide (ANP), C-type natriuretic peptide (CNP) and adrenomedullin are substrates for neprilysin and may play a role in the action of sacubitril/valsartan but have not been measured in existing clinical trials (in part because of the instability of these peptides and unfeasibility of measuring them in multi-centre, multi-national trials).
Indeed, ANP and CNP are more specific substrates for neprilysin than BNP. As has been mentioned above, cardiac fibrosis appears to be important in the process of LV remodelling in patients with asymptomatic LVSD and the development of HF-REF and is reflected in circulating biomarkers which may be influenced by sacubitril/valsartan
- Conditions
- Heart Failure
- Being tested
- sacubitril/valsartan, Valsartan
- Keywords
- sacubritil, valsartan, left ventricular remodelling, asymptomatic left ventricular systolic dysfunction, myocardial infarction
- Medical subject headings
- Heart Failure, Myocardial Infarction
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
sacubitril/valsartanDrug
Sacubitril is a prodrug neprilysin inhibitor used in combination with valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction.
ValsartanDrug
is an angiotensin II receptor antagonist (commonly called an ARB, or angiotensin receptor blocker), that is selective for the type I (AT1) angiotensin receptor.
| Study group | Role | What they receive |
|---|---|---|
| Sacubitril/valsartan | Experimental | 24mg/26mg (dose level 1), 49mg/51mg (dose level 2) and 97mg/103mg (dose level 3) twice daily Receives: Drug: sacubitril/valsartan |
| Valsartan | Experimental | 40mg (dose level 1), 80mg (dose level 2) and 160mg (dose level 3) twice daily. Receives: Drug: Valsartan |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change in Left Ventricular End Systolic Volume Index
Change in indexed left ventricular end-systolic volume (LVESVI) measured by cardiac MR measured in ml/m2
Measured: baseline and 12 months
Secondary outcomes (7)
Change in N-terminal Prohormone of B-type Natriuretic Peptide Levels
measured in pg/ml
Measured: baseline and 12 months
Change in High Sensitivity Troponin I Levels
measured in ng/L
Measured: baseline and 12 months
Change in Left Ventricular End-Diastolic Volume Index
Change in indexed left ventricular end-diastolic volume (LVEDVI) measured by cardiac MR measured in ml/m2
Measured: baseline and 12 months
Change in Left Atrial Volume Index
Change in indexed Left Atrial Volume (LAVI) measured by cardiac MR measured in ml/m2
Measured: baseline and 12 months
Change in Left Ventricular Ejection Fraction
Change in left ventricular ejection fraction (LVEF) measured by cardiac MR measured in percentage
Measured: baseline and 12 months
Change in Left Ventricular Mass Index
Change in indexed left ventricular mass (LVMI) measured by cardiac MR measured in grams/m2
Measured: baseline and 12 months
Change in Patient Well Being as Assessed by Patient Global Assessment Questionnaire
Change in patient well being as assessed by patient global assessment questionnaire which is a patient reported outcome measure that involves a patients own response to questions about their overall health and/or disease activity
Measured: 12 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted12 Jun 2018
- Study start1 Jul 2018
- Primary completion25 Jul 2020
- Study completion25 Jul 2020
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Posted resultsParticipant flow, outcome measures and adverse events reported by the sponsor.
- Publications (2)Papers the sponsor has linked to this study.
- Other trials for Heart FailureStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 3
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Model description
- Prospective, randomised, active-comparator, double-blinded study.
- Masking
- Quadruple blind
- Who is masked
- Participant, Care provider, Investigator, Outcomes assessor
- Enrolment
- 93 participants (actual)
Sponsor and investigators
- Lead sponsor
- NHS Greater Glasgow and Clyde
- Sponsor type
- University, hospital or other
- Collaborators
- University of Glasgow
- Responsible party
- Sponsor
- Investigators
- John McMurray, MBChB PhD, Principal investigator, NHS GGC and Glasgow University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03552575
- Sponsor's protocol ID
- GN16CA007
- Acronym
- RECOVER-LV
- Status last verified
- Apr 2022
- First submitted
- 29 May 2018
- Last updated
- 3 May 2023
- Results posted
- Yes, on ClinicalTrials.gov
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Brum WS, Docherty KF, Ashton NJ, Zetterberg H, Hansson O, McMurray JJV, Blennow K. Effect of Neprilysin Inhibition on Alzheimer Disease Plasma Biomarkers: A Secondary Analysis of a Randomized Clinical Trial. JAMA Neurol. 2024 Feb 1;81(2):197-200. doi: 10.1001/jamaneurol.2023.4719.
PubMed 38109077Docherty KF, Campbell RT, Brooksbank KJM, Dreisbach JG, Forsyth P, Godeseth RL, Hopkins T, Jackson AM, Lee MMY, McConnachie A, Roditi G, Squire IB, Stanley B, Welsh P, Jhund PS, Petrie MC, McMurray JJV. Effect of Neprilysin Inhibition on Left Ventricular Remodeling in Patients With Asymptomatic Left Ventricular Systolic Dysfunction Late After Myocardial Infarction. Circulation. 2021 Jul 20;144(3):199-209. doi: 10.1161/CIRCULATIONAHA.121.054892. Epub 2021 May 13.
PubMed 33983794
Study at a glance
From the registry record, last updated by the sponsor on 3 May 2023. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Effects of Sacubitril/Valsartan Compared to Valsartan on Left Ventricular Remodelling in Asymptomatic Left Ventricular Systolic Dysfunction After Myocardial Infarction: a Randomised, Double-blinded, Active-comparator, Cardiac-MR Based Trial
- ClinicalTrials.gov ID
- NCT03552575
- Acronym / sponsor ID
- RECOVER-LV / GN16CA007
- Conditions
- Heart Failure
- Keywords
- sacubritil, valsartan, left ventricular remodelling, asymptomatic left ventricular systolic dysfunction, myocardial infarction
- Phase
- Phase 3
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 93 participants (actual)
- Lead sponsor
- NHS Greater Glasgow and ClydeUniversity, hospital or other
- Collaborators
- University of Glasgow
- Study start
- 1 Jul 2018 (actual)
- Primary completion
- 25 Jul 2020 (actual)
- Study completion
- 25 Jul 2020 (actual)
- First posted
- 12 Jun 2018 (actual)
- Results
- Posted 3 May 2023
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Prior to reperfusion therapy, the major therapeutic breakthrough in myocardial infarction was the demonstration that ACE inhibitors or ARBs, given to prevent adverse "remodelling" (progressive dilatation and decline in systolic function) in high risk patients, reduced the likelihood of developing heart failure and the risk of death. The neurohumoral systems which are activated in patients after myocardial infarction (and in heart failure) are not all harmful and some endogenous systems may be protective. The best recognised of these is the natriuretic peptide system.
A- and B-type natriuretic peptides are secreted by the heart when it is stressed and these peptides promote vasodilation (reducing left ventricular wall stress), stimulate renal sodium and water excretion (i.e. antagonising the retention of salt and water characterising heart failure) and inhibit pathological growth i.e. hypertrophy and fibrosis (key components of the adverse left ventricular remodelling that occurs after infarction and in heart failure).The augmentation of plasma levels of endogenous natriuretic peptides can be achieved through inhibition of neutral endopeptidase, also known as neprilysin (NEP), which is responsible for the breakdown of natriuretic peptides. Recently, the addition of neprilysin inhibition to blockade of the RAAS (using sacubitril/valsartan), compared with RAAS blockade alone, reduced the risk of heart failure hospitalisation and death in patients with HF-REF. These exciting findings may lead to a new approach to the treatment of heart failure, with an angiotensin receptor neprilysin inhibitor (ARNI) replacing an ACE inhibitor as one of the fundamental treatments for this condition. We believe that the same approach may be beneficial in highrisk survivors of myocardial infarction. Recently, sacubitril/valsartan was shown to ameliorate adverse left ventricular remodelling in an experimental model of acute myocardial infarction. The objective of the present proposal is to gather "proof-ofconcept", mechanistic, evidence in humans to support adoption of this new approach in patients at high risk after myocardial infarction as a result of residual left ventricular systolic dysfunction.
Detailed description
The objective of the present proposal is to obtain information, which is currently not available, on the cardiac effects of sacubitril/valsartan in patients with LVSD, better characterise the neurohumoral actions of sacubitril/valsartan and gather "proof-ofconcept", mechanistic, evidence in humans to support adoption of this new treatment in patients at high risk after myocardial infarction as a result of residual LVSD.
Surprisingly, there is currently limited evidence about how sacubitril/valsartan works in humans. PARADIGM-HF was a large pragmatic mortality/morbidity trial with no mechanistic sub-studies and this is also true of a ongoing trial (PARADISE-MI) in acute myocardial infarction. Moreover, both trials either used or will use an ACE inhibitor (enalapril and ramipril, respectively), rather than an ARB as the active comparator for sacubitril/valsartan; use of valsartan in our study will allow us to precisely define the effects of neprilysin inhibition. A-type (or atrial) natriuretic peptide (ANP), C-type natriuretic peptide (CNP) and adrenomedullin are substrates for neprilysin and may play a role in the action of sacubitril/valsartan but have not been measured in existing clinical trials (in part because of the instability of these peptides and unfeasibility of measuring them in multi-centre, multi-national trials).
Indeed, ANP and CNP are more specific substrates for neprilysin than BNP. As has been mentioned above, cardiac fibrosis appears to be important in the process of LV remodelling in patients with asymptomatic LVSD and the development of HF-REF and is reflected in circulating biomarkers which may be influenced by sacubitril/valsartan
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind (participant, care provider, investigator, outcomes assessor)
- Number of arms
- 2
- Model description
- Prospective, randomised, active-comparator, double-blinded study.
| Arm | Type | Receives |
|---|---|---|
| Sacubitril/valsartan | Experimental | Drug: sacubitril/valsartan24mg/26mg (dose level 1), 49mg/51mg (dose level 2) and 97mg/103mg (dose level 3) twice daily |
| Valsartan | Experimental | Drug: Valsartan40mg (dose level 1), 80mg (dose level 2) and 160mg (dose level 3) twice daily. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (6 listed)
- Acute myocardial infarction (AMI) at least 3 months prior to recruitment
Key exclusion criteria (17 listed)
- Contraindication to CMR (ferrous prosthesis, implantable cardiac device or severe claustrophobia)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| sacubitril/valsartanSacubitril is a prodrug neprilysin inhibitor used in combination with valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction. | Drug | Sacubitril/valsartan |
| Valsartanis an angiotensin II receptor antagonist (commonly called an ARB, or angiotensin receptor blocker), that is selective for the type I (AT1) angiotensin receptor. | Drug | Valsartan |
Primary outcome
Change in Left Ventricular End Systolic Volume Index
Time frame: baseline and 12 months
Change in indexed left ventricular end-systolic volume (LVESVI) measured by cardiac MR measured in ml/m2
7 secondary outcomes
Change in N-terminal Prohormone of B-type Natriuretic Peptide Levels
Time frame: baseline and 12 months
Change in High Sensitivity Troponin I Levels
Time frame: baseline and 12 months
Change in Left Ventricular End-Diastolic Volume Index
Time frame: baseline and 12 months
Change in Left Atrial Volume Index
Time frame: baseline and 12 months
Change in Left Ventricular Ejection Fraction
Time frame: baseline and 12 months
Change in Left Ventricular Mass Index
Time frame: baseline and 12 months
Change in Patient Well Being as Assessed by Patient Global Assessment Questionnaire
Time frame: 12 months
Results and safety
Loading the posted results from ClinicalTrials.gov…
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 May 2023.
- Posted resultsParticipant flow, baseline, all outcome measures and adverse events.
- Derived from this study: PubMed 38109077Brum WS, Docherty KF, Ashton NJ, Zetterberg H, Hansson O, McMurray JJV, Blennow K. Effect of Neprilysin Inhibition on Alzheimer Disease Plasma Biomarkers: A Secondary Analysis of a Randomized Clinical Trial. JAMA Neurol. 2024 Feb 1;81(2):197-200. doi: 10.1001/jamaneurol.2023.4719.
- Derived from this study: PubMed 33983794Docherty KF, Campbell RT, Brooksbank KJM, Dreisbach JG, Forsyth P, Godeseth RL, Hopkins T, Jackson AM, Lee MMY, McConnachie A, Roditi G, Squire IB, Stanley B, Welsh P, Jhund PS, Petrie MC, McMurray JJV. Effect of Neprilysin Inhibition on Left Ventricular Remodeling in Patients With Asymptomatic Left Ventricular Systolic Dysfunction Late After Myocardial Infarction. Circulation. 2021 Jul 20;144(3):199-209. doi: 10.1161/CIRCULATIONAHA.121.054892. Epub 2021 May 13.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
John McMurray, MBChB PhD principal investigator
NHS GGC and Glasgow University
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 3 study testing sacubitril/valsartan and Valsartan in people with Heart Failure, run by NHS Greater Glasgow and Clyde at 2 sites in United Kingdom.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 6 inclusion and 17 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 3 May 2023. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites in United Kingdom. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 3 studies compare the treatment with the current standard treatment or a placebo in a large group, to confirm how well it works and watch for side effects.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Yes. Results are posted in the registry (first posted 3 May 2023). A summary is in the For doctors view, and the full results are on ClinicalTrials.gov.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Change in Left Ventricular End Systolic Volume Index (time frame: baseline and 12 months). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT03552575, which also lists 2 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 3 May 2023.