Myocardial FibrosisPhase 2PROTECT-AMINCT05531955
Pirfenidone Treat Myocardial Fibrosis After Acute Myocardial Infarction
A Phase 2 study testing Pirfenidone Oral Capsule in people with Myocardial Fibrosis, run by Shanghai Zhongshan Hospital at 1 site in China.
Trial summary
Acute myocardial infarction (AMI) is myocardial necrosis caused by acute and continuous ischemia and hypoxia of coronary artery. It can be complicated with arrhythmia, shock or heart failure, which is often life-threatening. Read more about this study
- Who is it for?
- Ages 18 to 80 years
- Conditions the study is for
- Myocardial Fibrosis
- What is being tested?
- Pirfenidone Oral Capsule
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 100 participants
- Where
- 1 siteChina
- Study dates
- 5 Aug 2022to Jun 2024
- Phase
- Phase 2
- Are there results?
- None posted in the registry
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 to 80 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Age 18 ~ 80 years old (including 18 and 80 years old), regardless of gender.
- Patients with acute anterior myocardial infarction 2-4 weeks after PCI.
- NT proBNP ≥ 800 pg / ml in patients with sinus rhythm and 2400 pg / ml in patients with atrial fibrillation.
- LVEF <50%.
- The patients volunteered to participate in the trial, with good compliance and the ability to understand and sign the informed consent before the study
Who cannot join
- Those who do not meet any of the inclusion criteria.
- Patients with non acute anterior myocardial infarction.
- Patients without PCI after myocardial infarction.
- Glomerular filtration rate (CKD-EPI equation) < 30 ml / min / 1.73 m2.
- Moderate or severe liver cirrhosis, or TBIL > 2 times ULN, ALT or AST > 3 times ULN caused by non cardiac reasons.
- Patients with malignant tumors.
Show all 19Show fewer
- Patients with dysphagia or clinical signs of absorption disorder or requiring parenteral nutrition.
- Patients with active peptic ulcer.
- Severe pulmonary hypertension (pulmonary systolic pressure > 70mmhg).
- Other diseases or complications that may affect the participation in the trial or put the patient at risk based on the judgment of the investigator.
- Allergic to the test drug or its components (e.g., lactose).
- Major surgery is planned during treatment.
- Women who are pregnant, breastfeeding or planning to become pregnant during the trial.
- Women of childbearing age are unwilling or unable to use highly effective contraceptive methods 28 days before administration or 3 months after administration.
- According to the researchers, the patients had alcohol or drug abuse.
- Patients with mental illness.
- Participate in clinical trials of other drugs.
- The researchers judged the participants who were unwell.
- Patients who need to use Nintedanib, pirfenidone and Amifostine at the same time.
Trial locations and contacts
1 site in 1 country.
About this study
Official title: A Study of Pirfenidone in the Treatment of Myocardial Fibrosis After Acute Myocardial Infarction: a Phase II Prospective, Randomized, Double-blind，Placebo Controlled Clinical Trial
Acute myocardial infarction (AMI) is myocardial necrosis caused by acute and continuous ischemia and hypoxia of coronary artery. It can be complicated with arrhythmia, shock or heart failure, which is often life-threatening. The disease is the most common in Europe and the United States, where about 1.5 million people suffer from myocardial infarction every year. China has shown an obvious upward trend in recent years, with at least 500000 new cases every year and at least 2 million current cases . At present, China has a high incidence rate of heart failure after myocardial infarction. The incidence of heart failure within 7 days after myocardial infarction is 19.3%, and the incidence of heart failure from 30 days to 6.7 years after myocardial infarction is 13.1%~37.5%. The incidence of heart failure after myocardial infarction significantly increases the risk of short-term and long-term death, and the prognosis is poor. At present, there is a lack of unified guidance and norms for the diagnosis, treatment and prevention and control strategies of heart failure after myocardial infarction. Cardiac remodeling is the basic pathological process of heart failure after myocardial infarction, and it is also one of the main factors affecting the prognosis of patients. Studies have shown that 30% of AMI have ventricular remodeling 6 months after percutaneous coronary intervention (PCI), and the risk of ventricular remodeling in anterior wall myocardial infarction is the highest. According to foreign literature data, the probability of ventricular remodeling after anterior wall acute myocardial infarction is about 13%, which is 1.9 times higher than that in other parts.Opening the infarct related coronary artery early can save the dying myocardium, reduce the infarct myocardial area and reduce the loss of cardiomyocytes.
Read the detailed description
It plays an important role in preventing or delaying the occurrence of heart failure after myocardial infarction.However,even if the blood supply of infarct related vessels is restored, the immune injury, inflammatory response and RAAS activation caused by apoptotic and necrotic cardiomyocytes after myocardial infarction will still directly lead to a series of pathophysiological changes and aggravate cardiac remodeling. Based on the above targets β Receptor blockers, ACEI / ARB / Arni and aldosterone receptor antagonists have become the cornerstone of drug therapy for cardiac remodeling after myocardial infarction. However, myocardial fibrosis also plays an important role in the process of cardiac remodeling after myocardial infarction. Ischemic death of cardiomyocytes after myocardial infarction can induce repair response, and the damaged tissue is replaced by fibrotic scar produced by fibroblasts and myofibroblasts. Although the initial reparative fibrosis is very important to prevent ventricular wall rupture, excessive fibrosis and reactive fibrosis in non infarcted areas, including myocardial interstitial and perivascular fibrosis, will cause changes in cardiac morphology and biomechanics, further aggravate cardiac remodeling, damage cardiac function, and eventually lead to heart failure. Therefore, inhibition of reactive fibrosis in non infarcted areas is an important supplement to the current treatment of traditional anti cardiac remodeling drugs. In order to reduce the degree of reactive fibrosis in non infarct areas, a potentially feasible method is to inhibit the signal pathway promoting fibrosis. TGF- β Signal pathway plays an important role in promoting fibrosis signal pathway. It can promote the proliferation of fibroblasts, the differentiation and transfer of myofibroblasts, the deposition of collagen and the survival of myofibroblasts, so it can inhibit TGF- β Signal pathway is an effective method to inhibit myocardial fibrosis.
Pirfenidone (PFD) is TGF- β The inhibitor can be used to delay the progression of idiopathic pulmonary fibrosis (IPF). Animal experiments also show that PFD can inhibit TGF- β Reduce myocardial fibrosis and improve the ability of myocardial contraction and relaxation. In the mouse model of dilated cardiomyopathy, it can effectively inhibit the pathological process of dilated cardiomyopathy, improve the degree of cardiac dilation and ventricular wall thickness. Preclinical studies have shown that PFD can inhibit myocardial fibrosis and protect the heart. A recently published phase II clinical study showed that compared with placebo, PFD significantly reduced EF value, preserved myocardial extracellular volume (ECV) and improved myocardial fibrosis in patients with heart failure (HFPEF). In view of the above background, we propose a research assumption: for patients after AMI, PFD drug intervention on the basis of standard treatment may achieve the effect of inhibiting myocardial fibrosis in non infarcted areas, so as to prevent or delay the occurrence of ventricular remodeling and heart failure after myocardial infarction, improve the quality of life and improve the prognosis of patients
- Conditions
- Myocardial Fibrosis
- Being tested
- Pirfenidone Oral Capsule, Placebo Oral Capsule
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Pirfenidone Oral CapsuleDrug
pirfenidone capsules were added to patients receiving basic treatment
Placebo Oral CapsuleOther
placebo oral capsules were added to patients receiving basic treatment
| Study group | Role | What they receive |
|---|---|---|
| Pirfenidone group | Experimental | Drug name:Pirfenidone Dosage Form:capsule Dosage:200mg three times a day in 1st week;400mg three times a day in 2ndweek;600mg three times a day in 3rd week~52th week. Receives: Drug: Pirfenidone Oral Capsule |
| Placebo group | Placebo comparator | Drug name:Placebo Dosage Form:capsule Dosage:200mg three times a day in 1st week;400mg three times a day in 2ndweek;600mg three times a day in 3rd week~52th week. Receives: Other: Placebo Oral Capsule |
What is being measured
The primary outcome is the main question the study is designed to answer.
Changes of the subjects'ECV
Compare the ECV of subjects
Measured: 52week
Secondary outcomes (6)
Cardiovascular death
Number of participants with cardiovascular death
Measured: 52week
Admission for heart failure
Number of participants for heart failure
Measured: 52week
Death
collect the case of death
Measured: 52week
Changes of LVE
compare the LVEF of the subjects
Measured: 52week
Changes of NT-proBNP
compare the NT-proBNP of the subjects
Measured: 52week
Changes of ST2
compare the ST2 of the subjects
Measured: 52week
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted8 Sep 2022
- Study start5 Aug 2022
- Primary completionMay 2024 (estimated)
- Study completionJun 2024 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (9)Papers the sponsor has linked to this study.
- Other trials for Myocardial FibrosisStudies of the same condition, open and under way.
- More trials run by Shanghai Zhongshan HospitalThe sponsor's other registered studies.
- 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 2
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind
- Who is masked
- Participant, Care provider, Investigator
- Enrolment
- 100 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Shanghai Zhongshan Hospital
- Sponsor type
- University, hospital or other
- Collaborators
- Beijing Continent Pharmaceutical Co, Ltd.
- Responsible party
- Sponsor
- Investigators
- Junbo Ge, Doctor, Principal investigator, Shanghai Zhongshan Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05531955
- Sponsor's protocol ID
- SHZS- F647-PIN-202201
- Acronym
- PROTECT-AMI
- Status last verified
- Nov 2022
- First submitted
- 18 Aug 2022
- Last updated
- 10 Nov 2022
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Talman V, Ruskoaho H. Cardiac fibrosis in myocardial infarction-from repair and remodeling to regeneration. Cell Tissue Res. 2016 Sep;365(3):563-81. doi: 10.1007/s00441-016-2431-9. Epub 2016 Jun 21.
PubMed 27324127Prabhu SD, Frangogiannis NG. The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. Circ Res. 2016 Jun 24;119(1):91-112. doi: 10.1161/CIRCRESAHA.116.303577.
PubMed 27340270Lee HC, Park JS, Choe JC, Ahn JH, Lee HW, Oh JH, Choi JH, Cha KS, Hong TJ, Jeong MH; Korea Acute Myocardial Infarction Registry (KAMIR) and Korea Working Group on Myocardial Infarction (KorMI) Investigators. Prediction of 1-Year Mortality from Acute Myocardial Infarction Using Machine Learning. Am J Cardiol. 2020 Oct 15;133:23-31. doi: 10.1016/j.amjcard.2020.07.048. Epub 2020 Jul 26.
PubMed 32811651Dondo TB, Hall M, Munyombwe T, Wilkinson C, Yadegarfar ME, Timmis A, Batin PD, Jernberg T, Fox KA, Gale CP. A nationwide causal mediation analysis of survival following ST-elevation myocardial infarction. Heart. 2020 May;106(10):765-771. doi: 10.1136/heartjnl-2019-315760. Epub 2019 Nov 15.
PubMed 31732655Lewis GA, Dodd S, Clayton D, Bedson E, Eccleson H, Schelbert EB, Naish JH, Jimenez BD, Williams SG, Cunnington C, Ahmed FZ, Cooper A, Rajavarma Viswesvaraiah, Russell S, McDonagh T, Williamson PR, Miller CA. Pirfenidone in heart failure with preserved ejection fraction: a randomized phase 2 trial. Nat Med. 2021 Aug;27(8):1477-1482. doi: 10.1038/s41591-021-01452-0. Epub 2021 Aug 12.
PubMed 34385704Graziani F, Lillo R, Crea F. Rationale for the Use of Pirfenidone in Heart Failure With Preserved Ejection Fraction. Front Cardiovasc Med. 2021 Apr 22;8:678530. doi: 10.3389/fcvm.2021.678530. eCollection 2021.
PubMed 33969025Lewis GA, Schelbert EB, Naish JH, Bedson E, Dodd S, Eccleson H, Clayton D, Jimenez BD, McDonagh T, Williams SG, Cooper A, Cunnington C, Ahmed FZ, Viswesvaraiah R, Russell S, Neubauer S, Williamson PR, Miller CA. Pirfenidone in Heart Failure with Preserved Ejection Fraction-Rationale and Design of the PIROUETTE Trial. Cardiovasc Drugs Ther. 2019 Aug;33(4):461-470. doi: 10.1007/s10557-019-06876-y.
PubMed 31069575Nguyen DT, Ding C, Wilson E, Marcus GM, Olgin JE. Pirfenidone mitigates left ventricular fibrosis and dysfunction after myocardial infarction and reduces arrhythmias. Heart Rhythm. 2010 Oct;7(10):1438-45. doi: 10.1016/j.hrthm.2010.04.030. Epub 2010 Apr 28.
PubMed 20433946Li C, Han R, Kang L, Wang J, Gao Y, Li Y, He J, Tian J. Pirfenidone controls the feedback loop of the AT1R/p38 MAPK/renin-angiotensin system axis by regulating liver X receptor-alpha in myocardial infarction-induced cardiac fibrosis. Sci Rep. 2017 Jan 16;7:40523. doi: 10.1038/srep40523.
PubMed 28091615
Study at a glance
From the registry record, last updated by the sponsor on 10 Nov 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- A Study of Pirfenidone in the Treatment of Myocardial Fibrosis After Acute Myocardial Infarction: a Phase II Prospective, Randomized, Double-blind，Placebo Controlled Clinical Trial
- ClinicalTrials.gov ID
- NCT05531955
- Acronym / sponsor ID
- PROTECT-AMI / SHZS- F647-PIN-202201
- Conditions
- Myocardial Fibrosis
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 100 participants (estimated)
- Lead sponsor
- Shanghai Zhongshan HospitalUniversity, hospital or other
- Collaborators
- Beijing Continent Pharmaceutical Co, Ltd.
- Study start
- 5 Aug 2022 (actual)
- Primary completion
- May 2024 (estimated)
- Study completion
- Jun 2024 (estimated)
- First posted
- 8 Sep 2022 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Acute myocardial infarction (AMI) is myocardial necrosis caused by acute and continuous ischemia and hypoxia of coronary artery. It can be complicated with arrhythmia, shock or heart failure, which is often life-threatening. The disease is the most common in Europe and the United States, where about 1.5 million people suffer from myocardial infarction every year. China has shown an obvious upward trend in recent years, with at least 500000 new cases every year and at least 2 million current cases . At present, China has a high incidence rate of heart failure after myocardial infarction. The incidence of heart failure within 7 days after myocardial infarction is 19.3%, and the incidence of heart failure from 30 days to 6.7 years after myocardial infarction is 13.1%~37.5%. The incidence of heart failure after myocardial infarction significantly increases the risk of short-term and long-term death, and the prognosis is poor. At present, there is a lack of unified guidance and norms for the diagnosis, treatment and prevention and control strategies of heart failure after myocardial infarction. Cardiac remodeling is the basic pathological process of heart failure after myocardial infarction, and it is also one of the main factors affecting the prognosis of patients. Studies have shown that 30% of AMI have ventricular remodeling 6 months after percutaneous coronary intervention (PCI), and the risk of ventricular remodeling in anterior wall myocardial infarction is the highest. According to foreign literature data, the probability of ventricular remodeling after anterior wall acute myocardial infarction is about 13%, which is 1.9 times higher than that in other parts.Opening the infarct related coronary artery early can save the dying myocardium, reduce the infarct myocardial area and reduce the loss of cardiomyocytes.
Detailed description
It plays an important role in preventing or delaying the occurrence of heart failure after myocardial infarction.However,even if the blood supply of infarct related vessels is restored, the immune injury, inflammatory response and RAAS activation caused by apoptotic and necrotic cardiomyocytes after myocardial infarction will still directly lead to a series of pathophysiological changes and aggravate cardiac remodeling. Based on the above targets β Receptor blockers, ACEI / ARB / Arni and aldosterone receptor antagonists have become the cornerstone of drug therapy for cardiac remodeling after myocardial infarction. However, myocardial fibrosis also plays an important role in the process of cardiac remodeling after myocardial infarction. Ischemic death of cardiomyocytes after myocardial infarction can induce repair response, and the damaged tissue is replaced by fibrotic scar produced by fibroblasts and myofibroblasts. Although the initial reparative fibrosis is very important to prevent ventricular wall rupture, excessive fibrosis and reactive fibrosis in non infarcted areas, including myocardial interstitial and perivascular fibrosis, will cause changes in cardiac morphology and biomechanics, further aggravate cardiac remodeling, damage cardiac function, and eventually lead to heart failure. Therefore, inhibition of reactive fibrosis in non infarcted areas is an important supplement to the current treatment of traditional anti cardiac remodeling drugs. In order to reduce the degree of reactive fibrosis in non infarct areas, a potentially feasible method is to inhibit the signal pathway promoting fibrosis. TGF- β Signal pathway plays an important role in promoting fibrosis signal pathway. It can promote the proliferation of fibroblasts, the differentiation and transfer of myofibroblasts, the deposition of collagen and the survival of myofibroblasts, so it can inhibit TGF- β Signal pathway is an effective method to inhibit myocardial fibrosis.
Pirfenidone (PFD) is TGF- β The inhibitor can be used to delay the progression of idiopathic pulmonary fibrosis (IPF). Animal experiments also show that PFD can inhibit TGF- β Reduce myocardial fibrosis and improve the ability of myocardial contraction and relaxation. In the mouse model of dilated cardiomyopathy, it can effectively inhibit the pathological process of dilated cardiomyopathy, improve the degree of cardiac dilation and ventricular wall thickness. Preclinical studies have shown that PFD can inhibit myocardial fibrosis and protect the heart. A recently published phase II clinical study showed that compared with placebo, PFD significantly reduced EF value, preserved myocardial extracellular volume (ECV) and improved myocardial fibrosis in patients with heart failure (HFPEF). In view of the above background, we propose a research assumption: for patients after AMI, PFD drug intervention on the basis of standard treatment may achieve the effect of inhibiting myocardial fibrosis in non infarcted areas, so as to prevent or delay the occurrence of ventricular remodeling and heart failure after myocardial infarction, improve the quality of life and improve the prognosis of patients
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind (participant, care provider, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Pirfenidone group | Experimental | Drug: Pirfenidone Oral CapsuleDrug name:Pirfenidone Dosage Form:capsule Dosage:200mg three times a day in 1st week;400mg three times a day in 2ndweek;600mg three times a day in 3rd week~52th week. |
| Placebo group | Placebo comparator | Other: Placebo Oral CapsuleDrug name:Placebo Dosage Form:capsule Dosage:200mg three times a day in 1st week;400mg three times a day in 2ndweek;600mg three times a day in 3rd week~52th week. |
Who may qualify
- Ages
- 18 to 80 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (5 listed)
- Age 18 ~ 80 years old (including 18 and 80 years old), regardless of gender.
- Patients with acute anterior myocardial infarction 2-4 weeks after PCI.
- NT proBNP ≥ 800 pg / ml in patients with sinus rhythm and 2400 pg / ml in patients with atrial fibrillation.
- LVEF <50%.
- The patients volunteered to participate in the trial, with good compliance and the ability to understand and sign the informed consent before the study
Key exclusion criteria (19 listed)
- Those who do not meet any of the inclusion criteria.
- Patients with non acute anterior myocardial infarction.
- Patients without PCI after myocardial infarction.
- Glomerular filtration rate (CKD-EPI equation) < 30 ml / min / 1.73 m2.
- Moderate or severe liver cirrhosis, or TBIL > 2 times ULN, ALT or AST > 3 times ULN caused by non cardiac reasons.
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 |
|---|---|---|
| Pirfenidone Oral Capsulepirfenidone capsules were added to patients receiving basic treatment | Drug | Pirfenidone group |
| Placebo Oral Capsuleplacebo oral capsules were added to patients receiving basic treatment | Other | Placebo group |
Primary outcome
Changes of the subjects'ECV
Time frame: 52week
Compare the ECV of subjects
6 secondary outcomes
Cardiovascular death
Time frame: 52week
Admission for heart failure
Time frame: 52week
Death
Time frame: 52week
Changes of LVE
Time frame: 52week
Changes of NT-proBNP
Time frame: 52week
Changes of ST2
Time frame: 52week
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 10 Nov 2022.
- Background: PubMed 27324127Talman V, Ruskoaho H. Cardiac fibrosis in myocardial infarction-from repair and remodeling to regeneration. Cell Tissue Res. 2016 Sep;365(3):563-81. doi: 10.1007/s00441-016-2431-9. Epub 2016 Jun 21.
- Background: PubMed 27340270Prabhu SD, Frangogiannis NG. The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. Circ Res. 2016 Jun 24;119(1):91-112. doi: 10.1161/CIRCRESAHA.116.303577.
- Background: PubMed 32811651Lee HC, Park JS, Choe JC, Ahn JH, Lee HW, Oh JH, Choi JH, Cha KS, Hong TJ, Jeong MH; Korea Acute Myocardial Infarction Registry (KAMIR) and Korea Working Group on Myocardial Infarction (KorMI) Investigators. Prediction of 1-Year Mortality from Acute Myocardial Infarction Using Machine Learning. Am J Cardiol. 2020 Oct 15;133:23-31. doi: 10.1016/j.amjcard.2020.07.048. Epub 2020 Jul 26.
- Background: PubMed 31732655Dondo TB, Hall M, Munyombwe T, Wilkinson C, Yadegarfar ME, Timmis A, Batin PD, Jernberg T, Fox KA, Gale CP. A nationwide causal mediation analysis of survival following ST-elevation myocardial infarction. Heart. 2020 May;106(10):765-771. doi: 10.1136/heartjnl-2019-315760. Epub 2019 Nov 15.
- Background: PubMed 34385704Lewis GA, Dodd S, Clayton D, Bedson E, Eccleson H, Schelbert EB, Naish JH, Jimenez BD, Williams SG, Cunnington C, Ahmed FZ, Cooper A, Rajavarma Viswesvaraiah, Russell S, McDonagh T, Williamson PR, Miller CA. Pirfenidone in heart failure with preserved ejection fraction: a randomized phase 2 trial. Nat Med. 2021 Aug;27(8):1477-1482. doi: 10.1038/s41591-021-01452-0. Epub 2021 Aug 12.
- Background: PubMed 33969025Graziani F, Lillo R, Crea F. Rationale for the Use of Pirfenidone in Heart Failure With Preserved Ejection Fraction. Front Cardiovasc Med. 2021 Apr 22;8:678530. doi: 10.3389/fcvm.2021.678530. eCollection 2021.
- Background: PubMed 31069575Lewis GA, Schelbert EB, Naish JH, Bedson E, Dodd S, Eccleson H, Clayton D, Jimenez BD, McDonagh T, Williams SG, Cooper A, Cunnington C, Ahmed FZ, Viswesvaraiah R, Russell S, Neubauer S, Williamson PR, Miller CA. Pirfenidone in Heart Failure with Preserved Ejection Fraction-Rationale and Design of the PIROUETTE Trial. Cardiovasc Drugs Ther. 2019 Aug;33(4):461-470. doi: 10.1007/s10557-019-06876-y.
- Background: PubMed 20433946Nguyen DT, Ding C, Wilson E, Marcus GM, Olgin JE. Pirfenidone mitigates left ventricular fibrosis and dysfunction after myocardial infarction and reduces arrhythmias. Heart Rhythm. 2010 Oct;7(10):1438-45. doi: 10.1016/j.hrthm.2010.04.030. Epub 2010 Apr 28.
- Background: PubMed 28091615Li C, Han R, Kang L, Wang J, Gao Y, Li Y, He J, Tian J. Pirfenidone controls the feedback loop of the AT1R/p38 MAPK/renin-angiotensin system axis by regulating liver X receptor-alpha in myocardial infarction-induced cardiac fibrosis. Sci Rep. 2017 Jan 16;7:40523. doi: 10.1038/srep40523.
- 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.
Junbo Ge, Doctor principal investigator
Shanghai Zhongshan Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing Pirfenidone Oral Capsule in people with Myocardial Fibrosis, run by Shanghai Zhongshan Hospital at 1 site in China.
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 5 inclusion and 19 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: status not confirmed, as of the sponsor's last update on 10 Nov 2022. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in China. 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. Some participants in this study may receive a placebo. 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 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Results are not available in the source record.
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?
Changes of the subjects'ECV (time frame: 52week). 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 NCT05531955, which also lists 9 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 10 Nov 2022.