Heart FailureNCT02997462
Monocyte Phenotypic Changes in Heart Failure
An observational study of Heart Failure and Decompensated Heart Failure, run by University of Michigan at 1 site in United States.
Trial summary
There are many treatments that can improve how long and how well people live with heart failure when they are outside the hospital. However, the investigators know less about how to effectively treat hospitalized heart failure patients so that they do not have to return to the hospital after they go home. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- Conditions the study is for
- Heart Failure, Decompensated Heart Failure
- How many people
- 60 participants
- Where
- 1 siteUnited States
- Study dates
- Nov 2011to 23 Jun 2022
- Phase
- Observational
- 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 years and older
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: Heart failure inpatients and age-matched controls
Who may be able to join
- 18 years of age or older
- Patients must be diagnosed with heart failure
- Patients must be hospitalized at the University of Michigan Hospital for treatment of heart failure symptoms.
- Must be greater than or equal to 65 years of age
Who cannot join
- Heart attack or other active problem with coronary artery disease
- Severe kidney failure or need for dialysis
- An active infection or inflammatory condition
- A need for treatment that affects the immune system (e.g. systemic steroids, immunomodulatory therapies)
- A planned surgery during this hospital admission, including heart transplant or other heart surgery
- Diabetes
Show all 13Show fewer
- High blood pressure
- Active cancer
- Heart disease
- Lung disease
- Liver disease
- Kidney disease
- Active smoker
Trial locations and contacts
1 site in 1 country.
United States1 site
University of Michigan Health System
Ann Arbor, Michigan, 48109
About this study
There are many treatments that can improve how long and how well people live with heart failure when they are outside the hospital. However, the investigators know less about how to effectively treat hospitalized heart failure patients so that they do not have to return to the hospital after they go home. Part of the problem is that the investigators don't understand all of the causes of worsening heart failure.
Previous studies by other researchers suggest that white blood cells called monocytes are over-active in heart failure. Under normal conditions monocytes help fight infections in the body, but over-active monocytes release chemicals that could cause abnormal function of the heart and blood vessels. The investigators' research group believes that over-active monocytes may be an important reason that heart failure worsens before hospitalization.
In this study the investigators will collect blood samples on the day a patient comes into the hospital, the day they return home, and the day they come back to the clinic for a follow-up appointment. The investigators will measure the inflammation in the bloodstream and the activity of monocytes from the patients' blood to see if there are changes in these measurements as heart failure improves. The investigators will also call each patient several times after they return home to ask questions about how they are doing.
Read the detailed description
With over 5 million Americans having heart failure (HF) today and an incidence approaching 10 per 1000 population among persons over the age of 65, HF is a major source or morbidity and mortality and a significant public health concern facing developed nations. In the US, decompensated heart failure is the most common reason for hospital admission among persons older than 65. Yet despite significant advances in the treatment of chronic heart failure, currently there are very few evidence-based strategies to treat acutely decompensated heart failure. The incidence of heart failure will likely continue to rise with the increasing prevalence of HF risk factors (advanced age, hypertension, obesity, diabetes, and other metabolic diseases). Accordingly, substantial efforts are underway to identify and treat populations at risk and to understand the molecular drivers of this heterogeneous disease.
The investigators understanding of the pathophysiology of heart failure has evolved from a 'cardiocentric' view focused on mechanical dysfunction to a more global view. Heart failure is now understood as a complex blend of structural, functional, and neurohormonal abnormalities manifested both locally and systemically. More recently, several groups have demonstrated abnormalities in the inflammatory cascade associated with both the initiation and the progression of heart failure. The innate immune system appears to modulate the inflammatory component of HF through several mechanisms including the production of inflammatory cytokines (tumor necrosis factor-α,TNFα; interleukin-6, IL6), reactive oxygen species, activation of the complement system, as well as through functional modification of endothelial cells and myeloid cell trafficking.
Monocytes and macrophages are two of the key myeloid mediators of acute and chronic inflammatory responses. Myeloid dysregulation has been implicated in the pathogenesis of diverse diseases including diabetes, tumor metastasis, pulmonary fibrosis, myocardial infarction, and atherosclerosis. Accumulating evidence suggests that myeloid subsets have distinct functional properties reflecting their polarization patterns and their interaction with the local microenvironment. As a framework to study their role in models of clinical diseases, myeloid populations have been broadly categorized as "inflammatory" and "anti-inflammatory" based on specific surface markers, cytokine potential, and other functional properties.
Although the role of myeloid populations in inflammatory disease is now appreciated, the molecular mechanisms linking these cells to clinical heart failure syndromes remain largely unknown. The investigators hypothesize that distinct myeloid subsets drive different phases of acute and chronic heart failure syndromes, and that identification of these subsets and their functional properties will provide further insight into the pathophysiology of clinical heart failure.
In order to initially characterize the roles that monocytes play across the spectrum of heart failure, the investigators will obtain whole-blood samples from acutely decompensated patients on the date of hospitalization, the date of transfer from the intensive care unit (ICU) to the general-care telemetry floor (if relevant), the date of hospital discharge, and at their first outpatient follow-up visit. Subjects will be recruited from the University of Michigan inpatient heart failure service, which admits approximately 75 patients for decompensated heart failure each month. Once the samples are obtained, the investigators will perform flow cytometry to characterize monocyte subsets and their flux in response to treatment. The investigators will also look at the production of reactive oxygen species by monocytes and will examine how cytokines and chemokines skew monocyte population subsets and their gene expression profiles. The investigators will also investigate the energetic state and flux (aerobic vs. anaerobic metabolic status) of the monocytes.
- Conditions
- Heart Failure, Decompensated Heart Failure
- Keywords
- Monocyte, Oxidative Stress, Endothelial Function, Congestive Heart Failure
- Medical subject headings
- Heart Failure
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Heart Failure | Heart Failure patients admitted to the ICU or Heart Failure Service. No changes in service-directed plan of care for patients. | |
| Healthy Control | Healthy, age-matched controls. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change in IL-6 between hospital admission and discharge
Cytokine
Measured: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Secondary outcomes (7)
Lys6c Hi and Lo, Mannose Receptor
Cell Surface Markers
Measured: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
IL-10, IL-13
Cytokine
Measured: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Gene Expression (iNOS, CCL2, Ym1, Fizz, VEGF, MMP2/9)
Monocyte gene expression
Measured: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
microRNA
miR155, let7, mir-33a
Measured: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Monocyte/macrophage morphology
Macrophages/monocytes will be classified based on their morphology
Measured: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Serum F-2 Isoprostanes
Oxidative stress marker
Measured: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
TNF-alpha
Marker of inflammation
Measured: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted20 Dec 2016 (estimated)
- Study startNov 2011
- Primary completion23 Jun 2022
- Study completion23 Jun 2022
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (7)Papers the sponsor has linked to this study.
- Other trials for Heart FailureStudies of the same condition, open and under way.
- More trials run by University of MichiganThe 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
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 60 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Michigan
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Scott L. Hummel, University of Michigan
- Investigators
- Scott Hummel, MD MS, Principal investigator, University of MichiganAdam Stein, MD, Principal investigator, University of MichiganSascha Goonewardena, MD, Principal investigator, University of Michigan
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02997462
- Sponsor's protocol ID
- HUM00049322
- Status last verified
- May 2024
- First submitted
- 19 Mar 2012
- Last updated
- 8 May 2024
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Seidler S, Zimmermann HW, Bartneck M, Trautwein C, Tacke F. Age-dependent alterations of monocyte subsets and monocyte-related chemokine pathways in healthy adults. BMC Immunol. 2010 Jun 21;11:30. doi: 10.1186/1471-2172-11-30.
PubMed 20565954Polidori MC, Pratico D, Savino K, Rokach J, Stahl W, Mecocci P. Increased F2 isoprostane plasma levels in patients with congestive heart failure are correlated with antioxidant status and disease severity. J Card Fail. 2004 Aug;10(4):334-8. doi: 10.1016/j.cardfail.2003.11.004.
PubMed 15309701Colombo PC, Banchs JE, Celaj S, Talreja A, Lachmann J, Malla S, DuBois NB, Ashton AW, Latif F, Jorde UP, Ware JA, LeJemtel TH. Endothelial cell activation in patients with decompensated heart failure. Circulation. 2005 Jan 4;111(1):58-62. doi: 10.1161/01.CIR.0000151611.89232.3B. Epub 2004 Dec 20.
PubMed 15611373Levine B, Kalman J, Mayer L, Fillit HM, Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med. 1990 Jul 26;323(4):236-41. doi: 10.1056/NEJM199007263230405.
PubMed 2195340Deswal A, Petersen NJ, Feldman AM, Young JB, White BG, Mann DL. Cytokines and cytokine receptors in advanced heart failure: an analysis of the cytokine database from the Vesnarinone trial (VEST). Circulation. 2001 Apr 24;103(16):2055-9. doi: 10.1161/01.cir.103.16.2055.
PubMed 11319194Mann DL, McMurray JJ, Packer M, Swedberg K, Borer JS, Colucci WS, Djian J, Drexler H, Feldman A, Kober L, Krum H, Liu P, Nieminen M, Tavazzi L, van Veldhuisen DJ, Waldenstrom A, Warren M, Westheim A, Zannad F, Fleming T. Targeted anticytokine therapy in patients with chronic heart failure: results of the Randomized Etanercept Worldwide Evaluation (RENEWAL). Circulation. 2004 Apr 6;109(13):1594-602. doi: 10.1161/01.CIR.0000124490.27666.B2. Epub 2004 Mar 15.
PubMed 15023878Aukrust P, Ueland T, Lien E, Bendtzen K, Muller F, Andreassen AK, Nordoy I, Aass H, Espevik T, Simonsen S, Froland SS, Gullestad L. Cytokine network in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 1999 Feb 1;83(3):376-82. doi: 10.1016/s0002-9149(98)00872-8.
PubMed 10072227
Study at a glance
From the registry record, last updated by the sponsor on 8 May 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Monocyte Phenotypic Changes in Heart Failure
- ClinicalTrials.gov ID
- NCT02997462
- Acronym / sponsor ID
- HUM00049322
- Conditions
- Heart Failure, Decompensated Heart Failure
- Keywords
- Monocyte, Oxidative Stress, Endothelial Function, Congestive Heart Failure
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 60 participants (actual)
- Lead sponsor
- University of MichiganUniversity, hospital or other
- Study start
- Nov 2011
- Primary completion
- 23 Jun 2022 (actual)
- Study completion
- 23 Jun 2022 (actual)
- First posted
- 20 Dec 2016 (estimated)
- 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.
There are many treatments that can improve how long and how well people live with heart failure when they are outside the hospital. However, the investigators know less about how to effectively treat hospitalized heart failure patients so that they do not have to return to the hospital after they go home. Part of the problem is that the investigators don't understand all of the causes of worsening heart failure.
Previous studies by other researchers suggest that white blood cells called monocytes are over-active in heart failure. Under normal conditions monocytes help fight infections in the body, but over-active monocytes release chemicals that could cause abnormal function of the heart and blood vessels. The investigators' research group believes that over-active monocytes may be an important reason that heart failure worsens before hospitalization.
In this study the investigators will collect blood samples on the day a patient comes into the hospital, the day they return home, and the day they come back to the clinic for a follow-up appointment. The investigators will measure the inflammation in the bloodstream and the activity of monocytes from the patients' blood to see if there are changes in these measurements as heart failure improves. The investigators will also call each patient several times after they return home to ask questions about how they are doing.
Detailed description
With over 5 million Americans having heart failure (HF) today and an incidence approaching 10 per 1000 population among persons over the age of 65, HF is a major source or morbidity and mortality and a significant public health concern facing developed nations. In the US, decompensated heart failure is the most common reason for hospital admission among persons older than 65. Yet despite significant advances in the treatment of chronic heart failure, currently there are very few evidence-based strategies to treat acutely decompensated heart failure. The incidence of heart failure will likely continue to rise with the increasing prevalence of HF risk factors (advanced age, hypertension, obesity, diabetes, and other metabolic diseases). Accordingly, substantial efforts are underway to identify and treat populations at risk and to understand the molecular drivers of this heterogeneous disease.
The investigators understanding of the pathophysiology of heart failure has evolved from a 'cardiocentric' view focused on mechanical dysfunction to a more global view. Heart failure is now understood as a complex blend of structural, functional, and neurohormonal abnormalities manifested both locally and systemically. More recently, several groups have demonstrated abnormalities in the inflammatory cascade associated with both the initiation and the progression of heart failure. The innate immune system appears to modulate the inflammatory component of HF through several mechanisms including the production of inflammatory cytokines (tumor necrosis factor-α,TNFα; interleukin-6, IL6), reactive oxygen species, activation of the complement system, as well as through functional modification of endothelial cells and myeloid cell trafficking.
Monocytes and macrophages are two of the key myeloid mediators of acute and chronic inflammatory responses. Myeloid dysregulation has been implicated in the pathogenesis of diverse diseases including diabetes, tumor metastasis, pulmonary fibrosis, myocardial infarction, and atherosclerosis. Accumulating evidence suggests that myeloid subsets have distinct functional properties reflecting their polarization patterns and their interaction with the local microenvironment. As a framework to study their role in models of clinical diseases, myeloid populations have been broadly categorized as "inflammatory" and "anti-inflammatory" based on specific surface markers, cytokine potential, and other functional properties.
Although the role of myeloid populations in inflammatory disease is now appreciated, the molecular mechanisms linking these cells to clinical heart failure syndromes remain largely unknown. The investigators hypothesize that distinct myeloid subsets drive different phases of acute and chronic heart failure syndromes, and that identification of these subsets and their functional properties will provide further insight into the pathophysiology of clinical heart failure.
In order to initially characterize the roles that monocytes play across the spectrum of heart failure, the investigators will obtain whole-blood samples from acutely decompensated patients on the date of hospitalization, the date of transfer from the intensive care unit (ICU) to the general-care telemetry floor (if relevant), the date of hospital discharge, and at their first outpatient follow-up visit. Subjects will be recruited from the University of Michigan inpatient heart failure service, which admits approximately 75 patients for decompensated heart failure each month. Once the samples are obtained, the investigators will perform flow cytometry to characterize monocyte subsets and their flux in response to treatment. The investigators will also look at the production of reactive oxygen species by monocytes and will examine how cytokines and chemokines skew monocyte population subsets and their gene expression profiles. The investigators will also investigate the energetic state and flux (aerobic vs. anaerobic metabolic status) of the monocytes.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Heart Failure | – | –Heart Failure patients admitted to the ICU or Heart Failure Service. No changes in service-directed plan of care for patients. |
| Healthy Control | – | –Healthy, age-matched controls. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- Heart failure inpatients and age-matched controls
Key inclusion criteria (4 listed)
- 18 years of age or older
- Patients must be diagnosed with heart failure
- Patients must be hospitalized at the University of Michigan Hospital for treatment of heart failure symptoms.
- Must be greater than or equal to 65 years of age
Key exclusion criteria (13 listed)
- Heart attack or other active problem with coronary artery disease
- Severe kidney failure or need for dialysis
- An active infection or inflammatory condition
- A need for treatment that affects the immune system (e.g. systemic steroids, immunomodulatory therapies)
- A planned surgery during this hospital admission, including heart transplant or other heart surgery
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Change in IL-6 between hospital admission and discharge
Time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Cytokine
7 secondary outcomes
Lys6c Hi and Lo, Mannose Receptor
Time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
IL-10, IL-13
Time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Gene Expression (iNOS, CCL2, Ym1, Fizz, VEGF, MMP2/9)
Time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
microRNA
Time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Monocyte/macrophage morphology
Time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Serum F-2 Isoprostanes
Time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
TNF-alpha
Time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 8 May 2024.
- Background: PubMed 20565954Seidler S, Zimmermann HW, Bartneck M, Trautwein C, Tacke F. Age-dependent alterations of monocyte subsets and monocyte-related chemokine pathways in healthy adults. BMC Immunol. 2010 Jun 21;11:30. doi: 10.1186/1471-2172-11-30.
- Background: PubMed 15309701Polidori MC, Pratico D, Savino K, Rokach J, Stahl W, Mecocci P. Increased F2 isoprostane plasma levels in patients with congestive heart failure are correlated with antioxidant status and disease severity. J Card Fail. 2004 Aug;10(4):334-8. doi: 10.1016/j.cardfail.2003.11.004.
- Background: PubMed 15611373Colombo PC, Banchs JE, Celaj S, Talreja A, Lachmann J, Malla S, DuBois NB, Ashton AW, Latif F, Jorde UP, Ware JA, LeJemtel TH. Endothelial cell activation in patients with decompensated heart failure. Circulation. 2005 Jan 4;111(1):58-62. doi: 10.1161/01.CIR.0000151611.89232.3B. Epub 2004 Dec 20.
- Background: PubMed 2195340Levine B, Kalman J, Mayer L, Fillit HM, Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med. 1990 Jul 26;323(4):236-41. doi: 10.1056/NEJM199007263230405.
- Background: PubMed 11319194Deswal A, Petersen NJ, Feldman AM, Young JB, White BG, Mann DL. Cytokines and cytokine receptors in advanced heart failure: an analysis of the cytokine database from the Vesnarinone trial (VEST). Circulation. 2001 Apr 24;103(16):2055-9. doi: 10.1161/01.cir.103.16.2055.
- Background: PubMed 15023878Mann DL, McMurray JJ, Packer M, Swedberg K, Borer JS, Colucci WS, Djian J, Drexler H, Feldman A, Kober L, Krum H, Liu P, Nieminen M, Tavazzi L, van Veldhuisen DJ, Waldenstrom A, Warren M, Westheim A, Zannad F, Fleming T. Targeted anticytokine therapy in patients with chronic heart failure: results of the Randomized Etanercept Worldwide Evaluation (RENEWAL). Circulation. 2004 Apr 6;109(13):1594-602. doi: 10.1161/01.CIR.0000124490.27666.B2. Epub 2004 Mar 15.
- Background: PubMed 10072227Aukrust P, Ueland T, Lien E, Bendtzen K, Muller F, Andreassen AK, Nordoy I, Aass H, Espevik T, Simonsen S, Froland SS, Gullestad L. Cytokine network in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 1999 Feb 1;83(3):376-82. doi: 10.1016/s0002-9149(98)00872-8.
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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.
Scott Hummel, MD MS principal investigator
University of Michigan
Adam Stein, MD principal investigator
University of Michigan
Sascha Goonewardena, MD principal investigator
University of Michigan
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Heart Failure and Decompensated Heart Failure, run by University of Michigan at 1 site in United States.
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 4 inclusion and 13 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 8 May 2024. 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 United States. 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.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
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 IL-6 between hospital admission and discharge (time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)). 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 NCT02997462, which also lists 7 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 8 May 2024; AzTrials last refreshed its copy on 28 Oct 2026.