AzTrials
AzTrials

DiabetesPhase 2/3P3NCT01052272

Impact of Diabetes on Left Ventricular Remodeling

A Phase 2/3 study testing Ramipril, Candesartan cilexetil and Allopurinol in people with Diabetes, run by University of Alabama at Birmingham at 1 site in United States.

Completed

Finished. The study has ended and is not enrolling. Results may be posted on the official record.

Official record
Search all trials

Trial summary

The investigators hypothesize that in patients with diabetes and acute myocardial infarction (MI), Ang II type-1 receptor blockade (AT1RB) attenuates left ventricle (LV) remodeling to a greater extent than angiotensin converting enzyme (ACE) inhibitor therapy and that the addition of xanthine oxidase (XO) inhibitor… Read more about this study

Who is it for?
Ages 21 years and older
Conditions the study is for
Diabetes
What is being tested?
Ramipril, Candesartan cilexetil and Allopurinol
Could I receive a placebo?
No, everyone receives an active treatment
How many people
72 participants
Where
1 siteUnited States
Study dates
Jul 2005to Nov 2010
Phase
Phase 2/3
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 21 years and older
  • All sexes
  • No healthy volunteers
  • Adult, Older adult

Who may be able to join

  • 21 years old or older
  • MI documented by increase in troponin > 0.78 ng/ml or CKMB ≥ 3% of total CK
  • Patients who have Type-2 diabetes defined by any one of the following:
  • Confirmed (i.e., two or more readings) fasting blood glucose >126mg/dl; or
  • Random glucose ≥200mg/dl; or
  • 2 hour glucose ≥200mg/dl following 75g of glucose; or
  • Current treatment with diet or oral agents directed at the control of hyperglycemia either alone or in combination with insulin; or
  • Current treatment with insulin with no prior history of diabetic ketoacidosis.

Who cannot join

  • Type-1 diabetes.
  • Class III or IV heart failure.
  • Cardiomyopathy (including hypertrophic and amyloidosis).
  • Congenital or pericardial diseases.
  • Intolerance to either ACE inhibitor, AT1-RB or allopurinol.
  • Renal failure with creatinine > 2.5 mg/dl.
Show all 14Show fewer
  • Renal artery stenosis.
  • Severe comorbidity such as liver disease or malignancy.
  • Pregnancy (negative pregnancy test and effective contraceptive methods are required prior to enrollment of females of childbearing potential (not post-menopausal or surgically sterilized).
  • Chronic steroid use.
  • Unable to understand or cooperate with protocol requirements.
  • Severe claustrophobia.
  • Presence of a pacemaker or non-removable hearing aid.
  • Presence of metal clips in the body.

Trial locations and contacts

1 site in 1 country.

United States1 site
  • University of Alabama at Birmingham

    Birmingham, Alabama, 35294-2180

Other trials in United States

About this study

Official title: Phase 2/3 Study of Effect of AT1RB Versus ACE Inhibitor in Addition to XO Inhibitor on Progression of LV Remodeling and Dysfunction in Diabetic Patients With Acute MI.

The investigators hypothesize that in patients with diabetes and acute myocardial infarction (MI), Ang II type-1 receptor blockade (AT1RB) attenuates left ventricle (LV) remodeling to a greater extent than angiotensin converting enzyme (ACE) inhibitor therapy and that the addition of xanthine oxidase (XO) inhibitor, Allopurinol, results in further improvement in LV remodeling and function in the follow-up phase after MI.

Read the detailed description

Following myocardial infarction (MI), the incidence of heart failure and mortality rates are approximately two-fold higher in patients with diabetes compared to those without diabetes. This increased risk for heart failure and mortality appears to be refractory to currently available treatments such as angiotensin converting enzyme (ACE) inhibitors, despite the effectiveness of such treatments in reducing overall morbidity and mortality following MI. Hyperglycemia stimulates cardiomyocyte angiotensin II (Ang II) formation, which has been implicated in increased myocyte cell death in diabetes. Furthermore, in humans, chymase is the predominant pathway of Ang II formation and this pathway of Ang II production is not blocked by ACE inhibition. Therefore, in diabetes where Ang II levels may already be elevated due to hyperglycemia the increase in Ang II formation associated with left ventricular (LV) remodeling continued Ang II formation from chymase could be particularly detrimental.

In addition to enhanced Ang II production, hyperglycemia and diabetes also amplify the production of reactive oxygen species (ROS). ROS are associated with increased in LV remodeling and myocyte apoptosis. Furthermore, xanthine oxidase (XO), an important source of ROS in myocytes, is increased in a rat model of myocardial infarction and in diabetes. Thus, increased XO-mediated ROS production following MI may be especially damaging in diabetic patients where ROS production is already elevated. Interestingly, acute treatment with Allopurinol, an inhibitor of XO, improves cardiac function in heart failure and improves endothelial dysfunction in patients with type-2 diabetes.

To test our hypothesis the investigators will investigate the following aims in diabetic patients after acute MI:

Aim 1: Show that the progression of LV remodeling and dysfunction in diabetic patients will be attenuated to greater extent by AT1RB than by ACE inhibitor.

Aim 2: Show that the addition of XO inhibition results in further attenuation of LV remodeling than with AT1RB or ACE inhibitor alone.

Aim 3: Show that baseline and follow-up LV remodeling and dysfunction and inflammatory markers differ in diabetic and non-diabetic patients post-MI.

Conditions
Diabetes
Being tested
Ramipril, Candesartan cilexetil, Allopurinol
Keywords
Diabetes, Acute MI, Ang II type-1 receptor blockade (AT1RB), LV remodeling, ACE inhibitor therapy, XO inhibitor, Allopurinol, Systolic dysfunction, Diastolic dysfunction, LV dimensions, Cardiac MRI
Medical subject headings
Diabetes Mellitus

What participants receive

What participants receive. In a randomised study each person is assigned to one group by chance.

  • RamiprilDrug

    Also called Altace

    The starting dose of Ramipril will be 2.5 mg once daily and rapidly titrated upward to 5 mg once daily after 5 days if systolic blood pressure is greater than 100 mmHg. After one month the patient will return to clinic for blood pressure check and will be titrated up to 10 mg once daily.

  • Candesartan cilexetilDrug

    Also called Atacand

    The starting dose of Candesartan cilexetil will be 4 mg or 8 mg once daily and doubled every 2 weeks, if systolic blood pressure is greater than 100 mmHg, to a maximum dose of 32 mg once daily. After one month the patient will return to clinic for blood pressure check and will be titrated up to 32 mg once daily.

  • AllopurinolDrug

    Also called Altace

    The starting dose of Allopurinol is 300 mg daily.

Study groups in NCT01052272
Study groupRoleWhat they receive
RamiprilActive comparatorThe starting dose of Ramipril will be 2.5 mg once daily and rapidly titrated upward to 5 mg once daily after 5 days if systolic blood pressure is greater than 100 mmHg. After one month the patient will return to clinic for blood pressure check and will be titrated up to 10 mg once daily.
Receives: Drug: Ramipril
Candesartan cilexetilActive comparatorThe starting dose of Candesartan cilexetil will be 4 mg or 8 mg once daily and doubled every 2 weeks, if systolic blood pressure is greater than 100 mmHg, to a maximum dose of 32 mg once daily. After one month the patient will return to clinic for blood pressure check and will be titrated up to 32 mg once daily.
Receives: Drug: Candesartan cilexetil
Ramipril and AllopurinolActive comparatorThe starting dose of Ramipril will be 2.5 mg once daily and rapidly titrated upward to 5 mg once daily after 5 days if systolic blood pressure is greater than 100 mmHg. After one month the patient will return to clinic for blood pressure check and will be titrated up to 10 mg once daily. It is anticipated that the starting dose of each drug will be initiated in hospital and that the second dose will be implemented prior to discharge from the hospital. The starting dose of Allopurinol is 300 mg daily.
Receives: Drug: Ramipril; Drug: Allopurinol
Candesartan cilexetil and AllopurinolActive comparatorThe starting dose of Candesartan cilexetil will be 4 mg or 8 mg once daily and doubled every 2 weeks, if systolic blood pressure is greater than 100 mmHg, to a maximum dose of 32 mg once daily. After one month the patient will return to clinic for blood pressure check and will be titrated up to 32 mg once daily. The starting dose of Allopurinol is 300 mg daily.
Receives: Drug: Candesartan cilexetil; Drug: Allopurinol

What is being measured

The primary outcome is the main question the study is designed to answer.

  1. Left Ventricular End Diastolic Volume Indexed to Body Surface Area (LVEDV/BSA)

    LVEDV/BSA: As an indicator of heart size, the blood volume of the heart is related to the body size. The relation of heart blood volume to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Diastolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals.

    Measured: 5 visits per Participant over 2 years (about every 6 months)

  2. Left Ventricular End-Diastolic Radius to Wall Thickness (LVED Radius/Wall Thickness)

    LVED Radius/Wall thickness As an indicator of heart muscle mass and heart volume chamber diameter, the end-diastolic radius indexed to end diastolic wall thickness determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a two-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Geometry. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes.

    Measured: 5 visits per Participant over 2 years (about every 6 months)

  3. Left Ventricular End-diastolic Mass Indexed to Left Ventricular End-diastolic Volume (LVED Mass/LVEDV)

    LVED Mass/LVEDV: As an indicator of heart muscle mass and heart blood volume, the mass indexed to end diastolic volume determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a three-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Geometry. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes.

    Measured: 5 visits per Participant over 2 years (about every 6 months)

  4. Left Ventricular Ejection Fraction (LVEF)

    LVEF is a calculation of heart pump function determined from the volume after complete filling minus the volume after complete contraction divided by the volume after complete filling. A value of 55% or greater is normal. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes

    Measured: 5 visits per Participant over 2 years (about every 6 months)

  5. Left Ventricular End Systolic Volume Indexed to Body Surface Area (LVESV/BSA)

    LVESV/BSA: The end systolic volume is the blood volume of the heart at the end of contraction and is an index of the pump function of the heart. This relation to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals.

    Measured: 5 visits per Participant over 2 years (about every 6 months)

  6. LV End Systolic Maximum Shortening (LVES Max Shortening)

    By identifying three points in three different planes in the heart muscle, the maximum shortening is the average of the difference between the distance between these three points at the end of filling of the heart and the end of contraction divided by the length at the end of filling times 100. The maximum shortening is a three dimensional analysis. The higher values indicate a healthy heart. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes.

    Measured: 5 visits per Participant over 2 years (about every 6 months)

  7. Peak Early Filling Rate Normalized to EDV

    The Peak Early Filling Rate Normalized to EDV is calculated from the slope of the volume during the early filling of the heart with respect to time. The higher values indicate a very healthy heart muscle and lower values are indicative of a very stiff muscle. This is a measure of LV Diastolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes.

    Measured: 5 visits per Participant over 2 years (about every 6 months)

Timeline

From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.

  1. First posted20 Jan 2010 (estimated)
  2. Study startJul 2005
  3. Primary completionNov 2010
  4. Study completionNov 2010

Resources

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 2/3
Primary purpose
Treatment
Allocation
Randomised
Intervention model
Factorial
Masking
None (open label)
Enrolment
72 participants (actual)
IDs, dates and publications
ClinicalTrials.gov ID
NCT01052272
Sponsor's protocol ID
F040105007
Acronym
P3
Status last verified
Nov 2012
First submitted
15 Jan 2010
Last updated
17 Dec 2012
Data monitoring committee
Yes

Publications

  • Solomon SD, St John Sutton M, Lamas GA, Plappert T, Rouleau JL, Skali H, Moye L, Braunwald E, Pfeffer MA; Survival And Ventricular Enlargement (SAVE) Investigators. Ventricular remodeling does not accompany the development of heart failure in diabetic patients after myocardial infarction. Circulation. 2002 Sep 3;106(10):1251-5. doi: 10.1161/01.cir.0000032313.82552.e3.

    PubMed 12208801
  • Mukamal KJ, Nesto RW, Cohen MC, Muller JE, Maclure M, Sherwood JB, Mittleman MA. Impact of diabetes on long-term survival after acute myocardial infarction: comparability of risk with prior myocardial infarction. Diabetes Care. 2001 Aug;24(8):1422-7. doi: 10.2337/diacare.24.8.1422.

    PubMed 11473080
  • Melchior T, Kober L, Madsen CR, Seibaek M, Jensen GV, Hildebrandt P, Torp-Pedersen C. Accelerating impact of diabetes mellitus on mortality in the years following an acute myocardial infarction. TRACE Study Group. Trandolapril Cardiac Evaluation. Eur Heart J. 1999 Jul;20(13):973-8. doi: 10.1053/euhj.1999.1530.

    PubMed 10361050
  • Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators. Lancet. 1993 Oct 2;342(8875):821-8.

    PubMed 8104270
  • Pfeffer MA, Braunwald E, Moye LA, Basta L, Brown EJ Jr, Cuddy TE, Davis BR, Geltman EM, Goldman S, Flaker GC, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators. N Engl J Med. 1992 Sep 3;327(10):669-77. doi: 10.1056/NEJM199209033271001.

    PubMed 1386652
  • Fiordaliso F, Leri A, Cesselli D, Limana F, Safai B, Nadal-Ginard B, Anversa P, Kajstura J. Hyperglycemia activates p53 and p53-regulated genes leading to myocyte cell death. Diabetes. 2001 Oct;50(10):2363-75. doi: 10.2337/diabetes.50.10.2363.

    PubMed 11574421
  • Fiordaliso F, Li B, Latini R, Sonnenblick EH, Anversa P, Leri A, Kajstura J. Myocyte death in streptozotocin-induced diabetes in rats in angiotensin II- dependent. Lab Invest. 2000 Apr;80(4):513-27. doi: 10.1038/labinvest.3780057.

    PubMed 10780668
  • Urata H, Healy B, Stewart RW, Bumpus FM, Husain A. Angiotensin II-forming pathways in normal and failing human hearts. Circ Res. 1990 Apr;66(4):883-90. doi: 10.1161/01.res.66.4.883.

    PubMed 2156635
  • Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001 Dec 13;414(6865):813-20. doi: 10.1038/414813a.

    PubMed 11742414
  • Giugliano D, Ceriello A, Paolisso G. Oxidative stress and diabetic vascular complications. Diabetes Care. 1996 Mar;19(3):257-67. doi: 10.2337/diacare.19.3.257.

    PubMed 8742574
  • Sorescu D, Griendling KK. Reactive oxygen species, mitochondria, and NAD(P)H oxidases in the development and progression of heart failure. Congest Heart Fail. 2002 May-Jun;8(3):132-40. doi: 10.1111/j.1527-5299.2002.00717.x.

    PubMed 12045381
  • Pimentel DR, Amin JK, Xiao L, Miller T, Viereck J, Oliver-Krasinski J, Baliga R, Wang J, Siwik DA, Singh K, Pagano P, Colucci WS, Sawyer DB. Reactive oxygen species mediate amplitude-dependent hypertrophic and apoptotic responses to mechanical stretch in cardiac myocytes. Circ Res. 2001 Aug 31;89(5):453-60. doi: 10.1161/hh1701.096615.

    PubMed 11532907
  • de Jong JW, Schoemaker RG, de Jonge R, Bernocchi P, Keijzer E, Harrison R, Sharma HS, Ceconi C. Enhanced expression and activity of xanthine oxidoreductase in the failing heart. J Mol Cell Cardiol. 2000 Nov;32(11):2083-9. doi: 10.1006/jmcc.2000.1240.

    PubMed 11040111
  • Matsumoto S, Koshiishi I, Inoguchi T, Nawata H, Utsumi H. Confirmation of superoxide generation via xanthine oxidase in streptozotocin-induced diabetic mice. Free Radic Res. 2003 Jul;37(7):767-72. doi: 10.1080/1071576031000107344.

    PubMed 12911273
  • Desco MC, Asensi M, Marquez R, Martinez-Valls J, Vento M, Pallardo FV, Sastre J, Vina J. Xanthine oxidase is involved in free radical production in type 1 diabetes: protection by allopurinol. Diabetes. 2002 Apr;51(4):1118-24. doi: 10.2337/diabetes.51.4.1118.

    PubMed 11916934

Questions about this trial

What is this clinical trial studying?

A Phase 2/3 study testing Ramipril, Candesartan cilexetil and Allopurinol in people with Diabetes, run by University of Alabama at Birmingham 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 8 inclusion and 14 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 17 Dec 2012. 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.

What does this combined 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.

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 17 Dec 2012). 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?

Left Ventricular End Diastolic Volume Indexed to Body Surface Area (LVEDV/BSA) (time frame: 5 visits per Participant over 2 years (about every 6 months)). The study lists 7 primary outcomes in all. 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 NCT01052272, which also lists 39 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 17 Dec 2012.

Free account

Log in to keep searching

You’ve used your 3 free searches. AzTrials is free: log in or create a free account to keep searching clinical trials and save the ones you want to follow.

Create a free accountLog in