Congenital Heart DiseaseNCT01656993
Antiplatelet Activity of Aspirin in Infants After Aortopulmonary and Cavopulmonary Shunts
An observational study of Congenital Heart Disease, run by University of Utah at 1 site in United States.
Trial summary
Background: Blood clots cause poor outcomes, including death, in babies with heart defects that require a surgical connection ("shunt") to provide blood flow to their lungs. Aspirin (ASA) blocks the part of the blood that helps clots form (platelets). Aspirin is used in babies with shunts to prevent blood clots. Read more about this study
- Who is it for?
- Ages 2 days to 12 months
- Conditions the study is for
- Congenital Heart Disease
- How many people
- 25 participants
- Where
- 1 siteUnited States
- Study dates
- Nov 2012to Dec 2014
- 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 2 days to 12 months
- All sexes
- No healthy volunteers
- Child
Study population: Infants undergoing cardiac surgery involving aortopulmonary and/or cavopulmonary shunts with planned aspirin treatment
Who may be able to join
- Undergoing cardiac surgery for a shunt and planned treatment with aspirin
- Age 2.0 days to 12 months
- Consent of parent or guardian
Who cannot join
- Known or suspected congenital or acquired coagulation disorders (such as hemophilia, von Willebrands disease, Glansmans thrombasthenia).
- History of aspirin use within 7 days of surgery.
- Platelet count < 50K prior to surgery.
- Weight < 2.5 kg.
- Prematurity defined as gestational age < 37 weeks.
Trial locations and contacts
1 site in 1 country.
United States1 site
Primary Children's Medical Center
Salt Lake City, Utah, 84113
About this study
Background: Blood clots cause poor outcomes, including death, in babies with heart defects that require a surgical connection ("shunt") to provide blood flow to their lungs. Aspirin (ASA) blocks the part of the blood that helps clots form (platelets). Aspirin is used in babies with shunts to prevent blood clots. The dose of aspirin given to babies is based on adult research. Because babies are different from adults, the investigators do not know if the dose is enough to block platelets, or if it is too much and may cause bleeding. The investigators can test the platelets using a blood test called Thromboelastography with Platelet Mapping (TEG-PM). This test needs a small amount of blood so it can be used in babies.
Hypothesis and Specific Aims: The investigators suspect the aspirin doses typically given babies are not enough to block platelets and prevent blood clots in their shunts. The investigators want to determine the percentage of babies whose platelets are not blocked enough (< 70% inhibition), by using TEG-PM. The investigators also want to determine how often bleeding or clots occur in babies receiving aspirin.
Read the detailed description
Background: Aortopulmonary and cavopulmonary shunts ("shunts") are surgically placed to provide pulmonary blood flow in infants with congenital heart disease who require the shunt for survival. Thrombosis occurs in about 17% of these shunted infants (Li et al, 2007; Monagle et al, 2012) with an associated morbidity of 23% and mortality of 7%.(Li et al, 2007) One study reported a third of all deaths were from shunt thrombosis.(Fenton, 2003) Despite insufficient evidence to guide appropriate dosing, current thromboprophylaxis guidelines recommend aspirin (ASA) for thrombus prevention in these high-risk infants. No therapeutic monitoring exists to ensure consistent and effective anticoagulation and prevent over-anticoagulation to minimize bleeding complications. Previous studies examining the effectiveness of ASA in shunt thrombosis prevention have conflicting results. The most recent large, prospective observational study showed a significant association between ASA use and lower risk of thrombosis and death (Li et al, 2007), but the study was limited by lack of standardized ASA dosing and failure to include adverse events. To further complicate the picture, adult studies have described a phenomenon termed "ASA resistance," where thrombosis occurs despite ASA therapy.(Frelinger et al, 2008; Heistein et al, 2008; Szczeklik et al, 2005; Frelinger et al, 2006) ASA resistance has not been adequately studied in the pediatric population leading to a knowledge gap between therapeutic dosing and the adequate prevention of thrombosis combined with minimization of bleeding complications. Thromboelastography with Platelet Mapping (TEG-PM) is a blood test that specifically evaluates the percentage of inhibition of the arachidonic acid pathway targeted by ASA. It can be used for serial monitoring of the adequacy of anticoagulation with ASA in shunted infants and to provide evidence of safe and effective dosages for its use in other pediatric populations.
Hypothesis and Specific Aims:
Hypothesis: The investigators hypothesize that ASA dosing by current guidelines (1-5 mg/kg/day) favors protection from bleeding complications and fails to achieve adequate inhibition of the arachidonic acid pathway to prevent thrombosis.
Specific Aim 1: The primary aim is to determine the percentage of infants treated with ASA after shunt surgery who have adequate (> 70%) inhibition of the arachidonic acid pathway as measured by TEG-PM.
Outcome: The percentage of arachidonic inhibition, as measured by TEG-PM, at 3 designated time points after starting ASA postoperatively. Therefore, TEG-PM will be measured at these designated time points:
- After the third dose of ASA
- At the first post-operative cardiology clinic visit (between 2 and 4 weeks after hospital discharge)
- At a follow-up cardiology clinic visit 3-6 months after the initiation of ASA
Specific Aim 2: The secondary aim is to describe the frequency of bleeding and thrombotic events while on ASA.
Outcome: The number of bleeding and thrombotic events from initiation of ASA therapy to end of study will be documented.
ASA administration: ASA will be initiated by the cardiac intensive care unit attending physician postoperatively, at a dose of 1-5 mg/kg/day, but no less than 20 mg per day; the initiation of ASA at 1-5 mg/kg/day is standard of care and recommended by the College of Chest Physicians (Monagle et al, 2012), albeit with limited evidence for its use. TEG-PM results obtained for research purposes will be available only to the research team. The dose of ASA will not be adjusted by results from the research TEG-PM. However, if bleeding or thrombosis occurs, TEG-PM is obtained by local practice and ASA dosing adjusted by the treating physician. If the dose of ASA is changed while the patient is hospitalized, TEG-PM will be obtained 2 hours after the third (adjusted or restarted) dose.
- Conditions
- Congenital Heart Disease
- Keywords
- Aspirin, ASA, aortopulmonary shunt, cavopulmonary shunt, shunt, TEG, Antiplatelet
- Medical subject headings
- Heart Defects, Congenital
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 |
|---|---|---|
| ASA activity | Participants (age 2.0 days to 12 months) undergoing cardiac surgery for a shunt and planned treatment with aspirin |
What is being measured
The primary outcome is the main question the study is designed to answer.
The percentage of arachidonic acid inhibition of platelets, as measured by TEG-PM after the initiation of ASA.
Measured: TEG-PM will be measured after the third dose of ASA is given postoperatively. (up to 6 months after surgery)
Secondary outcomes (3)
The percentage of arachidonic acid inhibition of platelets, as measured by TEG-PM at the first postoperative cardiology clinic visit.
Measured: The percentage of arachidonic acid inhibition will be measured at the first post-operative cardiology clinic vist (typically 2-4 weeks after hospital discharge)
The percentage of arachidonic acid inhibition of platelets, as measured by TEG-PM 3-6 months after surgery.
Measured: TEG-PM will be measured 3-6 months postoperatively to determine the percentage of arachidonic acid inhibition.
The number of bleeding and thrombotic events while patients are on ASA.
Measured: Patients will be monitored for bleeding and thrombotic events while on ASA for the duration of this study, thus for up to 1.5 years.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted3 Aug 2012 (estimated)
- Study startNov 2012
- Primary completionDec 2014
- Study completionDec 2014
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 Congenital Heart DiseaseStudies of the same condition, open and under way.
- More trials run by University of UtahThe 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
- 25 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Utah
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Dongngan Truong, University of Utah
- Investigators
- Dongngan Truong, MD, Principal investigator, University of Utah / Primary Children's Medical Center
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01656993
- Sponsor's protocol ID
- 55107
- Status last verified
- May 2017
- First submitted
- 26 Jul 2012
- Last updated
- 5 May 2017
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Li JS, Yow E, Berezny KY, Rhodes JF, Bokesch PM, Charpie JR, Forbus GA, Mahony L, Boshkov L, Lambert V, Bonnet D, Michel-Behnke I, Graham TP, Takahashi M, Jaggers J, Califf RM, Rakhit A, Fontecave S, Sanders SP. Clinical outcomes of palliative surgery including a systemic-to-pulmonary artery shunt in infants with cyanotic congenital heart disease: does aspirin make a difference? Circulation. 2007 Jul 17;116(3):293-7. doi: 10.1161/CIRCULATIONAHA.106.652172. Epub 2007 Jun 25.
PubMed 17592082Monagle P, Chan AKC, Goldenberg NA, Ichord RN, Journeycake JM, Nowak-Gottl U, Vesely SK. Antithrombotic therapy in neonates and children: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e737S-e801S. doi: 10.1378/chest.11-2308.
PubMed 22315277Fenton KN, Siewers RD, Rebovich B, Pigula FA. Interim mortality in infants with systemic-to-pulmonary artery shunts. Ann Thorac Surg. 2003 Jul;76(1):152-6; discussion 156-7. doi: 10.1016/s0003-4975(03)00168-1.
PubMed 12842531Frelinger AL, Li Y, Linden MD, Tarnow I, Barnard MR, Fox ML, Michelson AD. Aspirin 'resistance': role of pre-existent platelet reactivity and correlation between tests. J Thromb Haemost. 2008 Dec;6(12):2035-44. doi: 10.1111/j.1538-7836.2008.03184.x. Epub 2008 Oct 7.
PubMed 18983514Heistein LC, Scott WA, Zellers TM, Fixler DE, Ramaciotti C, Journeycake JM, Lemler MS. Aspirin resistance in children with heart disease at risk for thromboembolism: prevalence and possible mechanisms. Pediatr Cardiol. 2008 Mar;29(2):285-91. doi: 10.1007/s00246-007-9098-7. Epub 2007 Sep 25.
PubMed 17896127Szczeklik A, Musial J, Undas A, Sanak M, Nizankowski R. Aspirin resistance. Pharmacol Rep. 2005;57 Suppl:33-41.
PubMed 16415485Frelinger AL 3rd, Furman MI, Linden MD, Li Y, Fox ML, Barnard MR, Michelson AD. Residual arachidonic acid-induced platelet activation via an adenosine diphosphate-dependent but cyclooxygenase-1- and cyclooxygenase-2-independent pathway: a 700-patient study of aspirin resistance. Circulation. 2006 Jun 27;113(25):2888-96. doi: 10.1161/CIRCULATIONAHA.105.596627. Epub 2006 Jun 19.
PubMed 16785341
Study at a glance
From the registry record, last updated by the sponsor on 5 May 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Antiplatelet Activity of Aspirin in Infants After Aortopulmonary and Cavopulmonary Shunts
- ClinicalTrials.gov ID
- NCT01656993
- Acronym / sponsor ID
- 55107
- Conditions
- Congenital Heart Disease
- Keywords
- Aspirin, ASA, aortopulmonary shunt, cavopulmonary shunt, shunt, TEG, Antiplatelet
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 25 participants (actual)
- Lead sponsor
- University of UtahUniversity, hospital or other
- Study start
- Nov 2012 (actual)
- Primary completion
- Dec 2014 (actual)
- Study completion
- Dec 2014 (actual)
- First posted
- 3 Aug 2012 (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.
Background: Blood clots cause poor outcomes, including death, in babies with heart defects that require a surgical connection ("shunt") to provide blood flow to their lungs. Aspirin (ASA) blocks the part of the blood that helps clots form (platelets). Aspirin is used in babies with shunts to prevent blood clots. The dose of aspirin given to babies is based on adult research. Because babies are different from adults, the investigators do not know if the dose is enough to block platelets, or if it is too much and may cause bleeding. The investigators can test the platelets using a blood test called Thromboelastography with Platelet Mapping (TEG-PM). This test needs a small amount of blood so it can be used in babies.
Hypothesis and Specific Aims: The investigators suspect the aspirin doses typically given babies are not enough to block platelets and prevent blood clots in their shunts. The investigators want to determine the percentage of babies whose platelets are not blocked enough (< 70% inhibition), by using TEG-PM. The investigators also want to determine how often bleeding or clots occur in babies receiving aspirin.
Detailed description
Background: Aortopulmonary and cavopulmonary shunts ("shunts") are surgically placed to provide pulmonary blood flow in infants with congenital heart disease who require the shunt for survival. Thrombosis occurs in about 17% of these shunted infants (Li et al, 2007; Monagle et al, 2012) with an associated morbidity of 23% and mortality of 7%.(Li et al, 2007) One study reported a third of all deaths were from shunt thrombosis.(Fenton, 2003) Despite insufficient evidence to guide appropriate dosing, current thromboprophylaxis guidelines recommend aspirin (ASA) for thrombus prevention in these high-risk infants. No therapeutic monitoring exists to ensure consistent and effective anticoagulation and prevent over-anticoagulation to minimize bleeding complications. Previous studies examining the effectiveness of ASA in shunt thrombosis prevention have conflicting results. The most recent large, prospective observational study showed a significant association between ASA use and lower risk of thrombosis and death (Li et al, 2007), but the study was limited by lack of standardized ASA dosing and failure to include adverse events. To further complicate the picture, adult studies have described a phenomenon termed "ASA resistance," where thrombosis occurs despite ASA therapy.(Frelinger et al, 2008; Heistein et al, 2008; Szczeklik et al, 2005; Frelinger et al, 2006) ASA resistance has not been adequately studied in the pediatric population leading to a knowledge gap between therapeutic dosing and the adequate prevention of thrombosis combined with minimization of bleeding complications. Thromboelastography with Platelet Mapping (TEG-PM) is a blood test that specifically evaluates the percentage of inhibition of the arachidonic acid pathway targeted by ASA. It can be used for serial monitoring of the adequacy of anticoagulation with ASA in shunted infants and to provide evidence of safe and effective dosages for its use in other pediatric populations.
Hypothesis and Specific Aims:
Hypothesis: The investigators hypothesize that ASA dosing by current guidelines (1-5 mg/kg/day) favors protection from bleeding complications and fails to achieve adequate inhibition of the arachidonic acid pathway to prevent thrombosis.
Specific Aim 1: The primary aim is to determine the percentage of infants treated with ASA after shunt surgery who have adequate (> 70%) inhibition of the arachidonic acid pathway as measured by TEG-PM.
Outcome: The percentage of arachidonic inhibition, as measured by TEG-PM, at 3 designated time points after starting ASA postoperatively. Therefore, TEG-PM will be measured at these designated time points:
- After the third dose of ASA
- At the first post-operative cardiology clinic visit (between 2 and 4 weeks after hospital discharge)
- At a follow-up cardiology clinic visit 3-6 months after the initiation of ASA
Specific Aim 2: The secondary aim is to describe the frequency of bleeding and thrombotic events while on ASA.
Outcome: The number of bleeding and thrombotic events from initiation of ASA therapy to end of study will be documented.
ASA administration: ASA will be initiated by the cardiac intensive care unit attending physician postoperatively, at a dose of 1-5 mg/kg/day, but no less than 20 mg per day; the initiation of ASA at 1-5 mg/kg/day is standard of care and recommended by the College of Chest Physicians (Monagle et al, 2012), albeit with limited evidence for its use. TEG-PM results obtained for research purposes will be available only to the research team. The dose of ASA will not be adjusted by results from the research TEG-PM. However, if bleeding or thrombosis occurs, TEG-PM is obtained by local practice and ASA dosing adjusted by the treating physician. If the dose of ASA is changed while the patient is hospitalized, TEG-PM will be obtained 2 hours after the third (adjusted or restarted) dose.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| ASA activity | – | –Participants (age 2.0 days to 12 months) undergoing cardiac surgery for a shunt and planned treatment with aspirin |
Who may qualify
- Ages
- 2 days to 12 months
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child
- Study population
- Infants undergoing cardiac surgery involving aortopulmonary and/or cavopulmonary shunts with planned aspirin treatment
Key inclusion criteria (3 listed)
- Undergoing cardiac surgery for a shunt and planned treatment with aspirin
- Age 2.0 days to 12 months
- Consent of parent or guardian
Key exclusion criteria (5 listed)
- Known or suspected congenital or acquired coagulation disorders (such as hemophilia, von Willebrands disease, Glansmans thrombasthenia).
- History of aspirin use within 7 days of surgery.
- Platelet count < 50K prior to surgery.
- Weight < 2.5 kg.
- Prematurity defined as gestational age < 37 weeks.
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
The percentage of arachidonic acid inhibition of platelets, as measured by TEG-PM after the initiation of ASA.
Time frame: TEG-PM will be measured after the third dose of ASA is given postoperatively. (up to 6 months after surgery)
3 secondary outcomes
The percentage of arachidonic acid inhibition of platelets, as measured by TEG-PM at the first postoperative cardiology clinic visit.
Time frame: The percentage of arachidonic acid inhibition will be measured at the first post-operative cardiology clinic vist (typically 2-4 weeks after hospital discharge)
The percentage of arachidonic acid inhibition of platelets, as measured by TEG-PM 3-6 months after surgery.
Time frame: TEG-PM will be measured 3-6 months postoperatively to determine the percentage of arachidonic acid inhibition.
The number of bleeding and thrombotic events while patients are on ASA.
Time frame: Patients will be monitored for bleeding and thrombotic events while on ASA for the duration of this study, thus for up to 1.5 years.
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 5 May 2017.
- Background: PubMed 17592082Li JS, Yow E, Berezny KY, Rhodes JF, Bokesch PM, Charpie JR, Forbus GA, Mahony L, Boshkov L, Lambert V, Bonnet D, Michel-Behnke I, Graham TP, Takahashi M, Jaggers J, Califf RM, Rakhit A, Fontecave S, Sanders SP. Clinical outcomes of palliative surgery including a systemic-to-pulmonary artery shunt in infants with cyanotic congenital heart disease: does aspirin make a difference? Circulation. 2007 Jul 17;116(3):293-7. doi: 10.1161/CIRCULATIONAHA.106.652172. Epub 2007 Jun 25.
- Background: PubMed 22315277Monagle P, Chan AKC, Goldenberg NA, Ichord RN, Journeycake JM, Nowak-Gottl U, Vesely SK. Antithrombotic therapy in neonates and children: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e737S-e801S. doi: 10.1378/chest.11-2308.
- Background: PubMed 12842531Fenton KN, Siewers RD, Rebovich B, Pigula FA. Interim mortality in infants with systemic-to-pulmonary artery shunts. Ann Thorac Surg. 2003 Jul;76(1):152-6; discussion 156-7. doi: 10.1016/s0003-4975(03)00168-1.
- Background: PubMed 18983514Frelinger AL, Li Y, Linden MD, Tarnow I, Barnard MR, Fox ML, Michelson AD. Aspirin 'resistance': role of pre-existent platelet reactivity and correlation between tests. J Thromb Haemost. 2008 Dec;6(12):2035-44. doi: 10.1111/j.1538-7836.2008.03184.x. Epub 2008 Oct 7.
- Background: PubMed 17896127Heistein LC, Scott WA, Zellers TM, Fixler DE, Ramaciotti C, Journeycake JM, Lemler MS. Aspirin resistance in children with heart disease at risk for thromboembolism: prevalence and possible mechanisms. Pediatr Cardiol. 2008 Mar;29(2):285-91. doi: 10.1007/s00246-007-9098-7. Epub 2007 Sep 25.
- Background: PubMed 16415485Szczeklik A, Musial J, Undas A, Sanak M, Nizankowski R. Aspirin resistance. Pharmacol Rep. 2005;57 Suppl:33-41.
- Background: PubMed 16785341Frelinger AL 3rd, Furman MI, Linden MD, Li Y, Fox ML, Barnard MR, Michelson AD. Residual arachidonic acid-induced platelet activation via an adenosine diphosphate-dependent but cyclooxygenase-1- and cyclooxygenase-2-independent pathway: a 700-patient study of aspirin resistance. Circulation. 2006 Jun 27;113(25):2888-96. doi: 10.1161/CIRCULATIONAHA.105.596627. Epub 2006 Jun 19.
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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.
Dongngan Truong, MD principal investigator
University of Utah / Primary Children's Medical Center
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 Congenital Heart Disease, run by University of Utah 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 3 inclusion and 5 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 5 May 2017. 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?
The percentage of arachidonic acid inhibition of platelets, as measured by TEG-PM after the initiation of ASA. (time frame: TEG-PM will be measured after the third dose of ASA is given postoperatively. (up to 6 months after surgery)). 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 NCT01656993, 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 5 May 2017.