Coronary Artery DiseaseNCT01552161
Prevalence of Allergic Diseases and Atopy in Subjects With Coronary Artery Disease
An observational study of Coronary Artery Disease and Allergy, run by Medical University of Lodz at 1 site in Poland.
Trial summary
The purpose of this study is to estimate the prevalence of allergic diseases and atopy among patients with angiographically confirmed coronary artery disease as well as to assess levels of serum allergic inflammation markers in this population. Read more about this study
- Who is it for?
- Ages 30 years and older
- Conditions the study is for
- Coronary Artery Disease, Allergy, Asthma
- How many people
- 300 participants
- Where
- 1 sitePoland
- Study dates
- Apr 2010to Jun 2012
- 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 30 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Patients who underwent coronary angiography are eligible for the study.
Who may be able to join
- available result of coronary angiography
- able to express written informed consent for study participation
- able to perform forced expiratory manoeuvre for spirometry
Who cannot join
- ongoing infection
- exacerbation of chronic disorder (e.g. asthma, COPD, CVD, chronic kidney disease, neoplasm<10 years from complete remission)
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Prevalence of Allergic Diseases and Atopy in Patients With Angiographically Confirmed Coronary Artery Disease
The purpose of this study is to estimate the prevalence of allergic diseases and atopy among patients with angiographically confirmed coronary artery disease as well as to assess levels of serum allergic inflammation markers in this population.
Read the detailed description
Cardiovascular disease (CVD) is one of the leading causes of death, disability and medical resources use worldwide. Atherosclerosis remains the basic pathology found in CVD. Based on theoretical knowledge and animal experimental models it can be hypothesized that allergic inflammation affects atherosclerotic plaque formation/disruption. The exact nature of such interaction remains unknown.
The process most probably takes place at the molecular level and involves both: specific interleukin formation and mast cells recruitment. On the one hand some pro-allergic interleukins have been found to inhibit atherosclerotic plaque formation in experimental animal models. However, other hypothesis conclude that mediators released by mast cells might encourage hypoxemia of the heart muscle cells and thus promote their necrosis. Mast cells and eosinophils -typically associated with allergy - are both found in human heart muscle, cross sections of coronary arteries and atherosclerotic plaques.
Atopic patients who are prone to IgE-mediated mast cell activation seem to run a lower risk of sudden cardiac death after myocardial infarction. It may be associated with the fact that atopy produces a mild haemostatic imbalance similar to that typical of aspirin - moderately long bleeding time, depressed platelet aggregability and delayed generation of thrombin in clotting blood. Tryptase, one of the mediators released from mast cells widely used marker of anaphylaxis, has recently been shown to be increased in sera of patients with angiographically significant narrowings in coronary arteries. These results are in accordance with the previous finding of increased total IgE (antibody involved in type I allergic reaction) post myocardial infarction. Allergic myocardial infarction (also known as Kounis syndrome) - a condition in which heart muscle ischemia results from allergic insult sometimes even in the absence of permanent coronary artery lesions - is another hint supporting the hypothesis of possible interaction between allergy and cardiovascular diseases.
Despite relatively many reports studying the association at molecular, in vitro and clinical level, the research investigating the problem as a whole, connecting laboratory data with clinical picture, is scarce. Our research aims at providing epidemiological evidence on the prevalence of allergy and atopy as well as serum allergy markers profile in subjects with coronary artery disease.
Our study is dedicated to post-coronary angiography subjects willing to express informed consent for study participation.
Coronarography has been chosen as a verification tool for several reasons:
- it gives more accurate diagnosis of clinically relevant coronary narrowings than basic ECG, ECG exercise test or coronary angioCT
- it enables the distinction between typical angina pectoris and Prinzmetal's angina
- it has become a common procedure in Poland giving a relatively large and diverse cohort of patients undergoing the procedure whom we could address
- Conditions
- Coronary Artery Disease, Allergy, Asthma
- Keywords
- Angiography, Atherosclerosis, Asthma, Tryptase, Eosinophil cationic protein
- Medical subject headings
- Coronary Artery Disease, Hypersensitivity, Asthma, Atherosclerosis
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 |
|---|---|---|
| Patients with negative coronarography. | Subjects who underwent coronary angiography and were classified as having no critical lesions in coronary arteries (a lesion of up to 50% of artery lumen is accepted as non-critical). | |
| Patients with positive coronarography | Subjects who underwent coronary angiography and were classified as having critical lesions in coronary arteries (over 50% narrowing of artery lumen). |
What is being measured
The primary outcome is the main question the study is designed to answer.
Prevalence of allergic diseases
Asthma, allergic rhinitis, allergic concjunctivitis, atopic dermatitis, contact eczema, drug, food and insect venom allergy will be assessed through a structured questionnaire based on ISAAC and ECRHS questions regarding allergy symptoms.
Additionally:
Asthma diagnosis is verified through basic spirometry, reversibility test, skin prick tests and/or serum specific IgE.
Allergic rhinitis diagnosis is verified through skin prick tests and/or serum specific IgE.
Measured: Within a month from study recruitment completion.
Secondary outcomes (3)
Serum tryptase
Systemic tryptase will be measured with ImmunoCAP fluorescence enzyme immunoassay in patients sera.
Measured: Within a month from study recruitment completion.
Serum eosinophil cationic protein
Systemic eosinophil cationic protein (ECP) will be measured with ImmunoCAP fluorescence enzyme immunoassay in patients sera.
Measured: Within a month from study recruitment completion.
Prevalence of atopy.
Atopy is defined as increased serum total/specific IgE and/or positive skin prick tests in the absence of relevant allergy clinical symptoms.
Measured: Within a month from study recruitment completion.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted13 Mar 2012 (estimated)
- Study startApr 2010
- Primary completionApr 2012
- Study completionJun 2012
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (12)Papers the sponsor has linked to this study.
- Other trials for Coronary Artery DiseaseStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 300 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Medical University of Lodz
- Sponsor type
- University, hospital or other
- Collaborators
- Ministry of Science and Higher Education, Poland, European Union
- Responsible party
- Principal investigator, Piotr Kuna, MD, PhD, Medical University of Lodz
- Investigators
- Piotr Kuna, Prof., Principal investigator, Medical University of Lodz
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01552161
- Sponsor's protocol ID
- NN402374938
- Status last verified
- Jan 2014
- First submitted
- 9 Mar 2012
- Last updated
- 28 Jan 2014
- Results posted
- No
- Data monitoring committee
- No
Publications
Szczeklik A, Dropinski J, Gora PF. Serum immunoglobulin E and sudden cardiac arrest during myocardial infarction. Coron Artery Dis. 1993 Nov;4(11):1029-32. doi: 10.1097/00019501-199311000-00012.
PubMed 8173709Szczeklik A, Milner PC, Birch J, Watkins J, Martin JF. Prolonged bleeding time, reduced platelet aggregation, altered PAF-acether sensitivity and increased platelet mass are a trait of asthma and hay fever. Thromb Haemost. 1986 Dec 15;56(3):283-7.
PubMed 3563961Szczeklik A, Jawien J. Possible role of IgE in acute-phase response. Allergy. 1997 Nov;52(11):1149-50. doi: 10.1111/j.1398-9995.1997.tb00196.x. No abstract available.
PubMed 9404576Kauhanen P, Kovanen PT, Reunala T, Lassila R. Effects of skin mast cells on bleeding time and coagulation activation at the site of platelet plug formation. Thromb Haemost. 1998 Apr;79(4):843-7.
PubMed 9569202Wang J, Cheng X, Xiang MX, Alanne-Kinnunen M, Wang JA, Chen H, He A, Sun X, Lin Y, Tang TT, Tu X, Sjoberg S, Sukhova GK, Liao YH, Conrad DH, Yu L, Kawakami T, Kovanen PT, Libby P, Shi GP. IgE stimulates human and mouse arterial cell apoptosis and cytokine expression and promotes atherogenesis in Apoe-/- mice. J Clin Invest. 2011 Sep;121(9):3564-77. doi: 10.1172/JCI46028. Epub 2011 Aug 8.
PubMed 21821913Heikkila HM, Trosien J, Metso J, Jauhiainen M, Pentikainen MO, Kovanen PT, Lindstedt KA. Mast cells promote atherosclerosis by inducing both an atherogenic lipid profile and vascular inflammation. J Cell Biochem. 2010 Feb 15;109(3):615-23. doi: 10.1002/jcb.22443.
PubMed 20024959Kovanen PT. Mast cells in atherogenesis: actions and reactions. Curr Atheroscler Rep. 2009 May;11(3):214-9. doi: 10.1007/s11883-009-0033-7.
PubMed 19361353Lindstedt KA, Kovanen PT. Mast cells in vulnerable coronary plaques: potential mechanisms linking mast cell activation to plaque erosion and rupture. Curr Opin Lipidol. 2004 Oct;15(5):567-73. doi: 10.1097/00041433-200410000-00011.
PubMed 15361793Kovanen PT. Mast cells: multipotent local effector cells in atherothrombosis. Immunol Rev. 2007 Jun;217:105-22. doi: 10.1111/j.1600-065X.2007.00515.x.
PubMed 17498055Kwon JS, Kim YS, Cho AS, Cho HH, Kim JS, Hong MH, Jeong SY, Jeong MH, Cho JG, Park JC, Kang JC, Ahn Y. The novel role of mast cells in the microenvironment of acute myocardial infarction. J Mol Cell Cardiol. 2011 May;50(5):814-25. doi: 10.1016/j.yjmcc.2011.01.019. Epub 2011 Feb 3.
PubMed 21295578Deliargyris EN, Upadhya B, Sane DC, Dehmer GJ, Pye J, Smith SC Jr, Boucher WS, Theoharides TC. Mast cell tryptase: a new biomarker in patients with stable coronary artery disease. Atherosclerosis. 2005 Feb;178(2):381-6. doi: 10.1016/j.atherosclerosis.2004.09.008.
PubMed 15694948Kervinen H, Kaartinen M, Makynen H, Palosuo T, Manttari M, Kovanen PT. Serum tryptase levels in acute coronary syndromes. Int J Cardiol. 2005 Sep 30;104(2):138-43. doi: 10.1016/j.ijcard.2004.10.023.
PubMed 16168805
Study at a glance
From the registry record, last updated by the sponsor on 28 Jan 2014. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Prevalence of Allergic Diseases and Atopy in Patients With Angiographically Confirmed Coronary Artery Disease
- ClinicalTrials.gov ID
- NCT01552161
- Acronym / sponsor ID
- NN402374938
- Conditions
- Coronary Artery Disease, Allergy, Asthma
- Keywords
- Angiography, Atherosclerosis, Asthma, Tryptase, Eosinophil cationic protein
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 300 participants (estimated)
- Lead sponsor
- Medical University of LodzUniversity, hospital or other
- Collaborators
- Ministry of Science and Higher Education, Poland, European Union
- Study start
- Apr 2010
- Primary completion
- Apr 2012 (actual)
- Study completion
- Jun 2012 (actual)
- First posted
- 13 Mar 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.
The purpose of this study is to estimate the prevalence of allergic diseases and atopy among patients with angiographically confirmed coronary artery disease as well as to assess levels of serum allergic inflammation markers in this population.
Detailed description
Cardiovascular disease (CVD) is one of the leading causes of death, disability and medical resources use worldwide. Atherosclerosis remains the basic pathology found in CVD. Based on theoretical knowledge and animal experimental models it can be hypothesized that allergic inflammation affects atherosclerotic plaque formation/disruption. The exact nature of such interaction remains unknown.
The process most probably takes place at the molecular level and involves both: specific interleukin formation and mast cells recruitment. On the one hand some pro-allergic interleukins have been found to inhibit atherosclerotic plaque formation in experimental animal models. However, other hypothesis conclude that mediators released by mast cells might encourage hypoxemia of the heart muscle cells and thus promote their necrosis. Mast cells and eosinophils -typically associated with allergy - are both found in human heart muscle, cross sections of coronary arteries and atherosclerotic plaques.
Atopic patients who are prone to IgE-mediated mast cell activation seem to run a lower risk of sudden cardiac death after myocardial infarction. It may be associated with the fact that atopy produces a mild haemostatic imbalance similar to that typical of aspirin - moderately long bleeding time, depressed platelet aggregability and delayed generation of thrombin in clotting blood. Tryptase, one of the mediators released from mast cells widely used marker of anaphylaxis, has recently been shown to be increased in sera of patients with angiographically significant narrowings in coronary arteries. These results are in accordance with the previous finding of increased total IgE (antibody involved in type I allergic reaction) post myocardial infarction. Allergic myocardial infarction (also known as Kounis syndrome) - a condition in which heart muscle ischemia results from allergic insult sometimes even in the absence of permanent coronary artery lesions - is another hint supporting the hypothesis of possible interaction between allergy and cardiovascular diseases.
Despite relatively many reports studying the association at molecular, in vitro and clinical level, the research investigating the problem as a whole, connecting laboratory data with clinical picture, is scarce. Our research aims at providing epidemiological evidence on the prevalence of allergy and atopy as well as serum allergy markers profile in subjects with coronary artery disease.
Our study is dedicated to post-coronary angiography subjects willing to express informed consent for study participation.
Coronarography has been chosen as a verification tool for several reasons:
- it gives more accurate diagnosis of clinically relevant coronary narrowings than basic ECG, ECG exercise test or coronary angioCT
- it enables the distinction between typical angina pectoris and Prinzmetal's angina
- it has become a common procedure in Poland giving a relatively large and diverse cohort of patients undergoing the procedure whom we could address
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Patients with negative coronarography. | – | –Subjects who underwent coronary angiography and were classified as having no critical lesions in coronary arteries (a lesion of up to 50% of artery lumen is accepted as non-critical). |
| Patients with positive coronarography | – | –Subjects who underwent coronary angiography and were classified as having critical lesions in coronary arteries (over 50% narrowing of artery lumen). |
Who may qualify
- Ages
- 30 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients who underwent coronary angiography are eligible for the study.
Key inclusion criteria (3 listed)
- available result of coronary angiography
- able to express written informed consent for study participation
- able to perform forced expiratory manoeuvre for spirometry
Key exclusion criteria (2 listed)
- ongoing infection
- exacerbation of chronic disorder (e.g. asthma, COPD, CVD, chronic kidney disease, neoplasm<10 years from complete remission)
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
Prevalence of allergic diseases
Time frame: Within a month from study recruitment completion.
Asthma, allergic rhinitis, allergic concjunctivitis, atopic dermatitis, contact eczema, drug, food and insect venom allergy will be assessed through a structured questionnaire based on ISAAC and ECRHS questions regarding allergy symptoms. Additionally: Asthma diagnosis is verified through basic spirometry, reversibility test, skin prick tests and/or serum specific IgE. Allergic rhinitis diagnosis is verified through skin prick tests and/or serum specific IgE.
3 secondary outcomes
Serum tryptase
Time frame: Within a month from study recruitment completion.
Serum eosinophil cationic protein
Time frame: Within a month from study recruitment completion.
Prevalence of atopy.
Time frame: Within a month from study recruitment completion.
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 28 Jan 2014.
- Background: PubMed 8173709Szczeklik A, Dropinski J, Gora PF. Serum immunoglobulin E and sudden cardiac arrest during myocardial infarction. Coron Artery Dis. 1993 Nov;4(11):1029-32. doi: 10.1097/00019501-199311000-00012.
- Background: PubMed 3563961Szczeklik A, Milner PC, Birch J, Watkins J, Martin JF. Prolonged bleeding time, reduced platelet aggregation, altered PAF-acether sensitivity and increased platelet mass are a trait of asthma and hay fever. Thromb Haemost. 1986 Dec 15;56(3):283-7.
- Background: PubMed 9404576Szczeklik A, Jawien J. Possible role of IgE in acute-phase response. Allergy. 1997 Nov;52(11):1149-50. doi: 10.1111/j.1398-9995.1997.tb00196.x. No abstract available.
- Background: PubMed 9569202Kauhanen P, Kovanen PT, Reunala T, Lassila R. Effects of skin mast cells on bleeding time and coagulation activation at the site of platelet plug formation. Thromb Haemost. 1998 Apr;79(4):843-7.
- Background: PubMed 21821913Wang J, Cheng X, Xiang MX, Alanne-Kinnunen M, Wang JA, Chen H, He A, Sun X, Lin Y, Tang TT, Tu X, Sjoberg S, Sukhova GK, Liao YH, Conrad DH, Yu L, Kawakami T, Kovanen PT, Libby P, Shi GP. IgE stimulates human and mouse arterial cell apoptosis and cytokine expression and promotes atherogenesis in Apoe-/- mice. J Clin Invest. 2011 Sep;121(9):3564-77. doi: 10.1172/JCI46028. Epub 2011 Aug 8.
- Background: PubMed 20024959Heikkila HM, Trosien J, Metso J, Jauhiainen M, Pentikainen MO, Kovanen PT, Lindstedt KA. Mast cells promote atherosclerosis by inducing both an atherogenic lipid profile and vascular inflammation. J Cell Biochem. 2010 Feb 15;109(3):615-23. doi: 10.1002/jcb.22443.
- Background: PubMed 19361353Kovanen PT. Mast cells in atherogenesis: actions and reactions. Curr Atheroscler Rep. 2009 May;11(3):214-9. doi: 10.1007/s11883-009-0033-7.
- Background: PubMed 15361793Lindstedt KA, Kovanen PT. Mast cells in vulnerable coronary plaques: potential mechanisms linking mast cell activation to plaque erosion and rupture. Curr Opin Lipidol. 2004 Oct;15(5):567-73. doi: 10.1097/00041433-200410000-00011.
- Background: PubMed 17498055Kovanen PT. Mast cells: multipotent local effector cells in atherothrombosis. Immunol Rev. 2007 Jun;217:105-22. doi: 10.1111/j.1600-065X.2007.00515.x.
- Background: PubMed 21295578Kwon JS, Kim YS, Cho AS, Cho HH, Kim JS, Hong MH, Jeong SY, Jeong MH, Cho JG, Park JC, Kang JC, Ahn Y. The novel role of mast cells in the microenvironment of acute myocardial infarction. J Mol Cell Cardiol. 2011 May;50(5):814-25. doi: 10.1016/j.yjmcc.2011.01.019. Epub 2011 Feb 3.
- Background: PubMed 15694948Deliargyris EN, Upadhya B, Sane DC, Dehmer GJ, Pye J, Smith SC Jr, Boucher WS, Theoharides TC. Mast cell tryptase: a new biomarker in patients with stable coronary artery disease. Atherosclerosis. 2005 Feb;178(2):381-6. doi: 10.1016/j.atherosclerosis.2004.09.008.
- Background: PubMed 16168805Kervinen H, Kaartinen M, Makynen H, Palosuo T, Manttari M, Kovanen PT. Serum tryptase levels in acute coronary syndromes. Int J Cardiol. 2005 Sep 30;104(2):138-43. doi: 10.1016/j.ijcard.2004.10.023.
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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.
Piotr Kuna, Prof. principal investigator
Medical University of Lodz
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 Coronary Artery Disease and Allergy, run by Medical University of Lodz at 1 site in Poland.
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 2 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 28 Jan 2014. 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 Poland. 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?
Prevalence of allergic diseases (time frame: Within a month from study recruitment completion.). 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 NCT01552161, which also lists 12 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 28 Jan 2014.