Coronary Artery DiseasePIHSNCT02146872
Premature Coronary Artery Disease - Clinical and Molecular Genetic Aspects
An observational study of Coronary Artery Disease and Myocardial Infarction, run by Aarhus University Hospital Skejby at 1 site in Denmark.
Trial summary
Since finishing the sequencing of the human genome in 2003, genetic research in coronary artery disease (CAD) and other complex traits have developed dramatically. Recent genome-wide association studies have identified a considerable number of common genetic variants each associated with the disease. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Coronary Artery Disease, Myocardial Infarction, Atherosclerosis
- How many people
- 400 participants
- Where
- 1 siteDenmark
- Study dates
- Feb 2014to Feb 2016
- 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
- No healthy volunteers
- Adult, Older adult
Study population: Patients who has received a coronary intervention procedure at Aarhus University Hospital, Skejby (all interventions are registered in the West Denmark Heart Registry)
Who may be able to join
- Coronary intervention at Aarhus University Hospital, Skejby in the period 2006-2013
- Age < 40 years at the time of intervention in the above mentioned period
- Intervention on the basis of atherosclerosis
- Residency in Denmark
- > 6 months since last coronary procedure
- 1st degree relatives of patients participating in study part 1.
Show all 9Show fewer
- Age 30-65 years
- No prior diagnosis of coronary atherosclerosis on the basis of a coronary angiogram
- Families who are considered severely affected by atherosclerosis, evaluated on a basis of family size, number of affected and severity of disease (yet to be defined - depending on the actual cohort (pedigree analysis))
Who cannot join
- Interventions on transplanted hearts
- Abuse of cocaine/amphetamine in close relation to the intervention
- Obesity (BMI>30)
- Chronic kidney disease stage 4+5
- Chronic atrial fibrillation
- Former allergic contrast reaction
- Pregnancy
- None
Trial locations and contacts
1 site in 1 country.
Denmark1 site, 1 recruiting
- Recruiting
Aarhus University Hospital, Skejby
Aarhus, 8200
Morten K Christiansen, MD, +4578452259, morten.christiansen@ki.au.dk
Henrik K Jensen, MD PhD DMSc, +4578452033, d249688@dadlnet.dk
About this study
Since finishing the sequencing of the human genome in 2003, genetic research in coronary artery disease (CAD) and other complex traits have developed dramatically. Recent genome-wide association studies have identified a considerable number of common genetic variants each associated with the disease. This has led to a new understanding but also to the discovery of new therapeutical targets. However, each of the variants discovered only have minor effects on disease development and even the pooling of the variants only explains a minor percentage of the total heritability. It has been evident that rare or private mutations probably play a great role in the genetic architecture of CAD, especially among young and severely affected patients. These may only be identified by sequencing. Therefore, the investigators hypothesize, that the use of exome sequencing (the read-off of the entire protein-coding regions of the genome) and linkage analysis in families of extreme phenotype cases, will identify disease-causing genetic variants. From the West Denmark Heart Registry the investigators will enroll a minimum of 120 patients with atherosclerosis who have undergone a coronary artery revascularization procedure before the age of 40, to participate in study part 1. A pedigree analysis will be performed and cardiovascular (CVD) risk factors and current preventive treatment will be evaluated. 1. degree relatives aged 30-65 years, who are free of CAD, are invited to participate in study 2. CVD risk factors are evaluated as well as a CT coronary angiogram is performed to quantify the degree of asymptomatic coronary atherosclerosis. Families from study 1 and 2, who are considered severely affected by atherosclerosis, evaluated on a basis of family size, number of affected and severity of disease, will be selected for exome sequencing. Other relevant family members will be included as well as their CVD risk factors will be evaluated. Exome sequencing will be performed and variants found will be filtered on a basis of frequency, linkage analysis, gene position, existing knowledge and in-silico prediction tools. Possible findings will be validated by Sanger-sequencing and causality of new variants will subsequently be sought to be proven by relevant experimental studies.
Read the detailed description
Purposes Study part 1: Quantify the occurrence of risk factors of atherosclerosis among patients with very premature CAD in the Central Denmark Region and investigate to what degree patients are treated according to national guidelines.
Study part 2: Investigate the occurrence of CAD among middle-aged 1st degree relatives of established patients having very premature CAD.
Study part 3: Evaluate possible genetic "risk factors" in families with a high CAD prevalence using exome sequencing analysis.
Hypotheses Hypothesis 1: Patients with very premature CAD have modifiable risk factors, which are inadequately treated relative to current national guidelines.
Hypothesis 2: The occurrence of very premature CAD is associated with familial accumulation of the disease.
Hypothesis 3: The use of exome sequencing in selected families with phenotypic severe premature CAD will identify disease-causing genetic variants.
Method Study part 1. Patients suffering from premature CAD who have had a percutaneous coronary intervention (PCI) or coronary artery bypass graft operation (CABG) done before the age of 40 years will be selected from the West Denmark Heart Registry (VDHD). Specifically, patients treated at Aarhus University Hospital (AUH) in Skejby for myocardial infarction (MI), stable or unstable angina pectoris in the period of January 1st 2007 - December 31st 2013 will be recruited and the occurrence of registered risk factors be evaluated (sample indicates app. 170 patients per year). After informed consent is obtained, they will participate in this research study. Participants will be interviewed in the cardiac outpatient clinic at the Dep. of Cardiology, AUH, Skejby. The following information about cardiovascular risk factors will be collected; family history of atherosclerosis (a pedigree analysis will be performed and cases of diagnosed CVD will be identified), prior medical history (i.e. hypertension, dyslipidemia, diabetes, chronic kidney disease, vascular disease), smoking status and number of pack years, alcohol consumption and vascular symptoms (i.e. angina pectoris, intermittent claudication). Gathered information will be compared to the registered information in patient records and VDHD. In addition, information about localization of the invasive treatment, the degree of CAD, and the latest estimate of the left ventricular ejection fraction (LVEF) will be collated. All patients will be examined regarding height and weight, abdominal girth and a blood sample is collected. An automated office blood pressure measurement (Bp-TRU device) will be performed. Levels of creatinine (e-GFR), total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides and HbA1c will be measured. Further, a blood sample will be saved for prospective DNA analysis (below). The investigators will evaluate to what degree the treatment targets have been met in accordance with national guidelines. Analysis will be corrected to reflect changes in these treatment guidelines, which have occurred in recent years.
Study part 2. Patients from study 1 (index patients) are requested to establish contact to 1st degree relatives between 30 and 65 years of age for the purpose of participating in Study part 2. The form of contact follows regular department guidelines for contact to family members. 1st degree relatives who give their informed consent will be included in study part 2 (participants). Patient records from participants who are diagnosed with atherosclerosis will be obtained. Exclusion criteria will be former diagnosis of CAD by CTCA or percutaneous transluminal coronary angiography, chronic atrial fibrillation, renal failure (e-GFR < 30ml/min), obesity (BMI > 30 is indicative but body geometry plays a role), former allergic contrast reaction and pregnancy. A traditional risk profile and blood samples will be collected as in study part 1. Prior to the CTCA, LVEF is estimated by echocardiography. A CTCA is performed according to the standard protocol in the department. Initially the CT-scan is performed without contrast in order to estimate the coronary calcification by Agatstons method. Afterwards a scan is performed with 70 ml of iodine-containing contrast. ECG modulation and radiation-reduced protocols will be used so that an average participant (70 kg) may expect to receive a radiation dose below 3 mSv. The analysis of the contrast study will focus on automated- and semi-automated plaque quantification. Non-cardiac findings will be described according to department standard procedures by the Dep. of Radiology, AUH, Skejby, and medical intervention performed as clinically indicated.
Study part 3. Families from study part 1 and 2, who are considered severely affected by atherosclerosis, evaluated on a basis of family size, number of affected and severity of disease, will be selected. Family members (index patients, 1st degree relatives and if relevant also their 1st degree relatives) who consent,will be included in study part 3. Contact with relatives who have not yet participated in the project will be attempted as in study part 2. A traditional risk profile and a blood sample for DNA analysis (exome sequencing) will be requested if it has not already been obtained. The analysis takes place at Department of Molecular Medicine (MOMA), AUH, Skejby, who have the required equipment, software and laboratory expertise in performing the tests as well as the bioinformatic analysis. First, genomic DNA is purified and fragmented to a size of 200-500 base pairs. Illumina TruSeq libraries (to be used with the exome sequencing) will be produced at a Caliper Sciclone-robot where the exome enrichment with Nimblegens EZ in solution Exome v3 kit will also take place. The dataanalysis will be taking place at MOMA under the guidance of the MOMA staff. First sequences will be trimmed and aligned to the humane genome. Second, alignments will be fine-tuned before variants will be called, including single nucleotide variants and insertions/deletions of various size. The interpretation of the data will be taking place in the software program Cartagenia, which gives access to an abundance of public and commercial databases and also offers the opportunity of integrating private databases. Variants will be filtered on a basis of frequency, gene position, existing knowledge and different in-silico prediction tools. Possible significant findings will be validated by Sanger sequencing.
Statistical analysis At the found genotypes from study part 3, coupling analysis is performed to identify regions in the genome shared by disease-affected individuals. The use of pedigree analysis and coupling analysis substantially reduce the candidate intervals in the genome, thereby increasing the statistical power to identify disease-causing variants even in small families. Because the precise genetic architecture and family structure of the included families is not known, exact calculation of statistical power will not be possible. In case of a dominant monogenetic disease, a filtration only based on localization (coupling) reduces the potential variants by app. 80% within a pair of affected siblings and by more than 95% for monogenetic recessive diseases, if affected individuals from inbred families.
Research Biobank A research biobank will be established under The Institute of Clinical Medicine, Health, Aarhus University. A sample of 2x4 ml (BD Vacutainer K3E 7,2mg Ref. 368860) and 1x4ml (BD Vacutainer SST II Advance, Ref. 367957) blood from all participants in studies 1-3 will be submitted to the biobank for further analysis. The sampling is performed at AUH, Skejby or a glass and a return envelope will sent to the patient for the drawing of blood by their family physician. The sample is cryo-preserved and exome sequencing is performed on the participants of study part 3. The biobank will be carried on after the project has ended for the purpose of future research. In case of future analysis on the preserved material The Research Ethics Committee and the participant (if still alive) will be noticed before hand. Permission to store the biological material will be applied continuously according to specified intervals by The Danish Data Protection Agency. All participants may demand their biological material destroyed at any time.
- Keywords
- Coronary Artery Disease, Myocardial Infarction, Atherosclerosis, High-Throughput Nucleotide Sequencing, Sequence Analysis, DNA, Genetic Testing, Genetic Linkage
- Medical subject headings
- Coronary Artery Disease, Myocardial Infarction, 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 |
|---|---|---|
| Very Premature CAD | Patients who have received a coronary intervention procedure on the basis of atherosclerosis before the age of 40 | |
| Healthy middle-aged 1st degree relatives | Healthy 1st degree relatives aged 30-65 years of patients with very premature CAD. | |
| PCAD families | Families severely affected by premature CAD |
What is being measured
The primary outcome is the main question the study is designed to answer.
Number of patients with very premature coronary artery disease treated according to national guidelines
Evaluated on the basis of medical history, current medication, BP-TRU-measurement and measurement of blood lipids, and other lab tests.
Measured: At least 6 months after last coronary intervention procedure
Secondary outcomes (1)
Coronary artery lesions burden among middle-aged 1st degree relatives of patients with very premature coronary artery disease
Evaluated on the basis of the Agatston score and the number of coronary artery lesions on the coronary CT angiogram
Measured: At least 6 months after last coronary intervention procedure
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted26 May 2014 (estimated)
- Study startFeb 2014
- Primary completionFeb 2016 (estimated)
- Study completionFeb 2016 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (16)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
- Family based
- Time perspective
- Cross-sectional
- Enrolment
- 400 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Aarhus University Hospital Skejby
- Sponsor type
- University, hospital or other
- Collaborators
- University of Aarhus, Kong Christian IX og Dronning Louises Jubilæumslegat, Snedkermester Sophus Jacobsen and hustru Astrid Jacobsens Foundation
- Responsible party
- Principal investigator, Morten Krogh Christiansen, Aarhus University Hospital Skejby
- Investigators
- Morten K Christiansen, MD, Principal investigator, Aarhus University Hospital Skejby
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02146872
- Sponsor's protocol ID
- PIHS-KMA
- Other IDs
- 13517433
- Acronym
- PIHS
- Status last verified
- May 2014
- First submitted
- 2 May 2014
- Last updated
- 26 May 2014
- Results posted
- No
- Data monitoring committee
- No
Publications
Sing CF, Haviland MB, Templeton AR, Zerba KE, Reilly SL. Biological complexity and strategies for finding DNA variations responsible for inter-individual variation in risk of a common chronic disease, coronary artery disease. Ann Med. 1992 Dec;24(6):539-47. doi: 10.3109/07853899209167008.
PubMed 1485951Chow CK, Pell AC, Walker A, O'Dowd C, Dominiczak AF, Pell JP. Families of patients with premature coronary heart disease: an obvious but neglected target for primary prevention. BMJ. 2007 Sep 8;335(7618):481-5. doi: 10.1136/bmj.39253.577859.BE.
PubMed 17823190Marenberg ME, Risch N, Berkman LF, Floderus B, de Faire U. Genetic susceptibility to death from coronary heart disease in a study of twins. N Engl J Med. 1994 Apr 14;330(15):1041-6. doi: 10.1056/NEJM199404143301503.
PubMed 8127331Perk J, De Backer G, Gohlke H, Graham I, Reiner Z, Verschuren M, Albus C, Benlian P, Boysen G, Cifkova R, Deaton C, Ebrahim S, Fisher M, Germano G, Hobbs R, Hoes A, Karadeniz S, Mezzani A, Prescott E, Ryden L, Scherer M, Syvanne M, Scholte op Reimer WJ, Vrints C, Wood D, Zamorano JL, Zannad F; European Association for Cardiovascular Prevention & Rehabilitation (EACPR); ESC Committee for Practice Guidelines (CPG). European Guidelines on cardiovascular disease prevention in clinical practice (version 2012). The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts). Eur Heart J. 2012 Jul;33(13):1635-701. doi: 10.1093/eurheartj/ehs092. Epub 2012 May 3. No abstract available.
PubMed 22555213Mortensen MB, Sivesgaard K, Jensen HK, Comuth W, Kanstrup H, Gotzsche O, May O, Bertelsen J, Falk E. Traditional SCORE-based health check fails to identify individuals who develop acute myocardial infarction. Dan Med J. 2013 May;60(5):A4629.
PubMed 23673263Kessler T, Erdmann J, Schunkert H. Genetics of coronary artery disease and myocardial infarction--2013. Curr Cardiol Rep. 2013 Jun;15(6):368. doi: 10.1007/s11886-013-0368-0.
PubMed 23616109Hughes MF, Saarela O, Stritzke J, Kee F, Silander K, Klopp N, Kontto J, Karvanen J, Willenborg C, Salomaa V, Virtamo J, Amouyel P, Arveiler D, Ferrieres J, Wiklund PG, Baumert J, Thorand B, Diemert P, Tregouet DA, Hengstenberg C, Peters A, Evans A, Koenig W, Erdmann J, Samani NJ, Kuulasmaa K, Schunkert H. Genetic markers enhance coronary risk prediction in men: the MORGAM prospective cohorts. PLoS One. 2012;7(7):e40922. doi: 10.1371/journal.pone.0040922. Epub 2012 Jul 25.
PubMed 22848412Frazer KA, Murray SS, Schork NJ, Topol EJ. Human genetic variation and its contribution to complex traits. Nat Rev Genet. 2009 Apr;10(4):241-51. doi: 10.1038/nrg2554.
PubMed 19293820Cirulli ET, Goldstein DB. Uncovering the roles of rare variants in common disease through whole-genome sequencing. Nat Rev Genet. 2010 Jun;11(6):415-25. doi: 10.1038/nrg2779.
PubMed 20479773Sanger F, Nicklen S, Coulson AR. DNA sequencing with chain-terminating inhibitors. Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7. doi: 10.1073/pnas.74.12.5463.
PubMed 271968Choi M, Scholl UI, Ji W, Liu T, Tikhonova IR, Zumbo P, Nayir A, Bakkaloglu A, Ozen S, Sanjad S, Nelson-Williams C, Farhi A, Mane S, Lifton RP. Genetic diagnosis by whole exome capture and massively parallel DNA sequencing. Proc Natl Acad Sci U S A. 2009 Nov 10;106(45):19096-101. doi: 10.1073/pnas.0910672106. Epub 2009 Oct 27.
PubMed 19861545Erdmann J, Stark K, Esslinger UB, Rumpf PM, Koesling D, de Wit C, Kaiser FJ, Braunholz D, Medack A, Fischer M, Zimmermann ME, Tennstedt S, Graf E, Eck S, Aherrahrou Z, Nahrstaedt J, Willenborg C, Bruse P, Braenne I, Nothen MM, Hofmann P, Braund PS, Mergia E, Reinhard W, Burgdorf C, Schreiber S, Balmforth AJ, Hall AS, Bertram L, Steinhagen-Thiessen E, Li SC, Marz W, Reilly M, Kathiresan S, McPherson R, Walter U; CARDIoGRAM; Ott J, Samani NJ, Strom TM, Meitinger T, Hengstenberg C, Schunkert H. Dysfunctional nitric oxide signalling increases risk of myocardial infarction. Nature. 2013 Dec 19;504(7480):432-6. doi: 10.1038/nature12722. Epub 2013 Nov 10.
PubMed 24213632Bamshad MJ, Ng SB, Bigham AW, Tabor HK, Emond MJ, Nickerson DA, Shendure J. Exome sequencing as a tool for Mendelian disease gene discovery. Nat Rev Genet. 2011 Sep 27;12(11):745-55. doi: 10.1038/nrg3031.
PubMed 21946919Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M Jr, Detrano R. Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol. 1990 Mar 15;15(4):827-32. doi: 10.1016/0735-1097(90)90282-t.
PubMed 2407762Ott J. Analysis of Human Genetic Linkage. Third Ed. Baltimore: The John Hopkins University Press; 1999
Study at a glance
From the registry record, last updated by the sponsor on 26 May 2014. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Premature Coronary Artery Disease - Clinical and Molecular Genetic Aspects
- ClinicalTrials.gov ID
- NCT02146872
- Acronym / sponsor ID
- PIHS / PIHS-KMA
- Keywords
- Coronary Artery Disease, Myocardial Infarction, Atherosclerosis, High-Throughput Nucleotide Sequencing, Sequence Analysis, DNA, Genetic Testing, Genetic Linkage
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 400 participants (estimated)
- Lead sponsor
- Aarhus University Hospital SkejbyUniversity, hospital or other
- Collaborators
- University of Aarhus, Kong Christian IX og Dronning Louises Jubilæumslegat, Snedkermester Sophus Jacobsen and hustru Astrid Jacobsens Foundation
- Study start
- Feb 2014
- Primary completion
- Feb 2016 (estimated)
- Study completion
- Feb 2016 (estimated)
- First posted
- 26 May 2014 (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.
Since finishing the sequencing of the human genome in 2003, genetic research in coronary artery disease (CAD) and other complex traits have developed dramatically. Recent genome-wide association studies have identified a considerable number of common genetic variants each associated with the disease. This has led to a new understanding but also to the discovery of new therapeutical targets. However, each of the variants discovered only have minor effects on disease development and even the pooling of the variants only explains a minor percentage of the total heritability. It has been evident that rare or private mutations probably play a great role in the genetic architecture of CAD, especially among young and severely affected patients. These may only be identified by sequencing. Therefore, the investigators hypothesize, that the use of exome sequencing (the read-off of the entire protein-coding regions of the genome) and linkage analysis in families of extreme phenotype cases, will identify disease-causing genetic variants. From the West Denmark Heart Registry the investigators will enroll a minimum of 120 patients with atherosclerosis who have undergone a coronary artery revascularization procedure before the age of 40, to participate in study part 1. A pedigree analysis will be performed and cardiovascular (CVD) risk factors and current preventive treatment will be evaluated. 1. degree relatives aged 30-65 years, who are free of CAD, are invited to participate in study 2. CVD risk factors are evaluated as well as a CT coronary angiogram is performed to quantify the degree of asymptomatic coronary atherosclerosis. Families from study 1 and 2, who are considered severely affected by atherosclerosis, evaluated on a basis of family size, number of affected and severity of disease, will be selected for exome sequencing. Other relevant family members will be included as well as their CVD risk factors will be evaluated. Exome sequencing will be performed and variants found will be filtered on a basis of frequency, linkage analysis, gene position, existing knowledge and in-silico prediction tools. Possible findings will be validated by Sanger-sequencing and causality of new variants will subsequently be sought to be proven by relevant experimental studies.
Detailed description
Purposes Study part 1: Quantify the occurrence of risk factors of atherosclerosis among patients with very premature CAD in the Central Denmark Region and investigate to what degree patients are treated according to national guidelines.
Study part 2: Investigate the occurrence of CAD among middle-aged 1st degree relatives of established patients having very premature CAD.
Study part 3: Evaluate possible genetic "risk factors" in families with a high CAD prevalence using exome sequencing analysis.
Hypotheses Hypothesis 1: Patients with very premature CAD have modifiable risk factors, which are inadequately treated relative to current national guidelines.
Hypothesis 2: The occurrence of very premature CAD is associated with familial accumulation of the disease.
Hypothesis 3: The use of exome sequencing in selected families with phenotypic severe premature CAD will identify disease-causing genetic variants.
Method Study part 1. Patients suffering from premature CAD who have had a percutaneous coronary intervention (PCI) or coronary artery bypass graft operation (CABG) done before the age of 40 years will be selected from the West Denmark Heart Registry (VDHD). Specifically, patients treated at Aarhus University Hospital (AUH) in Skejby for myocardial infarction (MI), stable or unstable angina pectoris in the period of January 1st 2007 - December 31st 2013 will be recruited and the occurrence of registered risk factors be evaluated (sample indicates app. 170 patients per year). After informed consent is obtained, they will participate in this research study. Participants will be interviewed in the cardiac outpatient clinic at the Dep. of Cardiology, AUH, Skejby. The following information about cardiovascular risk factors will be collected; family history of atherosclerosis (a pedigree analysis will be performed and cases of diagnosed CVD will be identified), prior medical history (i.e. hypertension, dyslipidemia, diabetes, chronic kidney disease, vascular disease), smoking status and number of pack years, alcohol consumption and vascular symptoms (i.e. angina pectoris, intermittent claudication). Gathered information will be compared to the registered information in patient records and VDHD. In addition, information about localization of the invasive treatment, the degree of CAD, and the latest estimate of the left ventricular ejection fraction (LVEF) will be collated. All patients will be examined regarding height and weight, abdominal girth and a blood sample is collected. An automated office blood pressure measurement (Bp-TRU device) will be performed. Levels of creatinine (e-GFR), total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides and HbA1c will be measured. Further, a blood sample will be saved for prospective DNA analysis (below). The investigators will evaluate to what degree the treatment targets have been met in accordance with national guidelines. Analysis will be corrected to reflect changes in these treatment guidelines, which have occurred in recent years.
Study part 2. Patients from study 1 (index patients) are requested to establish contact to 1st degree relatives between 30 and 65 years of age for the purpose of participating in Study part 2. The form of contact follows regular department guidelines for contact to family members. 1st degree relatives who give their informed consent will be included in study part 2 (participants). Patient records from participants who are diagnosed with atherosclerosis will be obtained. Exclusion criteria will be former diagnosis of CAD by CTCA or percutaneous transluminal coronary angiography, chronic atrial fibrillation, renal failure (e-GFR < 30ml/min), obesity (BMI > 30 is indicative but body geometry plays a role), former allergic contrast reaction and pregnancy. A traditional risk profile and blood samples will be collected as in study part 1. Prior to the CTCA, LVEF is estimated by echocardiography. A CTCA is performed according to the standard protocol in the department. Initially the CT-scan is performed without contrast in order to estimate the coronary calcification by Agatstons method. Afterwards a scan is performed with 70 ml of iodine-containing contrast. ECG modulation and radiation-reduced protocols will be used so that an average participant (70 kg) may expect to receive a radiation dose below 3 mSv. The analysis of the contrast study will focus on automated- and semi-automated plaque quantification. Non-cardiac findings will be described according to department standard procedures by the Dep. of Radiology, AUH, Skejby, and medical intervention performed as clinically indicated.
Study part 3. Families from study part 1 and 2, who are considered severely affected by atherosclerosis, evaluated on a basis of family size, number of affected and severity of disease, will be selected. Family members (index patients, 1st degree relatives and if relevant also their 1st degree relatives) who consent,will be included in study part 3. Contact with relatives who have not yet participated in the project will be attempted as in study part 2. A traditional risk profile and a blood sample for DNA analysis (exome sequencing) will be requested if it has not already been obtained. The analysis takes place at Department of Molecular Medicine (MOMA), AUH, Skejby, who have the required equipment, software and laboratory expertise in performing the tests as well as the bioinformatic analysis. First, genomic DNA is purified and fragmented to a size of 200-500 base pairs. Illumina TruSeq libraries (to be used with the exome sequencing) will be produced at a Caliper Sciclone-robot where the exome enrichment with Nimblegens EZ in solution Exome v3 kit will also take place. The dataanalysis will be taking place at MOMA under the guidance of the MOMA staff. First sequences will be trimmed and aligned to the humane genome. Second, alignments will be fine-tuned before variants will be called, including single nucleotide variants and insertions/deletions of various size. The interpretation of the data will be taking place in the software program Cartagenia, which gives access to an abundance of public and commercial databases and also offers the opportunity of integrating private databases. Variants will be filtered on a basis of frequency, gene position, existing knowledge and different in-silico prediction tools. Possible significant findings will be validated by Sanger sequencing.
Statistical analysis At the found genotypes from study part 3, coupling analysis is performed to identify regions in the genome shared by disease-affected individuals. The use of pedigree analysis and coupling analysis substantially reduce the candidate intervals in the genome, thereby increasing the statistical power to identify disease-causing variants even in small families. Because the precise genetic architecture and family structure of the included families is not known, exact calculation of statistical power will not be possible. In case of a dominant monogenetic disease, a filtration only based on localization (coupling) reduces the potential variants by app. 80% within a pair of affected siblings and by more than 95% for monogenetic recessive diseases, if affected individuals from inbred families.
Research Biobank A research biobank will be established under The Institute of Clinical Medicine, Health, Aarhus University. A sample of 2x4 ml (BD Vacutainer K3E 7,2mg Ref. 368860) and 1x4ml (BD Vacutainer SST II Advance, Ref. 367957) blood from all participants in studies 1-3 will be submitted to the biobank for further analysis. The sampling is performed at AUH, Skejby or a glass and a return envelope will sent to the patient for the drawing of blood by their family physician. The sample is cryo-preserved and exome sequencing is performed on the participants of study part 3. The biobank will be carried on after the project has ended for the purpose of future research. In case of future analysis on the preserved material The Research Ethics Committee and the participant (if still alive) will be noticed before hand. Permission to store the biological material will be applied continuously according to specified intervals by The Danish Data Protection Agency. All participants may demand their biological material destroyed at any time.
Study design
- Observational model
- Family based
- Time perspective
- Cross-sectional
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| Very Premature CAD | – | –Patients who have received a coronary intervention procedure on the basis of atherosclerosis before the age of 40 |
| Healthy middle-aged 1st degree relatives | – | –Healthy 1st degree relatives aged 30-65 years of patients with very premature CAD. |
| PCAD families | – | –Families severely affected by premature CAD |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients who has received a coronary intervention procedure at Aarhus University Hospital, Skejby (all interventions are registered in the West Denmark Heart Registry)
Key inclusion criteria (9 listed)
- Coronary intervention at Aarhus University Hospital, Skejby in the period 2006-2013
- Age < 40 years at the time of intervention in the above mentioned period
- Intervention on the basis of atherosclerosis
- Residency in Denmark
- > 6 months since last coronary procedure
Key exclusion criteria (8 listed)
- Interventions on transplanted hearts
- Abuse of cocaine/amphetamine in close relation to the intervention
- Obesity (BMI>30)
- Chronic kidney disease stage 4+5
- Chronic atrial fibrillation
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
Number of patients with very premature coronary artery disease treated according to national guidelines
Time frame: At least 6 months after last coronary intervention procedure
Evaluated on the basis of medical history, current medication, BP-TRU-measurement and measurement of blood lipids, and other lab tests.
1 secondary outcome
Coronary artery lesions burden among middle-aged 1st degree relatives of patients with very premature coronary artery disease
Time frame: At least 6 months after last coronary intervention procedure
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 26 May 2014.
- Background: PubMed 1485951Sing CF, Haviland MB, Templeton AR, Zerba KE, Reilly SL. Biological complexity and strategies for finding DNA variations responsible for inter-individual variation in risk of a common chronic disease, coronary artery disease. Ann Med. 1992 Dec;24(6):539-47. doi: 10.3109/07853899209167008.
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- Human Genome Project Information ArchiveLink provided by the sponsor.
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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.
Morten K Christiansen, MD principal investigator
Aarhus University Hospital Skejby
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 Myocardial Infarction, run by Aarhus University Hospital Skejby at 1 site in Denmark.
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 9 inclusion and 8 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 26 May 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 Denmark. 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?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Each site lists its own contact: choose the nearest one under Trial locations. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Number of patients with very premature coronary artery disease treated according to national guidelines (time frame: At least 6 months after last coronary intervention procedure). 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 NCT02146872, which also lists 16 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 26 May 2014.