Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis
Background The prothrombotic defect factor V Leiden (FVL) may confer higher risk of ST‐segment–elevation myocardial infarction (STEMI), compared with non–ST‐segment–elevation acute coronary syndrome, and may be associated with more myocardial necrosis caused by higher thrombotic burden. Methods and...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2021-06-01
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| Series: | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
| Subjects: | |
| Online Access: | https://www.ahajournals.org/doi/10.1161/JAHA.120.020025 |
| _version_ | 1797607289151029248 |
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| author | Bakhtawar K. Mahmoodi Niclas Eriksson Gerrit J. A. Vos Karina Meijer Agneta Siegbahn Stefan James Lars Wallentin Jurriën M. ten Berg |
| author_facet | Bakhtawar K. Mahmoodi Niclas Eriksson Gerrit J. A. Vos Karina Meijer Agneta Siegbahn Stefan James Lars Wallentin Jurriën M. ten Berg |
| author_sort | Bakhtawar K. Mahmoodi |
| collection | DOAJ |
| description | Background The prothrombotic defect factor V Leiden (FVL) may confer higher risk of ST‐segment–elevation myocardial infarction (STEMI), compared with non–ST‐segment–elevation acute coronary syndrome, and may be associated with more myocardial necrosis caused by higher thrombotic burden. Methods and Results Patients without history of cardiovascular disease were selected from 2 clinical trials conducted in patients with acute coronary syndrome. FVL was defined as G‐to‐A substitution at nucleotide 1691 in the factor V (factor V R506Q) gene. Odds ratios were calculated for the association of FVL with STEMI adjusted for age and sex in the overall population and in the subgroups including sex, age (≥70 versus <70 years), and traditional cardiovascular risk factors. The peak biomarker levels (ie, creatine kinase‐myocardial band and high‐sensitivity troponin I or T) after STEMI were contrasted between FVL carriers and noncarriers. Because of differences in troponin assays, peak high‐sensitivity troponin levels were converted to a ratio scale. The prevalence of FVL mutation was comparable in patients with STEMI (6.0%) and non–ST‐segment–elevation acute coronary syndrome (5.8%). The corresponding sex‐ and age‐adjusted odds ratio was 1.06 (95% CI, 0.86–1.30; P=0.59) for the association of FVL with STEMI. Subgroup analysis did not show any differences. In patients with STEMI, neither the median peak creatine kinase‐myocardial band nor the peak high‐sensitivity troponin ratio showed any differences between wild‐type and FVL carriers (P for difference: creatine kinase‐myocardial band=0.33; high sensitivity troponin ratio=0.54). Conclusions In a general population with acute coronary syndrome, FVL did not discriminate between a STEMI or non–ST‐segment–elevation acute coronary syndrome presentation and was unrelated to peak cardiac necrosis markers in patients with STEMI. Registration URL: https://www.clinicaltrials.gov; Unique identifiers: NCT00391872 and NCT01761786. |
| first_indexed | 2024-03-11T05:28:06Z |
| format | Article |
| id | doaj.art-bf537e3efa32476abb9653f24fe9024a |
| institution | Directory Open Access Journal |
| issn | 2047-9980 |
| language | English |
| last_indexed | 2024-03-11T05:28:06Z |
| publishDate | 2021-06-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
| spelling | doaj.art-bf537e3efa32476abb9653f24fe9024a2023-11-17T17:20:07ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802021-06-01101110.1161/JAHA.120.020025Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial NecrosisBakhtawar K. Mahmoodi0Niclas Eriksson1Gerrit J. A. Vos2Karina Meijer3Agneta Siegbahn4Stefan James5Lars Wallentin6Jurriën M. ten Berg7Department of Cardiology St. Antonius Hospital Nieuwegein the NetherlandsUppsala Clinical Research Center Uppsala University Uppsala SwedenDepartment of Cardiology St. Antonius Hospital Nieuwegein the NetherlandsDivision of Hemostasis and Thrombosis Department of Hematology UMC GroningenUniversity of Groningen the NetherlandsUppsala Clinical Research Center Uppsala University Uppsala SwedenUppsala Clinical Research Center Uppsala University Uppsala SwedenUppsala Clinical Research Center Uppsala University Uppsala SwedenDepartment of Cardiology St. Antonius Hospital Nieuwegein the NetherlandsBackground The prothrombotic defect factor V Leiden (FVL) may confer higher risk of ST‐segment–elevation myocardial infarction (STEMI), compared with non–ST‐segment–elevation acute coronary syndrome, and may be associated with more myocardial necrosis caused by higher thrombotic burden. Methods and Results Patients without history of cardiovascular disease were selected from 2 clinical trials conducted in patients with acute coronary syndrome. FVL was defined as G‐to‐A substitution at nucleotide 1691 in the factor V (factor V R506Q) gene. Odds ratios were calculated for the association of FVL with STEMI adjusted for age and sex in the overall population and in the subgroups including sex, age (≥70 versus <70 years), and traditional cardiovascular risk factors. The peak biomarker levels (ie, creatine kinase‐myocardial band and high‐sensitivity troponin I or T) after STEMI were contrasted between FVL carriers and noncarriers. Because of differences in troponin assays, peak high‐sensitivity troponin levels were converted to a ratio scale. The prevalence of FVL mutation was comparable in patients with STEMI (6.0%) and non–ST‐segment–elevation acute coronary syndrome (5.8%). The corresponding sex‐ and age‐adjusted odds ratio was 1.06 (95% CI, 0.86–1.30; P=0.59) for the association of FVL with STEMI. Subgroup analysis did not show any differences. In patients with STEMI, neither the median peak creatine kinase‐myocardial band nor the peak high‐sensitivity troponin ratio showed any differences between wild‐type and FVL carriers (P for difference: creatine kinase‐myocardial band=0.33; high sensitivity troponin ratio=0.54). Conclusions In a general population with acute coronary syndrome, FVL did not discriminate between a STEMI or non–ST‐segment–elevation acute coronary syndrome presentation and was unrelated to peak cardiac necrosis markers in patients with STEMI. Registration URL: https://www.clinicaltrials.gov; Unique identifiers: NCT00391872 and NCT01761786.https://www.ahajournals.org/doi/10.1161/JAHA.120.020025cardiovascular diseasecardiovascular disease risk factorscoagulation/thrombosisfactor V Leidengenetic polymorphism |
| spellingShingle | Bakhtawar K. Mahmoodi Niclas Eriksson Gerrit J. A. Vos Karina Meijer Agneta Siegbahn Stefan James Lars Wallentin Jurriën M. ten Berg Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease cardiovascular disease cardiovascular disease risk factors coagulation/thrombosis factor V Leiden genetic polymorphism |
| title | Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis |
| title_full | Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis |
| title_fullStr | Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis |
| title_full_unstemmed | Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis |
| title_short | Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis |
| title_sort | factor v leiden does not modify the phenotype of acute coronary syndrome or the extent of myocardial necrosis |
| topic | cardiovascular disease cardiovascular disease risk factors coagulation/thrombosis factor V Leiden genetic polymorphism |
| url | https://www.ahajournals.org/doi/10.1161/JAHA.120.020025 |
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