Regular ArticleThrombin-activatable fibrinolysis inhibitor genetic polymorphisms as markers of the type of acute coronary syndrome
Section snippets
Materials and methods
We prospectively recruited 248 consecutive patients with ACS (190 [77%] male, 58 [23%] female, mean age 60.75, SD 13.30 years) from the Cardiology Department of the Hospital Clinic of Barcelona (Spain). Inclusion criteria were unstable angina or myocardial infarction. Unstable angina was defined by chest pain at rest, or progressive angina, or cardiac ischemic symptoms of ≥ 10 minutes of duration at rest, and ST segment changes on the electrocardiogram suggestive of ischemia. Myocardial
Results
One hundred forty seven (59.3%) patients had ST-segment elevation (STE) ACS, and 101 (40.7%) had non-STE ACS. All patients with STE developed an Q-wave MI, while 52/101 (21%) patients with non-STE had non-Q wave MI and 49 (19.8%) had unstable angina. Patients with STE ACS and non-STE ACS (unstable angina or non-Q wave MI) were analyzed separately.
One hundred and one (40.7%) patients were smokers, 70 (28.2%) had diabetes, 143 (57.7%) had dyslipemia, 133 (53.6%) had hypertension, and 34 (13.7%)
Discussion
We analyzed the role of genetic variations in fibrinolysis inhibitors PAI-1 and TAFI in relation to the clinical presentation of ACS. TAFI alleles + 1542G and 325Ile, associated with lower TAFI levels, were associated with non-STE ACS (non Q wave MI and unstable angina) in comparison with STE ACS.
In ACS, thrombus propagation over a disrupted arteriosclerotic plaque may occlude the coronary lumen to varying extents, resulting in different clinical manifestations. It is unclear why some patients
Conflict of interest statement
None declared.
Acknowledgments
This work was funded in part by the Ministerio de Ciencia e Innovación, Instituto de Salud Carlos III, (Red HERACLES RD06/0009) and grants FIS 02/0711 and FIS 05/0204 from the Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III, Spain.
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