Risk factors for sudden cardiac death from an acute ischemic event in general population : a case-control study
1University of Oulu, Faculty of Medicine, Department of Internal Medicine
|Online Access:||PDF Full Text (PDF, 0.9 MB)|
|Persistent link:|| http://urn.fi/urn:isbn:9789514290473
|Publish Date:|| 2009-04-14
|Thesis type:||Doctoral Dissertation
|Defence Note:||Academic dissertation to be presented, with the assent of the Faculty of Medicine of the University of Oulu, for public defence in Auditorium 10 of Oulu University Hospital, on April 24th, 2009, at 12 noon
Docent Lasse Oikarinen
Docent Vesa Virtanen
Specific prevention of sudden cardiac death (SCD) caused by an acute coronary event in the general population has remained a challenge for clinicians since the recognizable risk factors for this fatal outcome of an underlying coronary artery disease (CAD) may be partly the same as those of a non-fatal coronary event.
This case-control study was designed to compare genetic and several other factors between consecutive series of survivors (n = 644) and victims of SCD (n = 425) from an acute coronary event. Only subjects with an acute coronary event verified at medico-legal autopsy were included in the SCD group. As controls, 809 subjects without any history of CAD, acute myocardial infarction or aborted cardiac arrest were examined. Subjects to the sub-studies were drawn from these study populations. The increased risk for SCD in the general population was associated with family history of SCD, male gender, smoking, cardiac hypertrophy and the severity of CAD. In the present study, 100% mortality was observed when all these risk factors were present at the time of an acute coronary event. In the subjects with a family history of SCD, the increased risk of SCD was correlated with the severity of CAD without any clustering of coronary risk factors, suggesting that genetic factors affecting the accelerated progression of CAD may have an important role in familial SCD. However, polymorphisms of genes affecting thrombosis, which are believed to have effects on plaque progression and the consequences of plaque complications, were not associated with an increased risk for SCD.
The present results show that the risk of SCD at the time of an acute coronary event can be assessed by generally available methods. If a subject is a male smoker and has a family history of SCD, the risk of SCD is substantially increased. In our study sample the currently known polymorphisms affecting thrombosis did not have a major impact in risk stratification of genetic susceptibility for SCD. Simple association studies have clear shortcomings when they attempt to reveal genetic associations with complex outcomes and thus new research strategies are needed to elucidate the genetic background of SCD.
Acta Universitatis Ouluensis. D, Medica
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