Abstract P008: Ultra-Sensitive Troponin I Strongly Predicts Incident Coronary Heart Disease in the General Population Independently of Traditional Risk Factors. Results From the MONICA/KORA Augsburg Case-Cohort Study

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Wolfgang Koenig ◽  
Astrid Zierer ◽  
Mahir Karakas ◽  
Christa Meisinger ◽  
Annette Peters ◽  
...  

Background: High-sensitive (hs) troponin T and I assays as well as ultrasensitive (us) troponin I enable measurement of troponins in 65% to 98% of the general population. We prospectively investigated whether increased concentrations of us-troponin I are associated with an increased risk of coronary heart disease (CHD) after controlling for traditional risk factors. Methods: We conducted a population-based case cohort study in middle-aged healthy men and women within the MONICA/KORA Augsburg studies. Serum levels of us-troponin I (Single Molecule Counting technology, Singulex) were available in 2,745 men and women including 803 incident CHD cases. Geometric mean us-troponin I was 1.56 ng/L. Mean (SD) follow-up was 16.0 (5.8) years. Results: Baseline concentrations of us-troponin I were higher in cases compared to non-cases (geometric mean 2.56 vs. 1.49 ng/L, p<0.0001) and in men compared to women (geometric mean 1.93 vs. 1.27 ng/L, p<0.0001). After adjustment for variables of the Framingham Risk Score, the hazard ratio (HR) with 95% confidence interval (CI) for a CHD event in the top quartile compared to the bottom quartile was 2.76 (95% CI, 1.87-4.09). After additional adjustment for alcohol intake, physical activity, and body mass index, hazard ratios remained essentially unchanged. Conclusions: Troponin I measured by an us-assay was detectable in almost all subjects. This is the first population-based prospective study with long-term follow-up showing that even modestly increased concentrations of us troponin I are strongly associated with incident CHD independently of a variety of traditional risk factors.

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e105804 ◽  
Author(s):  
Davood Khalili ◽  
Farhad Haj Sheikholeslami ◽  
Mahmood Bakhtiyari ◽  
Fereidoun Azizi ◽  
Amir Abbas Momenan ◽  
...  

Author(s):  
Nancy Kreiger ◽  
Alan Tenenhouse ◽  
Lawrence Joseph ◽  
Tom Mackenzie ◽  
Suzette Poliquin ◽  
...  

ABSTRACTRelatively little is known about the factors in Canada which lead to osteoporosis and its concomitant fractures. The Canadian Multicentre Osteoporosis Study (CaMos) is a prospective cohort study which will estimate the incidence and prevalence of declining bone mass and fractures. The impact of osteoporosis in Canada will be assessed, including regional variation and the effect of various risk factors. The study will provide information for developing prevention programs. The cohort has been drawn from a random population-based sample of non-institutionalized men and women 25 years old or more and living within 50 km. of nine cities in Canada. Through telephone interviews 9,423 participants have been recruited. All answered an extensive questionnaire, and had physical measurements related to bone quality taken. This paper details the CaMos baseline and five-year follow-up protocol.


2007 ◽  
Vol 35 (1) ◽  
pp. 4-10 ◽  
Author(s):  
Lise Lund Håheim ◽  
Serena Tonstad ◽  
Ingvar Hjermann ◽  
Paul Leren ◽  
Ingar Holme

Aims: To test the association between body mass index (BMI) and other coronary risk factors and the risk of a fatal coronary heart disease (CHD) event in different time periods during follow-up. Methods: Prospective cohort study with a 21 year follow-up period. A screened sample of 14,403 men aged 40—49 years initially free of CHD. Risk of fatal CHD was calculated for 21 years' cumulative follow-up and for four consecutive 5-year periods. Results: After adjustment for age and the other risk factors, total cholesterol and systolic blood pressure retained their predictive strength for CHD mortality throughout follow-up. Though cigarette smoking remained a significant predictor, the relative risk decreased with time (test of trend: p=0.01). Intermediate to vigorous physical activity at leisure was protective for 10 years of follow-up and a question on mental stress for 5 years. The test of trend indicated that the risk associated with BMI increased with the duration of follow-up (p=0.002). Conclusions: Our data show that coronary risk factors predicted CHD mortality differently according to the length of follow-up, and suggest that the harm associated with obesity may take more than a decade to become evident, in contrast to the classical CHD risk factors.


2021 ◽  
pp. jech-2020-214358
Author(s):  
Pekka Martikainen ◽  
Kaarina Korhonen ◽  
Aline Jelenkovic ◽  
Hannu Lahtinen ◽  
Aki Havulinna ◽  
...  

BackgroundGenetic vulnerability to coronary heart disease (CHD) is well established, but little is known whether these effects are mediated or modified by equally well-established social determinants of CHD. We estimate the joint associations of the polygenetic risk score (PRS) for CHD and education on CHD events.MethodsThe data are from the 1992, 1997, 2002, 2007 and 2012 surveys of the population-based FINRISK Study including measures of social, behavioural and metabolic factors and genome-wide genotypes (N=26 203). Follow-up of fatal and non-fatal incident CHD events (N=2063) was based on nationwide registers.ResultsAllowing for age, sex, study year, region of residence, study batch and principal components, those in the highest quartile of PRS for CHD had strongly increased risk of CHD events compared with the lowest quartile (HR=2.26; 95% CI: 1.97 to 2.59); associations were also observed for low education (HR=1.58; 95% CI: 1.32 to 1.89). These effects were largely independent of each other. Adjustment for baseline smoking, alcohol use, body mass index, igh-density lipoprotein (HDL) and total cholesterol, blood pressure and diabetes attenuated the PRS associations by 10% and the education associations by 50%. We do not find strong evidence of interactions between PRS and education.ConclusionsPRS and education predict CHD events, and these associations are independent of each other. Both can improve CHD prediction beyond behavioural risks. The results imply that observational studies that do not have information on genetic risk factors for CHD do not provide confounded estimates for the association between education and CHD.


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