Background: Type D personality is associated with an increased morbidity and mortality risk in cardiovascular disease patients, but the mechanisms explaining this risk are unclear. We examined whether Type D was associated with coronary artery disease (CAD) risk factors, estimated risk of developing CAD, and previous cardiac events.
Design: Cross-sectional study in the general Icelandic population.
Methods: A random sample of 4753 individuals (mean age 49.1 ± 12.0 years; 49% men) from the REFINE-Reykjavik study completed assessments for Type D personality and conventional CAD risk factors. Ten-year risk of developing CAD was estimated with the Icelandic risk calculator.
Results: Type D personality (22% of sample) was associated with a higher prevalence of hypertension (35 vs. 31%, p = 0.009), but less use of hypertension medication (58 vs. 65%, p = 0.013) in hypertensives, more diabetes (6 vs. 4%, p = 0.023), wider waist circumference (p = 0.007), and elevated body mass index (p = 0.025) and blood lipids (p < 0.05). Type D individuals reported less physical exercise (p = 0.000) and more current (26 vs. 21%, p = 0.003) and former smoking (48 vs. 44%, p = 0.036). Estimates of 10-year risk of CAD were higher in Type D individuals (12.4%, 95% CI 1.9 to 23.8%), and Type Ds reported more previous cardiac events than non-Type Ds (5 vs. 3%, p < 0.01; OR 1.71, 95% CI 1.21 to 2.42).
Conclusions: In the general Icelandic population, Type D personality was associated with differences in lifestyle-related CAD risk factors, a higher estimated risk of developing CAD, and higher incidence of previous cardiac events. Unhealthy lifestyles may partly explain the adverse cardiovascular effect of Type D personality.
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http://dx.doi.org/10.1177/2047487312441723 | DOI Listing |
Sci Rep
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Molecular Biology and Genetics Laboratory (LGBM), UFMS - Federal University of Mato Grosso do Sul, Três Lagoas, Brazil.
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Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, 3-25-8 Nishi-shimbashi, Minato-ku, Tokyo, 105-8461, Japan.
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Institute of Pathology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Pathogenic activating mutations in the fibroblast growth factor receptor 3 (FGFR3) drive disease maintenance and progression in urothelial cancer. 10-15% of muscle-invasive and metastatic urothelial cancer (MIBC/mUC) are FGFR3-mutant. Selective targeting of FGFR3 hotspot mutations with tyrosine kinase inhibitors (e.
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