Association of Genetic Variation in Coronary Artery Disease-Related Loci With the Risk of Heart Failure With Preserved Versus Reduced Ejection Fraction.
Association of Genetic Variation in Coronary Artery Disease-Related Loci With the Risk of Heart Failure With Preserved Versus Reduced Ejection Fraction.
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冠状动脉疾病相关位点的遗传变异与保留射血分数与减少射血分数的心力衰竭风险的关联。
DOI：
10.1161/circulationaha.117.032491
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发表时间：
2018
期刊：
影响因子：
37.8
通讯作者：
Vasan,RamachandranS
中科院分区：
文献类型：
--
作者：
Andersson,Charlotte;Lyass,Asya;Lin,Honghuang;Køber,Lars;Larson,MartinG;Vasan,RamachandranS
A total of 4390 participants (mean age, 65 years; 55% women) were included. Mean values and distribution of GRS by HF development are presented in the Figure (A). We confirmed a statistically significant association of GRS with incident CAD in our sample (sex-and age-adjusted hazard ratio 1.97 [95% confidence interval, 1.51–2.58] per 1 U GRS, P< 0.0001). During follow-up (mean, 12 years; limits, 0.1–27 years), 472 participants (11%) developed HF (196 HFPEF and 212 HFREF; 64 HF cases were unclassified because of unknown ejection fraction). The GRS was associated with any HF and HFREF, but not with HFPEF (Figure [B]); P for equal hazard ratios HFREF versus HFPEF= 0.0045. Additional adjustments for baseline and interim myocardial infarction and for the 10-year estimated risk of cardiovascular disease did not alter these associations (Figure [B]). Also, the differences in hazard ratios associated with GRS (for HFREF versus HFPEF) remained statistically significant (P= 0.04). The risk of developing HF associated with a high GRS burden was not modified by the occurrence of either a baseline or an interim myocardial infarction or by a high 10-year estimated Framingham Risk Score (P for interactions> 0.5). The GRS was not significantly associated with post-HF mortality among any of the groups: hazard ratios were 0.90 (0.71–1.14) for any HF (371 deaths); 0.79 (0.54–1.14) for HFPEF (175 deaths); and 0.87 (0.62–1.21) for HFREF (156 deaths). In conclusion, a GRS for CAD was strongly associated with the risk for incident HFREF but not HFPEF in our sample, suggesting that CAD may contribute differentially to the propensity for these 2 conditions. Because our GRS captured only a modest part of the variability in CAD risk, more studies are warranted to establish if CAD may be a causal factor for the development of HFPEF, or if it is simply a frequent concomitant in elderly people presenting with the condition. Additional investigations are also needed to understand if competing risks could, in part, explain the lack of association between the GRS and the risk of developing HFPEF (ie, that people with several risk factors for CAD tend to develop HFREF before they can develop HFPEF), although we did not observe any effect modification by myocardial infarction or a high 10-year risk of developing cardiovascular disease. Other limitations to bear in mind when interpreting the data include the small study sample of predominantly white people of European ancestry and the definition of HF, which was based on the Framingham Study criteria (and only included hospitalized events).
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将内源合成的脂氧合酶产物酯化成粒细胞脂质。
影响因子：
2.9
作者：
R. Bonser;M. Siegel;S. Chung;R. McConnell;P. Cuatrecasas
通讯作者：
P. Cuatrecasas
影响因子：
6.5
作者：
F. Field;S. Mathur
通讯作者：
F. Field;S. Mathur
小鼠针对同种异体皮肤移植物的免疫反应中的巨噬细胞细胞毒性。
影响因子：
4.4
作者：
A. Dimitriu;M. Dy;N. Thomson;J. Hamburger
通讯作者：
J. Hamburger
DOI：
10.1042/bj0830460
发表时间：
1962
期刊：
The Biochemical journal
影响因子：
--
作者：
S. Murthy;J. Ganguly
通讯作者：
J. Ganguly
DOI：
10.1016/0005-2760(85)90175-4
发表时间：
1985
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
Mathur,SN;Field,FJ;Megan,MB;Armstrong,ML
通讯作者：
Armstrong,ML