scholarly journals Relationship Between Number of Multiple Risk Factors and Coronary Artery Disease Risk With and Without Diabetes Mellitus

2019 ◽  
Vol 104 (11) ◽  
pp. 5084-5090 ◽  
Author(s):  
Mayuko Yamada-Harada ◽  
Kazuya Fujihara ◽  
Taeko Osawa ◽  
Masahiko Yamamoto ◽  
Masanori Kaneko ◽  
...  

Abstract Purpose To determine the degree of control of multiple risk factors under real-world conditions for coronary artery disease (CAD) according to the presence or absence of diabetes mellitus (DM) and to determine whether reaching multifactorial targets for blood pressure (BP), low-density lipoprotein-cholesterol (LDL-C), HbA1c, and current smoking is associated with lower risks for CAD. Methods We investigated the effects on subsequent CAD of the number of controlled risk factors among BP, LDL-C, HbA1c, and current smoking in a prospective cohort study using a nationwide claims database of 220,894 individuals in Japan. Cox regression examined risks over a 4.8-year follow-up. Results The largest percentage of participants had two risk factors at target in patients with DM (39.6%) and subjects without DM (36.4%). Compared with those who had two targets achieved, the risks of CAD among those who had any one and no target achieved were two and four times greater, respectively, regardless of the presence of DM. The effect of composite control was sufficient to bring CAD risk in patients with DM below that for subjects without DM with any two targets achieved, whereas the risk of CAD in the DM group with all four risk factors uncontrolled was 9.4 times more than in the non-DM group who had achieved two targets. Conclusions These findings show that composite control of modifiable risk factors has a large effect in patients with and without DM. The effect was sufficient to bring CAD risk in patients with DM below that in the non-DM group who had two targets achieved.

1979 ◽  
Vol 8 (3) ◽  
pp. 407-418 ◽  
Author(s):  
Larry S. Webber ◽  
Antonie W. Voors ◽  
Sathanur R. Srinivasan ◽  
Ralph R. Frerichs ◽  
Gerald S. Berenson

1987 ◽  
Vol 83 (4) ◽  
pp. 609-612 ◽  
Author(s):  
Ivana Zavaroni ◽  
Elizabeth Dall'aglio ◽  
Enzo Bonora ◽  
Orsola Alip ◽  
Mario Passeri ◽  
...  

2003 ◽  
Vol 462 (1-3) ◽  
pp. 139-143 ◽  
Author(s):  
Alex I Malinin ◽  
Dan Atar ◽  
Kevin P Callahan ◽  
Marcus E McKenzie ◽  
Victor L Serebruany

1991 ◽  
Vol 32 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Yoshiyu TAKEDA ◽  
Junichiro MIFUNE ◽  
Kuniaki TAGA ◽  
Senshu HIFUMI ◽  
Yoshifumi TAKAHASHI ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Bernd Stratmann ◽  
Katrin Richter ◽  
Ruichao Wang ◽  
Zhonghao Yu ◽  
Tao Xu ◽  
...  

Coronary artery disease (CAD) is a common complication of type 2 diabetes mellitus (T2D). This case-control study was done to identify metabolites with different concentrations between T2D patients with and without CAD and to characterise implicated metabolic mechanisms relating to CAD. Fasting serum samples of 57 T2D subjects, 26 with (cases) and 31 without CAD (controls), were targeted for metabolite profiling of 163 metabolites. To assess the association between metabolite levels and CAD, partial least squares (PLS) analysis and multivariate logistic regression analysis with adjustment for CAD risk factors and medications were performed. We observed a separation of cases and controls with two classes of metabolites being significantly associated with CAD, including phosphatidylcholines, and serine. Four metabolites being independent from the common CAD risk factors displaying best separation between cases and controls were further selected. Addition of the metabolite concentrations to risk factor analysis raised the area under the receiver-operating-characteristic curve from 0.72 to 0.88 (p=0.020), providing improved sensitivity and specificity for CAD classification. Serum phospholipid and serine levels independently discriminate T2D patients with and without CAD. Oxidative stress and reduced antioxidative capacity lead to lower metabolite concentrations probably due to changes in membrane composition and accelerated phospholipid degradation.


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