Abstract
BackgroundObservational and experimental studies have thus far been unable to resolve whether the CYBA C242T polymorphism is associated with coronary artery disease (CAD). Therefore, we undertook a comprehensive meta-analysis to more precisely evaluate the influence of this polymorphism on CAD and potential biases.MethodsWe screened MEDLINE, Embase, CNKI, Wanfang and CBM up to January 2013 and extracted data from 22 studies with 9,279 CAD patients and 9,349 controls. A random-effects model was exploited to synthesize the inconsistent outcomes of the individual studies, while addressing between-study heterogeneity and publication bias.ResultsThe CYBA C242T polymorphism conformed to Hard-Weinberg Equilibrium for all studies (P>0.05). Overall comparison of the T allele with the C allele produced a non-significant risk estimate for CAD but with striking heterogeneity (T versus C: P = 0.87, OR = 0.99, 95%CI 0.89–1.11, Pheterogeneity<0.0001, I2 = 67.8%). However, subgroup analysis by ethnicity documented that the T allele carriers had a marginal risk increase (21%) of CAD among Caucasians (recessive genetic model: P = 0.05, 95%CI 1.00–1.46, Pheterogeneity = 0.15, I2 = 29.1%). Then data were divided into study design, the significance of CAD risk increase was substantially strengthened in matched case-control studies (allele comparison: P = 0.02, OR = 1.13, 95%CI 1.02–1.26, Pheterogeneity = 0.24, I2 = 21.6%).Further meta-regression analysis identified that a large proportion of heterogeneity was explained by body mass index (BMI) (P = 0.03, OR = 1.07, 95%CI 1.01–1.15) and study design (P = 0.03, OR = 1.30, 95%CI 1.02–1.64).There was no obvious publication bias as verified by funnel plot and Egger's linear regression test (t = −0.25, P = 0.81 for allele comparison).ConclusionTaken together, our results suggested the CYBA C242T polymorphism might be a risk-conferring factor on developing CAD and BMI and study design were probable sources of between-study heterogeneity.
Highlights
Coronary artery disease (CAD) and myocardial infarction (MI) are principal public health contributors to worldwide death and disability, and as such are primary causes of economic burden [1]
Oxidative stress is thought to play a pivotal role in the pathophysiology of atherosclerosis, which is manifested as increased availability of reactive oxygen species (ROS) and reactive nitrogen species because of an imbalanced redox state
The data from 26 studies depicting the association between the C242T polymorphism and coronary artery disease (CAD) risk were pooled into the provisional data set
Summary
Coronary artery disease (CAD) and myocardial infarction (MI) are principal public health contributors to worldwide death and disability, and as such are primary causes of economic burden [1]. The multiple potential pathologic pathways of CAD have been widely investigated, ranging from cholesterol accumulation to plaque rupture with thrombus formation [3]. Among these pathways, oxidative stress is thought to play a pivotal role in the pathophysiology of atherosclerosis, which is manifested as increased availability of reactive oxygen species (ROS) and reactive nitrogen species because of an imbalanced redox state. Observational and experimental studies have far been unable to resolve whether the CYBA C242T polymorphism is associated with coronary artery disease (CAD). We undertook a comprehensive meta-analysis to more precisely evaluate the influence of this polymorphism on CAD and potential biases
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