In the present study, we found the prognostic value of MAR in patients who underwent PCI and demonstrated higher MAR value was independently associated with adverse outcomes of patients who underwent PCI.
Considering the high prevalence and poor prognosis of CHD, the early diagnostic biomarkers for patients with CHD are in need. Vascular inflammation plays a crucial role in the progression of CHD, and inflammation-based biomarkers have been shown previously [15–17], such as monocyte [18], high-sensitivity C-reactive protein and serum albumin [19]. However, it is still elusive which cell plays a role in initiation of the cascade processes.
Atherosclerosis has long been associated with chronic inflammation, and monocytes and monocyte-derived macrophages account for the coronary plaque progression [20]. Circulating monocytes populate plaques and adhere to the dysfunctional endothelial surface via binding to leukocyte adhesion molecules only expressed by abnormal endothelial cells [21, 22]. Cao et al have reported that all stages of atherogenesis, from the earliest lesions (fatty strips) to the formation of complex plaque, are associated with macrophages which are considered as a driving force [23]. In another recent study, efficient degradation of CCR2 mRNA in monocytes attenuated the number of monocytes in atherosclerotic plaques, reduced the infarct size following coronary artery occlusion [24], which may be a novel therapeutic strategy for CHD patients undergoing PCI. Serum albumin is considered as a negative acute-phase protein in the progression of inflammation [25]. As previous studies demonstrated, low serum albumin concentration can predict the clinical outcome of acute myocardial infarction [12]. As shown in Table 1, age, gender, smoking, Cr and UA have significant differences between the 2 groups. Aging, gender and smoking are often characterized by a number of dysfunctional conditions including: myocardial sarcopenia, hypertrophy, vascular hyperpermeability, hypertension, inflammation, and functional impairment [26–30]. Increasing evidence demonstrates that age is a major risk factor in cardiac-related morbidity and mortality resulting from the decrease of the self-renewal of yolk sac-derived resident macrophages that play a key role in the post-MI repair and maintaining the cardiac homeostasis with age [31]. Ovaries removed or natural menopausal women exhibit systematic inflammation [32]. CHD has been considered to be male disease [28] because men are at a greater risk of CVD than women [29], who may decrease significantly the secretion of pro-inflammatory markers interleukin-6 (IL-6), IL-1, TNF-α via the estrogen [33]. Smoking has been known as an independent risk factor of atherosclerosis via promoting inflammation, thrombosis, and oxidative stress [30]. There are no doubts that age, gender, smoking, etc are confounding factors in our study, while after including these confounding factors in the multivariate Cox regression analysis, we still obtained positive results which demonstrated that the high MAR is an independent risk factor for ACM and CM in patients who underwent PCI.
To the best of our knowledge, it is the first time to demonstrate the MAR, which is a novel, powerful, inexpensive and effective predictor for outcomes of CHD after PCI. There are some limitations in our study. Firstly, we did not monitor the dynamic change of their variables. Secondly, our study is a single retrospective cohort design. Thirdly, we failed to collect inflammatory markers such as high sensitive C reaction protein (hsCRP) and erythrocyte sedimentation rate (ESR). Besides, to demonstrate the association between MAR and the outcomes of CHD after PCI, our study needs to be further verified by a multi-center, prospective study. And we expect more researches about the mechanism of MAR will be explored.