When the anterior coronary arterioles and arterioles have structural abnormalities and or dysfunction under the action of various risk factors, resulting in exertional angina pectoris or there is objective evidence of myocardial ischemia, we call it coronary microvascular disease(CMVD)[12].The abnormal structure and dysfunction of coronary microcirculation can affect the metabolic process of the cardiovascular, which have a great impact on the occurrence, development, evolution and prognosis of cardiovascular diseases. It has also been reported that cardiovascular disease can also induce and aggravate the structural abnormalities and dysfunction of coronary microcirculation[13]. At present, coronary intervention and coronary artery bypass grafting are commonly used in clinical myocardial reperfusion treatment, which can open the narrow epicardial coronary artery in time, but can not solve the problem of abnormal myocardial blood perfusion caused by coronary microcirculation. Therefore, if we can find a simple index to identify coronary microcirculation disease, it has important clinical significance to improve the prognosis of patients with coronary microvascular disease.
Clinical studies on risk factors related to coronary microvascular disease are still few. The research team of Li et al.[14] found that C-reactive protein in the coronary microvascular disease group was significantly higher than that in the non coronary microvascular disease group, suggesting that inflammatory response may be involved in the pathogenesis of coronary microvascular disease; Gokce et al.[15] found that the platelet aggregation rate in the coronary microvascular disease group was significantly higher than that in the non coronary microvascular disease group, suggesting that the dysfunction of platelets may play a role in the process of coronary microvascular disease; The research report of Yildiz et al.[16] suggested that the increase of blood uric acid in patients with coronary microvascular diseas as one of the risk factors of cardiovascular disease. Some researches suggested that coronary microvascular disease may be related to obesity[17], smoking[18], hyperlipidemia, hypoalbuminemia, insulin resistance[19]. However, there is no final conclusion about the indicators for identifying coronary microvascular disease.
In our study, we found that compared with Non-CMVD group, patients in CMVD group had a higher proportion of female, high blood pressure and type 2 diabetes, it is consistent with the previous research results of Bairey[20]et al. In the comparison of the two groups of laboratory indicators, we found that platelet count, C-reactive protein, TG concentration were increased in patients of CMVD group, accompanied by decreased albumin levels and high-density lipoprotein cholesterol. Previous studies by Goel PK[21] have shown that the increase of platelet aggregation rate will lead to high shear stress and slow blood flow, accelerate endothelial cell damage, and easily lead to microvascular dysfunction.
The increased expression of inflammatory factors such as C-reactive protein will lead to the aggravation of vascular endothelial oxidative stress, the decline of endothelial mediated vascular motor function, and the decline of the fibrinolytic capacity of the body. These factors are important pathophysiological mechanisms of coronary microvascular lesions[22].
High triglyceride and low high density lipoprotein will accelerate the speed of lipid peroxidation and the degree of endothelial cell damage, resulting in microcirculation disturbance[23].Previous studies have shown that low albumin levels can lead to systemic inflammatory response and excessive oxidative stress, easy to lead to microvascular diseases[24].
Studies have confirmed that TG and HDL-C are the main index reflecting the body's blood lipid, which are related to the occurrence of atherosclerosis[25]. TG/HDL-C is a new composite index, it is not only can reflect the disorder of blood lipid metabolism, but also is related to insulin resistance[26]. Previous studies on lipid parameters and coronary flow reserve fraction in patients with inflammatory bowel disease found that compared with the healthy control group with CFR ≥ 2, the patients with CFR < 2 had higher TG concentration and lower HDL-C concentration. It suggests that TG and HDL-C may be related to coronary microvascular disease[27].
In our study, we found that TG/HDL-C in CMVD group was higher than that in Non-CMVD group, multivariate logistic regression analysis indicated that Crp, female, albumin and TG/HDL-C were independent risk factors for CMVD. Compared with Crp, female and albumin, the area under TG/HDL-C curve was the largest, indicating that TG/HDL-C is more efficient in identifying coronary microvascular diseases.
The mechanism by TG/HDL-C is associated with coronary microvascular disease is unclear and it may be related to insulin resistance. Insulin resistance can directly exacerbate vascular endothelial cell injury, activate the damage repair mechanism of the body, and accelerate the aggregation of platelets, white blood cells, and other inflammatory factors[28]. Meanwhile, when insulin resistance, the compensatory increase in the number of vascular smooth muscle cells and the decrease in the content of the body's own vasodilator factors lead to the imbalance of vascular contraction and expansion, vascular endothelial damage and cause microvascular endothelial dysfunction[29]. In addition, when insulin resistance occurs, the expression of serum adiponectin and adhesion molecules in vivo also increases, which in turn affects the body's own vascular regulation and accelerates vascular endothelial injury and myocardial ischemia[30].
Limitations
There are still some limitations in this study. Firstly, our research is a single-center study with small sample size, so selection bias cannot be ruled out. Secondly, the specific mechanism of TG/HDL-C on coronary microcirculation disease is still unknown. Further experimental verification is needed to obtain more supporting evidence and clarify the mechanism. Thirdly, the follow-up of the study case is still in progress, so there is no further analysis on the prognosis. In the future, more samples are needed to conduct a prospective multi-center study to further validate our conclusions.