The main findings of this study are as follows: firstly, High LMR and APTT are independent predictors of incomplete occlusion of infarct-related vessels in NSTEMI patients; secondly, When the LMR is greater than 4.77, 79.3% of the infarct-related vessels in NSTEMI patients are incomplete occlusion. When the LMR is less than 4.77, 66.2% of the infarct-related vessels in NSTEMI patients are complete occlusion, and the prediction accuracy is 70.0%.
NSTEMI is dangerous and has a high mortality and disability rate. Early and non-invasive evaluation of the severity of coronary artery disease in NSTEMI patients is helpful to carry out risk stratification management, reduce the incidence of complications and improve the prognosis. Especially for NSTEMI patients with complete vascular occlusion, early intervention has better clinical and angiographic results than conservative treatment or delayed PCI(9). This may be because complete vascular occlusion tends to have larger infarct area and worse clinical prognosis(10). Coronary atherosclerotic plaque rupture and acute thrombosis are the main pathological basis of NSTEMI. The activation of inflammatory cells and enhanced inflammatory response can lead to plaque instability, accelerate plaque rupture and promote thrombosis(11). Lymphocytes and monocytes are important inflammatory cells in the body. They both play an important role in the occurrence, development and rupture of coronary atherosclerotic plaque. Studies have shown that the decrease of lymphocytes can aggravate the load of coronary atherosclerotic plaques, accelerate the formation of plaque lipid necrotic cores, and weaken the fibrous caps of plaques. It is an important reason for the rupture of coronary atherosclerotic plaques(4, 12). Studies have shown that monocytes can adhere to the intima of the arteries and directly damage the vascular endothelium, and then enter the subintimal space of the artery wall and differentiate into macrophages. Through their own scavenger receptors, they can take up a large amount of oxidized-LDL to generate foam cells. This results in the decrease of plaque stability. In addition, monocyte-macrophages can also increase the risk of plaque rupture by secreting a variety of inflammatory factors, promoting the production of matrix metalloproteinases and inducing apoptosis of smooth muscle cells(3). The results of this study showed that the average lymphocyte count of the incomplete occlusion group tended to be higher than that of the complete occlusion group, and the average monocyte count tended to be lower than that of the complete occlusion group. The average LMR in incomplete occlusion group was significantly higher than that of the occlusion group, which is consistent with the previous research conclusions(13).
When myocardial infarction occurs, the patient's sympathetic nerve excites and releases a large amount of catecholamines, which may interact with α2-adrenergic receptors on platelets to convert factor XII into XIIa, or activate factor XII through the kininase system. The activation of factor XII initiates the endogenous coagulation pathway, which is monitored by APTT and is characterized by the shortening of APTT(14). Acute myocardial infarction is related to enhanced blood coagulation. In the case of unstable angina pectoris or endothelial injury, the body's hypercoagulable state can lead to complete occlusion of the coronary arteries. In this study, the APTT of the complete occlusion group was significantly shorter than that of the incomplete occlusion group, and the results were consistent with previous studies.
Shock index can reflect the perfusion status of tissue and coronary artery. It increases when acute blood volume decreases and left ventricular function is impaired. It is negatively correlated with cardiac output index, left ventricular stroke volume and mean arterial pressure. It is reported that STEMI patients with elevated shock index on admission have more obvious myocardial and microvascular injury(15). This study found that the admission shock index of the complete vascular occlusion group was significantly higher than that of the incomplete occlusion group, which is consistent with the results of previous studies.
Wang's research results showed that 27% of NSTEMI patients had complete occlusion of criminal vessels. This part of the patients had a larger infarct size and a higher 6-month mortality rate(2). The incidence of complete vascular occlusion in NSTEMI patients in our study is inconsistent with the results of Wang et al. This may be because our study is a single-center retrospective study and there is a certain selection bias. In addition, the sample size included in our study is small, and there is a certain sampling error.
Diabetes, hypertension, smoking, etc. are related to higher incidence of cardiovascular disease, more severe vascular diseases and worse clinical outcomes(16). Our study also shows a trend that the incidence of diabetes, hypertension, and smoking in the complete occlusion group is higher than that in the incomplete occlusion group. If the sample size is enlarged, this trend may show statistical significance.
Limitations
Limitations of this study include that this is a single-center retrospective study, most of the patients are male, the sample size is small, and the distribution of infarct-related blood vessels is not recorded. In addition, some NSTEMI patients may have recanalization after complete vascular infarction. When TIMI blood flow is greater than grade 0 during coronary angiography, these patients will be divided into incomplete occlusion group. Therefore, the conclusions of this study still need to be further confirmed by prospective, multi-center and large sample studies.