This study verified the different characteristics between AMI and non-AMI patients among with typical clinical manifestations. Patients with higher APoB/APoA1 ratio and non-HDL/HDL ratio, especially the former, had higher risk of AMI. They both had significantly positive associations with Gensini score, which indicated the severity of the coronary stenosis. When combining these two parameters, it did not show much greater impact when revealing cardiovascular risks on AMI than that expected from the individual contribution.
In the present study, the traditional risk factors such as male, smoking and drinking history were different between AMI and non-AMI group, which was verified by other studies [8]. CHD refers to the hardening, narrowing and rupture of coronary arteries caused by excessive accumulation of cholesterol substances in the artery walls. Its root reason is known as atherosclerosis, while atherogenic dyslipidemia plays a key role in this process. Atherogenic dyslipidemia consisted of abnormal aggregation of lipoproteins, including elevated levels of TC, ApoB and LDL particles, and decreased levels of HDL particles and ApoA1 [17, 18], which were founded in our study as well.
Interestingly, we found that oxygen saturation in AMI group was lower than non-AMI group (97.7 ± 1.40 VS 98.7 ± 1.41, P < 0.001) which may indicate the utility of oxygen therapy. However, it is controversial in previous studies and calls for further investigations [19, 20]. Lipids profile including APoB/APoA1 ratio and non-HDL/HDL ratio were significantly and independently associated with an increasing risk of AMI and APoB/ APoA1 ratio was the most obvious related factors, which was in accordance with previous studies [21, 22].
We also found that the relative risk of AMI in top quartile subgroup compared with bottom subgroup was 8.929 for APoB/ APoA1 ratio and 1.346 for non-HDL/HDL ratio, which indicated that the higher values of these two ratios were better predictors of AMI, the results were similar to the UKPDS [23]. Furthermore, our study found that APoB/APoA1 ratio and non-HDL/HDL ratio had the first and second strongest associations with Gensini score, respectively, which indicated the severity of the coronary stenosis.
Our analysis also discovered high APoB/APoA1 ratio and high non-HDL/HDL ratio combination might enhance their ability to predict the incidence of AMI (n = 75, 79.79%). APoB/APoA1 ratio (AUC = 0.833) was more useful in predicting a greater risk of AMI than non-HDL/HDL ratio (AUC = 0.728), ApoB (AUC = 0.551) and other lipids profile. The differences between APoB, APoB/APoA1 ratio and non-HDL/HDL ratio in predicting the risk of AMI were probably associated with the essences of these lipids profile. ApoB was present in atherogenic lipoproteins including LDL, intermediate-density lipoprotein and very-low-density lipoprotein, its level indicated the number of atherogenic lipoprotein particles. ApoA1 was a major constituent of HDL, an anti-atherogenic apolipoprotein appeared to reverse the cholesterol transport [24, 25]. The ratio of APoB/APoA1 could represent the balance between the atherogenic and anti-atherogenic lipoproteins, and maybe a good predictor of AMI [7]. Non-HDL could be calculated by simply subtracting HDL from TC, which comprised all the cholesterol contained in LDL, VLDL and IDL. Thus, it was the cholesterol in the atherogenic particles and has been recommended as a target, especially in patients with high non-fasting TG levels by the National Cholesterol Education Program guidelines (NCEP ATP III 2002) [26]. It has often been used as a surrogate measure of circulating atherogenic lipoproteins, the increases in the non-HDL/HDL ratio was as strongly associated with the risk of AMI, which was shown in previous studies [27, 28]. In a study among obese Indian men, ApoB/ApoA1 ratio and non-HDL/HDL ratio were elevated significantly and were more prone to develop cardiovascular diseases [29].
It has been reported that the severity of coronary stenosis was a valuable predictor for future cardiovascular events. But the relationship between APoB/APoA1 ratio, non-HDL/HDL ratio with Gensini score were less investigated. It is reported that APoB/APoA1 ratio was significantly associated with the multi-branches and Gensini score in the CHD patients [30]. Similarly, high atherogenic lipid levels also enhanced the risk the fibrinogen induced coronary atherosclerosis [31]. In our study, the correlation between APoB, LDL, APoB/APoA1 ratio, non-HDL /HDL ratio and Gensini score was significantly obvious.
Studies have investigated the joint effects of different lipids, and the results vary [13, 32]. A ten-year follow-up showed no greater impact on CHD than their individual contributions when combing triglycerides (TGs), total cholesterol (TC) and high density lipoprotein cholesterol (HDLC) [14]. To our knowledge, no previous studies have explored the value of combination of ApoB/ApoA1 ratio and non-HDL/HDL ratio in predicting the risk of AMI. When combining the APoB/APoA1 ratio and non-HDL/HDL ratio, the predictive value (AUC = 0.838) was higher than any individual parameters but no much greater than APoB/APoA1 ratio alone (AUC = 0.833). Furthermore, its sensitivity (71.2%) and specificity (85.7%) increased, but only a limited improvement relative to APoB/APoA1 ratio. The notion that the combination confers unexpected levels of risk is unsubstantiated by our data.