Our study was the first time to demonstrate the relationship between the Apo A1 / Apo B ratio and ACS in CAPD patients. The association remained significant even after adjustment for traditional CVD risk factors such as age, prior CVD history, smoking, triglycerides, total cholesterol, HDL-C, LDL-C, hemoglobin, and Apo B. Moreover, Apo A1 / Apo B may be used as a predictor of the occurrence of future ACS.
Hyperlipidemia is a known risk factor for CVD in CKD patients. CKD appears to weaken the classical relationship between the lipid and CVD. Elevated very-low-density lipoprotein and low HDL-C have been shown to increase coronary heart disease risk in CKD patients [12, 13]. However, no significant association was found between LDL-C and cardiovascular outcomes. Moreover,some earlier studies[14–16] have failed to confirm an association between HDL-C, LDL-C, or triglyceride levels and CVD mortality. Similarly, our study indicated that total cholesterol and LDL-C were significantly higher in the ACS group than in the non-ACS group, but these two lipid parameters were not correlated with ACS. The study by Chang et al even came to the opposite conclusion that an increased triglyceride / HDL-C ratio was associated with reduced CVD mortality in hemodialysis patients. Therefore, the association between dyslipidemia and CVD in the CKD population is very complicated.
Apo A1 is the main component of HDL and is closely related to CVD. A study of 299 patients with ST-segment elevation myocardial infarction (STEMI) found that high baseline apoA1 levels were associated with reduced risk of STEMI. Apo B is present on the surface of LDL, and cellular recognition and uptake of LDL are mainly achieved by recognition of Apo B. Higher level of Apo B can increase the incidence of coronary heart disease, even if LDL levels are normal. Moreover, Apo B was significantly associated with CVD-related mortality. Our study suggested that Apo A1 levels were higher in the non-ACS group than in the ACS group, while Apo B showed the opposite. Unfortunately, we did not conclude that Apo A1 or Apo B was associated with ACS.
The Apo A1 / Apo B ratio provides a better summary of the burden of dyslipidemia than conventional lipids and lipoproteins. Some studies have confirmed that the Apo B / Apo A1 ratio was superior to LDL and HDL cholesterol in predicting cardiovascular events. Bodde MC et al found that elevated Apo B / Apo A1 ratio was associated with an increased risk of STEMI, but not LDL-C, after adjustment for age, sex, and statin therapy. In maintenance hemodialysis patients, each SD increase in the Apo B / Apo A1 ratio increased all-cause mortality or CVD-related mortality by 16%. In our study, similar results were found, adjusted for traditional CVD influencing factors, Apo A1 / Apo B and ACS were independently associated. Furthermore, the area under the ROC curve for Apo A1 / Apo B was 0.79 (95% CI: 0.69–0.88, p < 0.01). This suggests that Apo A1 / Apo B may be well used as a predictor for the future occurrence of ACS in CAPD patients.
Inflammation may affect Apo A1 metabolism to some extent in patients with renal failure, and CRP was also found to be significantly higher in the CVD group than in the non-CVD group. However, no correlation was found between CRP and Apo A1, Apo B, and Apo A1 / Apo B in the binary correlation analysis. Therefore, apolipoproteins do not simply mediate the occurrence of ACS through an inflammatory state, and the specific mechanism requires further investigation.
Our study has some limitations. This study was a retrospective small sample study, and the conclusion needs to be confirmed by prospective large sample studies in the future. Secondly, due to the voluntary principle, the enrolled patients pay more attention to their physical health than the non-enrolled patients, so the research population may have a certain degree of selection bias, which cannot well represent the general CAPD patients. Finally, it was unclear how dyslipidemia affected the development of ACS.