As far as our knowledge, this was the first study among Chinese type 2 diabetes with stable CAD to demonstrate that fasting TG on admission was an useful predictor for adverse outcomes independent of other traditional prognostic variables in the era of revascularization and statin therapy. The main findings of the present study are threefold. First, according to baseline characteristics of the current study, patients with higher fasting TG levels (≥1.2 mmol/L) were more prominent at groups of middle aged and higher BMI. Moreover, patients at high TG groups prone to be accompanied with other various dyslipidemia, impaired fasting glucose, high levels of inflammatory and oxidative response biomarkers such as leucocyte count, neutrophil count and uric acid. Second, in agreement with previous studies, as showed in ROC curves and bar graphs, our data further demonstrated that elevated fasting TG levels might be conferred to a useful discriminator for the presence of adverse events in diabetic patients with SAP. Third, both chi-squared for trend and multivariate Cox proportional regression analysis after adjusted major potential confounders were consistently indicated that fasting TG could provide with prognostic information in diabetic population with stable CAD and remained as an independent predictor for early outcome. Kaplan-Meier curve for cumulative event-free survival indicated that the high levels of TG were associated with increased adverse prognosis although the rate of statin administration and stent implantation were not different between the groups. Apparently, the present study not only confirmed the previous studies but also provided the novel information concerning the role of TG in predicting early outcomes in diabetic patients with stable CAD, especially in the era of revascularization and statin therapy.
Several lines of evidence have revealed a positive relation between TG and CAD and clinical outcomes in patients with or without diabetes owing to the role of TG-rich lipoproteins in atherothrombosis. The Copenhagen Male Study, which followed 2,906 white men over 8 years, demonstrated that fasting TG was independently associated with the incidence of CAD . Data from Multiple Risk Factor Intervention Trial confirmed that either non-fasting or fasting TG is an independent risk factor for CAD . Several mata-analyses showed that high concentration of TG was an independent risk factor for the morbidity and mortality rates of CAD in primary prevention [8–10]. Moreover, the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study detected that combination therapy using lipid-lowering drugs for regulating both LDL-C and TG could lead to a significant benefit in patients with metabolic syndrome but not to those without . Recently, Kasai et al. observed 1836 patients who underwent complete revascularization between 1984 and 1992, and evaluated the association between fasting TG level and all-cause and cardiac mortality for a median follow-up of 10.5-year period . They found that elevated fasting TG levels were associated with increased risk of cardiac death after complete coronary revascularization. However, they did not demonstrated that there were significant associations of age, gender, presence of diabetes, levels of TC and HDL-C, the use of statins with all-cause and cardiac death in their subgroup analysis.
The disparities of our data from their study were summarized as followings: firstly, their patients were enrolled between 1984 and 1992 duration in which optimal pharmacological therapy for CAD was not widely performed clinically. Besides, prior cases were subjected to percutaneous coronary intervention (PCI) with simple balloon angioplasty, and no patients received stent implantation; Finally, the population received coronary artery bypass grafting (CABG) in previous studies were as higher as 32%. In current study, including subjects were confined at diabetic patients with an relatively short-term duration (from June 2011 through March 2012). Among studied population, majority of patients were received statin therapeutics, and their profiles of major lipid disorders were significantly improved such as perfect of targeted LDL-C. We affirmed that baseline fasting TG was a powerful predictor for early outcome in diabetic patients with stable CAD, similar to the evidence from American Heart Association which has recently suggested that the independent predictive values of TG levels as a causal factor in development of CAD remains as debatable . Obviously, our study extended previous studies in that data provided the vital prognostic information regarding the role of fasting TG in diabetic subjects with stable CAD.
At the same time, our data suggested that patients with higher levels of admission fasting TG were more prone to receive revascularizations. The underlying hypothesis of current results might be consisted in three aspects. To begin with, high levels of fasting TG were not only implied with the severe disorder of glycolipid metabolism, but also low-grade of systematic inflammatory response, vascular dysfunction and potentially atherosclerotic progress in these settings [2, 28–31]. Secondly, with the advent of statin therapeutic era, the directly pivotal role of LDL-C on the atherogenesis has been favorably controlled (an average of LDL-C = 2.4 ± 0.9 mmol/L in the studied population). Nonetheless, It has been reported that the residual risks of atherogenic dyslipidemia have been increasingly prominent and gradually emerged as a leading impeller of cardiovascular disease and its future event [32, 33]. Therefore, the badly impacts of TG were not adjusted by multivariable analysis especially in the patients received of successfully complete revascularization and ideal glycemic control. Regarding to the current study population, all patients who had indications of revascularization were received complete intervention. Thirdly, several prior studies about secondary prevention of fasting TG had led to very similar results about the HR values (approximate to 1.5) [16, 34]. Although those study population had different background of demographics and comorbidities, the reproducible of above result strikingly supported the consistent hypothesis that TG was an independent predictor of adverse outcome. Fourthly, epidemical cohorts about primary prevention also suggested a direct association between relatively high levels of TG and incidence of CAD and mortality [8–10]. Finally, our findings also supported the viewpoint that high levels of TG might be very probably to have potential impacts on the vasculature before the establishments of formal diagnosis for hypertriglyceridemia and led to fasting glucose impaired and/or overt atherosclerosis disease alone or coupled with other risk biomarkers [30, 32, 35].
Nonetheless, the limitations of our study are obvious. First of all, the sample scale of the current study was relatively small and enrolled patients were entirely Chinese Han population. Besides, the duration of follow-up period was comparably in short term and unavoidably led to the bias for totally observing the outcome. Furthermore, the main method of revascularization of present investigation was confined to drug eluting stent implantation and although it might be mostly analogous to the real world of China, it inevitably implied with high incidence of target vascular revascularization. Besides, as the universal utilization of statin therapeutics, it will be difficult to deploy a subset analysis on the effect of statin therapy. Finally, our investigation failed to compare the predictive values of fasting and non-fasting TG at these settings.
Taken together, although TG was a paradox marker all along, the results of our study clearly suggested that high level of fasting TG (≥1.2 mmol/L) was an independent indicator of early outcome for diabetic patients with SAP as like as HBA1c and number of affected coronary arteries. Whether should be set a strict target value of fasting TG specifically for diabetic population with stable CAD aimed to reverse the “atypical atherogenic dyslipidemia” need to be seriously considered.