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Epidemiological evidence
In the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22 (PROVE IT-TIMI 22) trial, it was demonstrated that, among patients receiving statin therapy following acute coronary syndrome, an on-treatment fasting TG level <150 mg/dL (<1.7 mmol/L) was associated with a reduction in recurrent coronary heart disease risk versus higher TG levels (Table 1), even after adjustment for HDL-C and LDL-C levels (hazard ratio 0.8; P=0.025).10 A wealth of epidemiological evidence exists, demonstrating that both fasting and nonfasting TG levels are significant predictors of cardiovascular events, even in individuals who have already achieved guideline-recommended LDL-C levels with lipid-lowering therapy.64–68
Table 1
Table 1
Key studies investigating the association between triglycerides and cardiovascular disease
However, nonfasting TG levels are thought to be a much stronger predictor of cardiovascular events than fasting TG levels. The Women’s Health Study (n=26,509) showed that both fasting and nonfasting TG levels were strongly associated with an increased risk of cardiovascular events, independent of baseline cardiovascular risk factors (age, blood pressure, smoking, and use of hormone therapy). However, after adjustment for TC and HDL-C levels and indicators of insulin resistance, the association between fasting TG levels and the risk of cardiovascular events was no longer significant (P=0.90). In contrast, the association between nonfasting TG levels and cardiovascular risk remained strong even after adjustment for other lipid levels and markers of insulin resistance (P=0.006).67 Likewise, two prospective cohort studies using data from the Copenhagen City Heart Study found that the cumulative incidence of cardiovascular events (ischemic stroke, MI, ischemic heart disease) and all-cause mortality were strongly associated with increasing nonfasting TG levels (all P<0.001) (Table 1). That being said, these associations were not adjusted for other lipid parameters.66,68
A number of studies have found that the association between plasma TG levels (both fasting and nonfasting) and cardiovascular risk is often attenuated once adjusted for other lipid parameters, including HDL-C and non-HDL-C. An analysis conducted by the Emerging Risk Factors Collaboration, which included data from 302,430 individuals from 68 long-term prospective studies, demonstrated that there was a significant and stepwise association between fasting and nonfasting TG levels and CVD risk. However, this association was no longer significant after adjustment for HDL-C and non-HDL-C (Table 1).64 Likewise, in a combined analysis of the Incremental Decrease in End Points through Aggressive Lipid Lowering (IDEAL) and Treating to New Targets (TNT) trials in patients achieving low LDL-C (<70 mg/dL [1.8 mmol/L]), CVD risk increased incrementally with increasing on-treatment fasting TG level, with patients in the highest quintile experiencing a 63% higher rate of cardiovascular events than those in the lowest quintile (P<0.001). However, this association was also attenuated (P=0.044) after adjustment for HDL-C and apoB/apoA1 (Table 1).65 Elevated TG levels are closely associated with higher levels of non-HDL-C and apoB and low levels of HDL-C,2 and this may explain why this association is weakened after adjustment for these parameters.
Elevated remnant cholesterol levels, which directly correlate with elevated levels of TRLs, have also been shown to be associated with CVD. Using data from 73,513 subjects, Varbo et al30 found that every 88.6 mg/dL (1 mmol/L) increase in remnant cholesterol was associated with a 2.8-fold increase in CVD risk, independent of low HDL-C.
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