No abstract

Aims We investigated the association of fasting triglycerides with cardiovascular disease (CVD) mortality. Methods and results This cohort study included US adults from the National Health and Nutrition Examination Surveys from 1988 to 2014. CVD mortality outcomes were ascertained by linkage to the National Death Index records. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of triglycerides for CVD mortality. The cohort included 26,570 adult participants, among which 3,978 had diabetes. People with higher triglycerides had a higher prevalence of diabetes at baseline. The cohort was followed up for a mean of 12.0 years with 1,492 CVD deaths recorded. A 1-natural-log-unit higher triglyceride was associated with a 30% higher multivariate-adjusted risk of CVD mortality in participants with diabetes (HR, 1.30; 95% CI, 1.08-1.56) but not in those without diabetes (HR, 0.95; 95% CI, 0.83-1.07). In participants with diabetes, people with high triglycerides (200-499 mg/dL) had a 44% (HR, 1.44; 95% CI, 1.12-1.85) higher multivariate-adjusted risk of CVD mortality compared with those with normal triglycerides (<150 mg/dL). The findings remained significant when diabetes was defined by fasting glucose levels alone, or after further adjustment for the use of lipid-lowering medications, or after the exclusion of those who took lipid-lowering medications. Conclusions This study demonstrates that fasting triglycerides of ≥200 mg/dl are associated with an increased risk of CVD mortality in patients with diabetes but not in those without diabetes. Future clinical trials of new treatments to lower triglycerides should focus on patients with diabetes.

Background and Aims: Both fasting and non-fasting levels of triglyceride have been shown positively associated with all-cause mortality. It is unknown whether fasting status modifies this association. This study aimed to address this question.Methods: This study included 34,512 US adults (27,036 fasting and 7476 nonfasting participants). All-cause mortality was ascertained by linkage to the National Death Index records. Cox proportional hazards models were used to estimate hazard ratios of triglyceride for mortality.Results: This cohort was followed up for a mean of 13.0 years. During the follow-up, 8491 all-cause deaths were recorded. A 1-natural-log-unit increase in triglyceride was associated with an 8% higher multivariate-adjusted risk of all-cause mortality.Interaction analyses showed that fasting status interacted with triglyceride in predicting all-cause mortality. Sub-analyses showed that a 1-natural-log-unit increase in triglyceride was associated with a 17% higher multivariate-adjusted risk of all-cause mortality in the nonfasting subcohort; however, there lacked such an association in the fasting sub-cohort. Similarly, high (200-499 mg/dL) and very high levels of triglyceride (≥500 mg/dL) were associated with higher all-cause mortality risks compared with low normal triglyceride (<100 mg/dL) only in the nonfasting subcohort. Conclusion:This study found that, compared to fasting triglyceride, nonfasting triglyceride was more sensitive in predicting all-cause mortality. This study supports the initiatives by some guidelines to recommend the use of nonfasting triglycerides for risk assessment.

We investigated the association of dietary intake of major types of fatty acids with heart disease mortality in a general adult cohort with or without a prior diagnosis of myocardial infarction (MI). This cohort study included US adults who attended the National Health and Nutrition Examination Surveys from 1988 to 2014. Heart disease mortality was ascertained by linkage to the National Death Index records through 31 December 2015. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of fatty acid intake for heart disease mortality. This cohort included 45,820 adults among which 1,541 had a prior diagnosis of MI. Participants were followed up for 532,722 person-years (mean follow-up, 11.6 years), with 2,313 deaths recorded from heart disease being recorded. Intake of saturated (SFAs) and monounsaturated fatty acids (MUFAs) was associated with heart disease mortality after adjustment for all the tested confounders. In contrast, a 5% higher calorie intake from polyunsaturated fatty acids (PUFAs) was associated with a 9% (HR, 0.91; 95% CI 0.83–1.00; P = 0.048) lower multivariate-adjusted risk of heart disease mortality. Sub-analyses showed that this inverse association was present in those without a prior diagnosis of MI (HR,0.89; 95% CI 0.80–0.99) but not in those with the condition (HR, 0.94; 95% CI 0.75–1.16). The lack of association in the MI group could be due to a small sample size or severity and procedural complications (e.g., stenting and medication adherence) of the disease. Higher PUFA intake was associated with a favourable lipid profile. However, further adjustment for plasma lipids did not materially change the inverse association between PUFAs and heart disease mortality. Higher intake of PUFAs, but not SFAs and MUFAs, was associated with a lower adjusted risk of heart disease mortality in a large population of US adults supporting the need to increase dietary PUFA intake in the general public.

It is unknown whether non-fasting plasma glucose (PG) is associated with cardiovascular disease (CVD) mortality. This study aimed to investigate this association in US adults. This study included adults from the National Health and Nutrition Examination Surveys from 1988 to 2014. Mortality outcomes were ascertained by linkage to the National Death Index records. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of PG for CVD mortality. Among 34,907 participants, 1956, 5564, and 27,387 had PG from participants in early non-fasting, late non-fasting, and fasting states, respectively (defined as a period since last calorie intake of 0–2.9, 3.0–7.9, or ≥ 8.0 h, respectively). This cohort was followed up for 455,177 person-years (mean follow-up, 13.0 years), with 2,387 CVD deaths being recorded. After adjustment for all confounders including hemoglobin A1c (HbA1c), only late non-fasting PG (continuous, natural log-transformed) was positively associated with CVD mortality risks (hazard ratio, 1.73; 95% confidence interval 1.12–2.67). Higher late non-fasting PG (dichotomous, at a cut-off of 105, 110, or 115 mg/dL) was associated with higher CVD mortality risks. In addition, at the cut-off of 115 mg/dL, higher late non-fasting PG was associated with higher CVD mortality risks in those with either a normal (< 5.7%) or prediabetic HbA1c level (from 5.7 to 6.4%). In conclusion, late non-fasting PG predicts CVD mortality independent of HbA1c. Late non-fasting PG with a cut-off of 115 mg/dL may be used to identify those at high CVD risk.