Higher nonfasting triglycerides increase the risk of heart failure

Nonfasting Triglycerides, Low-Density Lipoprotein Cholesterol, and Heart Failure Risk: Two Cohort Studies of 113 554 Individuals

Literature - Varbo A and Nordestgaard BG. - ATVB 2018; published online ahead of print


There are strong associations between high concentrations of nonfasting TGs and risk of ischemic stroke, MI, ischemic heart disease (IHD), and all-cause mortality [1,2], as well as between TGs, diabetes and HF [3,4]. Hence, high concentrations of nonfasting TGs might also be associated with HF, although existing data have led to conflicting results [5-7].

In this study, it was evaluated whether high concentrations of nonfasting TGs and LDL-c are associated with a higher risk of HF in the general population. For this purpose 103 860 individuals with 2146 cases of HF from the Copenhagen General Population Study (2003–2014) were included, and the results were confirmed in the Copenhagen City Heart Study with 9694 individuals and 1447 cases of HF (1991–1994) and with minimal use of statins.

Individuals were divided into groups by their concentrations of nonfasting triglycerides and LDL-c, based on clinically meaningful cut points and without excluding extremely high concentrations, since they represent theoretically the highest risk of HF.

Main results

  • When compared with low nonfasting TGs (below 1 mmol/L or 88 mg/dL), stepwise higher nonfasting TGs were associated with a stepwise higher HF risk, with multivariable adjusted HRs ranging from 1.32 (95% CI: 1.06–1.65) for nonfasting TGs of 1-1.99 mmol/L (88-175 mg/dL) to 2.59 (95% CI: 1.48–4.54) for nonfasting TGs ≥5 mmol/L (440 mg/dL).
  • The HR for HF for a 1 mmol/L (88 mg/dL) higher concentration of nonfasting TGs was 1.19 (95% CI: 1.12–1.26), which was similar after stratification for conventional HF risk factors. There was no evidence for interactions between nonfasting TGs and HF risk factors.
  • The analysis of the Copenhagen City Heart Study confirmed the findings of the Copenhagen General Population Study: compared with low nonfasting TGs, multivariable adjusted HRs for nonfasting TGs of 1-1.99 mmol/L ranged from 1.28 (95% CI: 0.93–1.75) to 2.33 (95% CI: 1.22–4.45) for nonfasting TGs ≥5 mmol/L.
  • The cumulative incidence of HF was higher for stepwise higher nonfasting TGs: the subHRs ranged from 1.17 (95% CI: 1.04–1.32) for nonfasting TGs of 1-1.99 mmol/L to 1.95 (95% CI: 1.45–2.63) for nonfasting TGs ≥5 mmol/L, when compared with individuals with low nonfasting TGs.
  • The proportion of effect mediated through IHD was 34% (95% CI: 26%–49%), for MI 22% (95% CI: 16%–32%), and for IHD without MI 13% (95% CI: 9%–18%).
  • There was no association between stepwise higher LDL-c concentrations and HF risk. The HR for HF for a 1 mmol/L (38.6 mg/dL) higher LDL-c was 0.95 (95% CI; 0.88–1.04).


Stepwise higher concentrations of nonfasting TGs were associated with stepwise higher risk of HF, which was not the case for LDL-c. These findings support the need for further investigations examining whether TG and remnant cholesterol lowering in those with high concentrations would lower the HF risk.


1. Freiberg JJ, Tybjaerg-Hansen A, Jensen JS, et al. Nonfasting triglycerides and risk of ischemic stroke in the general population. JAMA.2008;300:2142–2152.

2. Di Angelantonio E, Sarwar N, Perry P, et al. Major lipids, apolipoproteins, and risk of vascular disease. JAMA 2009;302:1993–2000.

3. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62:e147–e239.

4. Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosisnand treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2016;18:891–975.

5. Ingelsson E, Arnlöv J, Sundström J, et al. Novel metabolic risk factors for heart failure. J Am Coll Cardiol. 2005;46:2054–2060.

6. Bahrami H, Bluemke DA, Kronmal R, et al. Novel metabolic risk factors for incident heart failure and their relationship with obesity: the MESA (Multi-Ethnic Study of Atherosclerosis) study. J Am Coll Cardiol. 2008;51:1775–1783.

7. Dhingra R, Sesso HD, Kenchaiah S, et al. Differential effects of lipids on the risk of heart failure and coronary heart disease: the Physicians’ Health Study. Am Heart J. 2008;155:869–875.

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