4.7 Article

Nonfasting cholesterol and triglycerides and association with risk of myocardial infarction and total mortality: the Copenhagen City Heart Study with 31 years of follow-up

Journal

JOURNAL OF INTERNAL MEDICINE
Volume 270, Issue 1, Pages 65-75

Publisher

WILEY
DOI: 10.1111/j.1365-2796.2010.02333.x

Keywords

absolute risk; arteriosclerosis; hypercholesterolaemia; lipids; risk prediction

Funding

  1. Danish Heart Foundation
  2. Danish Medical Research Council
  3. European Union [FP-2005-LIFESCIHEALTH-6, 037631]
  4. Herlev Hospital and Rigshospitalet, Copenhagen University Hospital
  5. AstraZeneca
  6. Abbott
  7. Merck
  8. Pfizer
  9. Sanofi Aventis
  10. Karo-Bio
  11. Boehringer Ingelheim

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Langsted A, Freiberg JJ, Tybjaerg-Hansen A, Schnohr P, Jensen GB, Nordestgaard BG (Herlev Hospital, Herlev; University of Copenhagen; Bispebjerg Hospital; and Rigshospitalet, Copenhagen O, Denmark). Nonfasting cholesterol and triglycerides and association with risk of myocardial infarction and total mortality: the Copenhagen City Heart Study with 31 years of follow-up. J Intern Med 2011; 270: 65-75. Objectives. We compared the ability of very high levels of nonfasting cholesterol and triglycerides to predict risk of myocardial infarction and total mortality. Design. Prospective study from 1976 to 1978 until 2007. Setting. Danish general population. Participants. Randomly selected population of 7581 women and 6391 men, of whom 768 and 1151 developed myocardial infarction and 4398 and 4416 died, respectively. Participation rate was 72%, and follow-up was 100% complete. Less than 2% of participants were taking lipid-lowering therapy. Results. Compared to women with cholesterol < 5 mmol L-1, multivariate-adjusted hazard ratios for myocardial infarction ranged from 1.3 [95% confidence interval (CI): 0.9-1.8] for a cholesterol level of 5.0-5.99 mmol L-1 to 2.5 (95% CI: 1.6-4.0) for cholesterol >= 9 mmol L-1 (trend: P < 0.0001). Compared with women with nonfasting triglycerides < 1 mmol L) 1, hazard ratios for myocardial infarction ranged from 1.5 (95% CI: 1.2-1.8) for triglycerides of 1.0-1.99 mmol L-1 to 4.2 (95% CI: 2.5-7.2) for triglycerides >= 5 mmol L-1 (p < 0.0001). In men, corresponding hazard ratios ranged from 1.2 (95% CI: 1.0-1.5) to 5.3 (95% CI: 3.6-8.0) for cholesterol (P < 0.0001) and from 1.3 (95% CI: 1.0-1.6) to 2.1 (95% CI: 1.5-2.8) for triglycerides (P < 0.0001). Increasing cholesterol levels were not consistently associated with total mortality in women (trend: P = 0.39) or men (P = 0.02). By contrast, compared with women with triglycerides < 1 mmol L-1, multivariate-adjusted hazard ratios for total mortality ranged from 1.1 (95% CI: 1.0-1.2) for triglycerides of 1.0-1.99 mmol L-1 to 2.0 (95% CI: 1.5-2.9) for triglycerides >= 5 mmol L-1 (trend: P < 0.0001); corresponding hazard ratios in men ranged from 1.1 (95% CI: 1.0-1.2) to 1.5 (95% CI: 1.2-1.7) (P < 0.0001). Conclusions. Stepwise increasing levels of nonfasting cholesterol and nonfasting triglycerides were similarly associated with stepwise increasing risk of myocardial infarction, with nonfasting triglycerides being the best predictor in women and nonfasting cholesterol the best predictor in men. Even more surprisingly, only increasing levels of nonfasting triglycerides were associated with total mortality, whereas increasing cholesterol levels were not.

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