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13
| 3 | 2009
Klinisk Biokemi i Norden
prevention do not recognize elevated triglycerides as
a risk factor for stroke (3,27).
By using a prospective study with 31 years follow-up
of 13,000 individuals from the Danish general popula-
tion, the Copenhagen City Heart Study, and by using
nonfasting rather than the fasting triglycerides used
in several former studies (27,30,32-33), and by having
more statistical power than any former study (27-34),
a previously unnoticed association between stepwise
increases in levels of nonfasting triglycerides and step-
wise increases in risk of ischemic stroke with no thres-
hold effect was recently reported (Figure 4)(11). The
highest levels of nonfasting triglycerides ≥5 mmol/L
predicted a 5 and 3 fold increased risk of ischemic
stroke in women and men in the general population.
In support of these findings, the Women’s Health
Study showed that upper versus lower tertiles of
nonfasting triglycerides, but not fasting triglycerides,
associated with increased risk of ischemic stroke (10).
This and other former studies on fasting as well as on
nonfasting triglycerides did not attempt to associate
very high levels of triglycerides with risk of ischemic
stroke (10,27-33), and therefore were not able to
detect that very high levels of triglycerides associate
with very high risk of ischemic stroke in both men
and women as shown in Figure 4.
Nonfasting triglycerides and early death
In a prospective study with 26 years follow-up of
13,000 individuals from the Danish general popula-
tion, the Copenhagen City Heart Study, nonfasting
triglycerides ≥5 mmol/L predicted a 4 and 2 fold
risk of early death in women and men (Figure 5)(9).
A previously unnoticed association between step-
wise increases in levels of nonfasting triglycerides
and stepwise increases in risk of early death with no
threshold effect was also detected.
Because myocardial infarction and ischemic stroke
are major causes of early death, and given the above-
mentioned results (Figure 3 and 4), it seems likely
that the association between elevated levels of non-
fasting triglycerides and risk of early death is caused
by death from these two diseases secondary to devel-
opment of atherosclerosis.
From nonfasting triglycerides and remnants to
atherogenesis
Mechanistically, the explanation for the above-
(Fortsætter side 14)
Foto: Henrik Alfthan
Figure 5.
Hazard ratios for total death for increasing levels
of nonfasting triglycerides. Values are from the Copenhagen
City Heart Study with 26 years follow-up. Multifactorial
adjustment was for age, total cholesterol, body mass index,
hypertension, diabetes mellitus, smoking, alcohol consumption,
physical inactivity, lipid lowering therapy, and in women also
for postmenopausal status and hormone replacement therapy.
Modified from Nordestgaard et al. JAMA 2007; 298: 299-308.
