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| 3 | 2009
Klinisk Biokemi i Norden
mentioned findings is most likely straightforward.
Elevated levels of nonfasting triglycerides indicate
the presence of elevated levels of remnant lipopro-
teins (Figure 2 and 6), lipoproteins that directly
cause atherosclerosis and consequently myocardial
infarction, ischemic stroke and ultimately early death.
Thus, it is not triglycerides per se that cause athero-
sclerosis, but rather the cholesterol content of rem-
nant lipoproteins.
Because all human cells can degrade triglycerides
but not cholesterol, and because remnant lipopro-
teins like LDL carry large amounts of cholesterol,
it is the cholesterol content of remnant particles that
upon entrance into the arterial intima (Figure 6) can
cause atherosclerosis (12,35-36). Like LDL, remnant
lipoproteins can enter into the arterial intima (22-23),
and may even be trapped preferentially within the
arterial wall (24-26,37).
In support of this mechanism, patients with geneti-
cally large amounts of remnant lipoproteins in plasma
develop premature atherosclerosis (20). In addition,
patients with familial forms of hypertriglyceridemia
have an increased risk of cardiovascular death (19).
Also, heterozygosity for genetic defects in lipoprotein
lipase, the plasma enzyme degrading triglycerides,
associates with elevated triglyceride levels as well as
increased risk of ischemic heart disease (16,38-39).
Furthermore, patients with the familial chylomicro-
nemia syndrome who during part of their life due
to lipid lowering treatment have triglyceride levels
down to 3-7 mmol/L, and consequently have remnant
lipoproteins in plasma rather than chylomicrons, also
develop premature atherosclerosis (40).
Conclusion
These new data open the possibility that nonfasting
rather than fasting lipid profiles are used for car-
diovascular risk prediction. Also in favor of the use
of nonfasting samples is the fact that lipid profiles
change minimally in response to normal food intake
(7-8). On the basis of such evidence, hospitals in
Copenhagen and elsewhere in Denmark now use
nonfasting lipid profiles as the standard and sug-
gest a repeat fasting triglyceride measurement only
if nonfasting concentrations exceed 4 mmol/L (352
mg/dL) (41-42). If implemented, this would simplify
blood sampling for lipid measurements for millions
of patients worldwide. Indirectly, this then pos-
(Fortsat fra side 13)
Figure 6.
Influx and efflux of LDL and remnant lipoproteins
between plasma and the arterial intima, the site of atheros-
clerotic lesions. Cholesterol (dark gray) and triglycerides (light
grey) exchange between triglyceride-rich remnant lipoproteins
and HDL particles. Therefore, high levels of triglycerides asso-
ciate with low levels of HDL cholesterol, and vice versa.
sibly could improve compliance for lipid lowering
treatments.
Acknowledgement
Supported by a Specific Targeted Research Project
grant from the European Union, Sixth Framework
Programme Priority (FP-2005-LIFESCIHEALTH-6)
contract 037631, the Danish Medical Research
Council, the Danish Heart Foundation, the Research
Fund at Rigshospitalet, Copenhagen University
Hospital, and the Copenhagen County Foundation.
Foto: Henrik Alfthan
