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| 3 | 2009
Klinisk Biokemi i Norden
increased risk of cardiovascular events (10). Although
previous studies found that elevated fasting triglycer-
ides also associate with increased risk of cardiovas-
cular disease (13-15), the study from the Women’s
Health Study (10) together with the one from the
Copenhagen City Heart Study (9) highlight that non-
fasting levels of triglycerides may be better than fast-
ing levels at predicting risk of cardiovascular disease.
In women versus men, a better predictive ability of
nonfasting triglycerides was observed for myocardial
infarction (Figure 3)(9), in accordance with similar
findings for fasting triglyceride levels in some (13-14),
but not all previous meta-analyses (15). However,
stratified analyses suggested that the predictive ability
of nonfasting triglycerides in young men who only
consume small amounts of alcohol was similar to
that in women (9). Therefore, because large alcohol
intake often leads to increased triglyceride levels,
and because these triglyceride-rich lipoproteins may
differ from most remnant lipoproteins present in
nonfasting plasma (type V versus type IIb hyper-
lipidemia), it is likely that high alcohol intake may
have confounded the association between triglyceride
levels and risk of myocardial infarction and ischemic
heart disease in recent (9) and former studies.
There are other very different diseases and causes
for hypertriglyceridemia, and that may be another
major reason for the previous uncertainty of whether
or not hypertriglyceridemia leads to increased risk of
cardiovascular disease. Patients with extreme triglyc-
eride levels above 25 mmol/L and the familial chy-
lomicronemia syndrome rarely develop atherosclero-
sis (16). With such extreme triglyceride levels, most
lipoproteins in plasma are very large (17). These giant
lipoproteins do not enter into the arterial intima (18),
and therefore cannot cause atherosclerosis. However,
patients with moderate hypertriglyceridemia and
conditions like familial hypertriglyceridemia, familial
combined hyperlipidemia, metabolic syndrome, and
remnant hyperlipidemia do in fact develop premature
atherosclerosis (16,19-21). At moderate hypertriglyc-
eridemia, chylomicron remnants and VLDL remnants
are present in plasma. These smaller triglyceride-rich
lipoproteins do enter into the arterial intima (22-23),
appear to be preferentially trapped within the arterial
wall (24-26), and thus may cause atherosclerosis lead-
ing to myocardial infarction, ischemic heart disease
and ultimately early death.
Nonfasting triglycerides and ischemic stroke
The role of triglycerides in risk of ischemic stroke
was previously controversial (27-34). Even the most
recent European and American guidelines on stroke
Figure 3.
Hazard ratios for myocardial infarction for increas-
ing 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, alco-
hol 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.
(Fortsat fra side 11)
Figure 4.
Hazard ratios for ischemic stroke for increas-
ing levels of nonfasting triglycerides. Values are from the
Copenhagen City Heart Study with 31 years follow-up.
Multifactorial adjustment was for age, total cholesterol, hyper-
tension, smoking, alcohol consumption, atrial fibrillation, lipid
lowering therapy, and in women also for postmenopausal sta-
tus and hormone replacement therapy. Modified from Freiberg
et al. JAMA 2008; 300: 2142-2152.
