Background and Aims: Elevated Lp(a) levels are a significant cardiovascular
risk factor, particularly for young individuals and for subjects with conc
omitant high LDL cholesterol. increased Lp(a) is believed to be linked to a
n enhanced production of the lipoprotein, controlled by genetic factors; it
can be reduced by agents such as nicotinic acid lowering free fatty acid i
nflow to the liver
Methods and Results: L-carnitine, a natural compound stimulating fatty acid
oxidation at the mitochondrial level, was tested in a double blind study i
n 36 subjects with Lp(a) levels ranging between 40-80 mg/dL, in most with c
oncomitant LDL cholesterol and triglyceride elevations. L-carnitine (2 g/da
y) significantly reduced Lp(a) levels (-7.7% vs baseline and -11.7% vs plac
ebo treatment), the reduction being more dramatic in the subjects with the
more marked elevations. In particular in the L-carnitine group, 14 out of 1
8 subjects (77.8%) had a significant reduction of Lp(a) vs only 7 out of 18
(38.9%) in the placebo group (chi (2) = 4.11, p = 0.0452). In a significan
t number of subjects the reduction of Lp(a) resulted in a return of this ma
jor cardiovascular risk parameter to the normal range.
Conclusions: L-carnitine offers a potentially useful therapeutic agent for
atherogenic conditions characterized by high Lp(a) levels, also in view of
the excellent tolerability and essential lack of major side effects. (C) 20
00, Medikal Press.