Background and aims: Elevated Lp(a) levels are a significant cardiovascular risk factor, particularly for young individuals and for subjects with concomitant high LDL cholesterol. Increased Lp(a) is believed to be linked to an enhanced production of the lipoprotein, controlled by genetic factors; it can be reduced by agents such as nicotinic acid, lowering free fatty acid inflow 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 in 36 subjects with Lp(a) levels ranging between 40-80 mg/dL, in most with concomitant LDL cholesterol and triglyceride elevations. L-carnitine (2 g/day) significantly reduced Lp(a) levels (-7.7% vs baseline and -11.7% vs placebo treatment), the reduction being more dramatic in the subjects with the more marked elevations. In particular, in the L-carnitine group, 14 out of 18 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 significant number of subjects the reduction of Lp(a) resulted in a return of this major 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.