Complementary Alternative Cardiovascular Medicine

Chapter 7 / Nutrachemicals and CVD 109
CARNITINE
Carnitine is an amino acid derivative that is found in all body cells,
especially striated muscles. It is synthesized in the liver, kidneys, and
brain from the amino acids lysine and methionine. Two analogs of carnitine,
acetyl-L-carnitine (ALC) and propionyl-L-carnitine (PLC), have
been used. Carnitine plays an important role in the transport of free fatty
acids (FFA) across the inner mitochondrial membranes for ATP production.
As a cofactor, carnitine enhances carbohydrate metabolism and
reduces toxic metabolites produced during ischemic conditions. Although
its approved indications are primary/secondary carnitine deficiencies, it is
widely used in multiple cardiovascular conditions.
Role in CVD
L-carnitine may beneficially affect cardiac function and also may
have cardioprotective activity resulting from its antioxidant effects. It
may also lower, to a variable extent, the plasma triglycerides and elevate
high-density lipoprotein (HDL)-cholesterol levels.
Both free and total myocardial carnitine levels are reduced during
periods of prolonged acute ischemia. This is noted significantly in the
ischemic zone, and mild reductions are noted in the adjacent nonischemic
areas. This reduction is associated with a significant elevation in FFAs
and toxic ester levels, with a reduction in ATP and creatine phosphate.
These intracellular changes in the ischemic myocardium can result in a
poor outcome after acute myocardial infarction (AMI). It has been suggested
that carnitine supplementation may mitigate ischemic injury. The
beneficial effects may include enhanced glucose oxidation, preservation
of myocardial carnitine, reduction in loss of high-energy phosphates,
and reduction in the accumulation of toxic esters. These metabolic
changes could translate into better clinical outcomes, such as reduction
in cardiac arrhythmias, preservation of myocardial function, and ST
elevation (36).
There are few trials suggesting the beneficial role of carnitine in patients
with acute myocardial infarction. Rebuzzi et al. (37) found that L-carnitine
reduced the extent of myocardial infarction if given within 8 h of symptom
onset. The CEDIM (L-Carnitine Ecocardiografia Digitalizzata
Infarto Miocardico) trial (38) studied patients after their first anterior
wall myocardial infarction. In this double-blind, randomized controlled
trial, 472 patients were treated with either L-carnitine (iv for 5 d, followed
by orally) or a placebo for 12 mo. Although there was no change
in overall ejection fractions, there were significant reductions in left
ventricular diastolic and systolic dimension in the active group. The