There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
Anoxia or ischemia causes an accumulation of long-chain fatty acid esters mainly because
of the inhibition of B oxidation. These compounds have deleterious effects on cellular
and intracellular membranes. They also inhibit mitochondrial adenine nucleotide translocase
inducing inhibition of ATP within the mitochondrial matrix, thus rendering it unavailable
for myocardial cell contractility. L-carnitine (L-C) protects against these negative
effects by decreasing the acylcoenzyme A (acyl CoA) through formation of the corresponding
acyl carnitine that is less harmful and diffuses freely across the cell membrane.
To assess the effects of L-C in preserving the ischemic myocardium following acute
myocardium infarction (MI) and in limiting the extent of ischemic damage, we studied
14 patients with acute MI (13 male, one female, mean age 55 years, range 38–72 years).
Acute MI was anterior in nine patients, inferior in three patients and combined in
two patients. Twelve patients admitted concurrently with acute MI (10 male, one female,
mean age 56.5 years) served as the control group. Following admission all patients
and controls were subjected to reperfusion therapy in the form of primary PCI (12
patients) and thrombolytic treatment (four patients), while only 12 patients were
out of the reperfusion window and were started on conservative medical treatment.
Twenty-four hours following therapeutic intervention, the study group received oral
L-C in a dose of 1.8 g daily, following a baseline study by M-mode and 2D echocardiography
together with rest myocardial perfusion imaging using Tc99 sesta MIBI scintigraphy
before and after 1 month of L-C administration. Both imaging techniques were repeated
and the serum L-C level was measured in our laboratory and maintained at 20 ± 5 mg/l.
Echocardiographic parameters assessed included left ventricular end diastolic diameter,
left ventricular end systolic diameter and ejection fraction (EF). Scintigraphically
the myocardium was divided into 20 segments to assess RWMA with application of a 0–4
scoring system to obtain the initial ischemic segment (summed score) and the difference
between the two summed scores in both studies with an estimated LVEF from gated SPECT
techniques. Compared with the control group on conventional therapy, the L-C group
exhibited a significantly greater EF from a baseline reading of 57% and 49%, respectively,
to 53% and 56.7% after L-C treatment, respectively (i.e. 12% improvement in EF in
the L-C group vs 7% decline in the control group). Assessed by scintigraphy the summed
score for the L-C group declined from 34.8% to 20.5% following treatment vs 17.5%
and 21% for the control group (i.e. 41% improvement in the study group vs 16% worsening
in the control group), with a significantly lower myocardium salvage (44.3% in the
study group vs -20% in control group).
In conclusion, as a metabolic supplement the early administration of L-C to patients
with acute MI provides a significant metabolic support to the ischemic myocardium,
helping to limit consequence sequences of ischemic damage and to improve viability.