- Poster presentation
- Open Access
L-carnitine deficiency in acute myocardium infarction: prevalence and therapeutic effects of repletion
© BioMed Central Ltd 2006
- Published: 21 March 2006
- Myocardial Perfusion Imaging
- Acute Myocardium Infarction
- Fatty Acid Ester
- Gated SPECT
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.