Differences in The Expression of Lectin-like Oxidised Low-Density Lipoprotein Receptor-1 in Human Epicardial and Intramyocardial Coronary Arteries - European Medical Journal

Differences in The Expression of Lectin-like Oxidised Low-Density Lipoprotein Receptor-1 in Human Epicardial and Intramyocardial Coronary Arteries

3 Mins
Andreas Synetos,1 Stauros Spyropoulos,2 Maria Gazouli,3 Despina Perrea,3 Konstantinos Toutouzas,1 Dimitris Tousoulis,1 Yiannis Chloroyiannis2

The authors have declared no conflicts of interest.

EMJ Cardiol. ;5[1]:37-38. Abstract Review No. AR1.
Intramyocardial paradox, atherosclerosis, inflammation

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

The difference in atherogenic properties of intramyocardial coronary arteries (ICA) and epicardial coronary arteries (ECA), known as the intramyocardial paradox, has been a point of interest for many investigators. Briefly, ICA and ECA covered by myocardial bridges appear to be resistant to atherosclerosis, while ECA that are in close contact to epicardial adipose tissue (EAT) appear to be more vulnerable to atherosclerosis. This effect can be explained partly by the mechanical properties of the arteries and by the close anatomical relation of the EAT and the inflammatory interaction between ECA and EAT.1-3 The aim of the study was to test the possible involvement of lectin-like oxidised-low-density lipoprotein receptor-1 (LOX-1) on the initiation of the intramyocardial paradox. Previous studies have shown that LOX-1 is involved in the initiation of atherosclerosis, but with no reference on its expression at the ICA and ECA course.4,5 In patients with coronary artery disease (CAD) that underwent coronary artery bypass grafting, we investigated whether there was a difference in LOX-1 expression between the intramyocardial and the epicardial parts of the coronary arteries.


We studied 13 consecutive male patients who underwent coronary artery bypass graft surgery due to three vessel occlusive CAD at the Department of Cardiac Surgery, Euroclinic of Athens, Athens, Greece. All patients underwent total arterial myocardial revascularisation using both pedicled mammary arteries and a radial artery, with a mean of 3.6 grafts per patient. During the dissection and the grafting process, we obtained a rhomboid-shaped total wall ECA and ICA sample, with a long axis of 7–9 mm and a short axis of ~1 mm, of the vessels from each patient. We further used reverse transcription-polymerase chain reaction for LOX-1 messenger ribonucleic acid (mRNA) and the total mRNA was directly extracted from ECA and ICA samples by the acid guanidinium-phenol-chloroform method using RNeasy kit (Qiagen, Düsseldorf, Germany). Each LOX-1 mRNA was normalised with a band of the relative internal reference GAPDH mRNA. The relative intensities of the bands of interest were analysed using Gel Doc 2000 (Bio-Rad Labs, Hercules, California, USA) and expressed as a ratio to the GAPDH mRNA band. Statistical analysis was performed with the commercially available software (SPSS Inc., Chicago, Illinois, USA). Quantitative data were presented as rates or mean value ± standard deviation. Probability values were two-sided from the Student’s t test for continuous variables. Non-continuous values were compared by a chi-square test. One-way analysis of variance was used to compare mean LOX-1/GAPDH between the two groups. A value of p<0.05 was considered significant.


Regarding the revascularisation process, we recorded absolute safety with zero early mortality for all patients and a mean hospital duration stay of 6.2 days. We used a mean number of 3.6 arterial grafts in each patient. LOX-1 mRNA was expressed in all samples from both ECA and ICA, and interestingly there was a significant difference between the expression of LOX-1 in ECA and ICA samples, as mean LOX-1/GAPDH ratio was 0.48±0.07 for the ECA samples compared to 0.35±0.03 for the ICA samples, p<0001. This higher expression of LOX-1 in the extramyocardial segments of the coronary arteries in patients with CAD can contribute to the explanation of the intramyocardial paradox, although further studies are needed to clarify the extent of the effects induced by many other factors, including coronary microcirculation, shear stress, and EAT.

Chatzizisis YS, Giannoglou GD. Myocardial bridges spared from atherosclerosis: Overview of the underlying mechanisms. Can J Cardiol. 2009;25(4):219-2. Scher AM. Absence of atherosclerosis in human intramyocardial coronary arteries: A neglected phenomenon. Atherosclerosis. 2000;149(1):1-3. Sacks HS, Fain JN. Human epicardial adipose tissue: A review. Am Heart J. 2007;153(6):907-17. Inoue K et al. Overexpression of lectin-like oxidized low-density lipoprotein receptor-1 induces intramyocardial vasculopathy in apolipoprotein e-null mice. Circ Res. 2005;97(2):176-84. Sawamura T et al. An endothelial receptor for oxidized lowdensity lipoprotein. Nature. 1997;386:73-7.

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