Clinical Utility of Serum Lipocalin-2 in Coronary Artery Disease
MarwaElazab Mahmoud;
Abstract
Coronary atherosclerosis with subsequent superimposition of an arterial thrombus over an underlying disrupted atherosclerotic plaque represents the major pathogenic process in CAD.
Atherosclerosis is defined as thickening of arterial wall as a result of the accumulation of calcium and fatty materials such as cholesterol and triglyceride leading to reduction of arterial wall elasticity. The buildup of an atheromatous plaque is a slow process, developed over a period of several years through a complex series of cellular events occurring within the arterial wall, and in response to a variety of local vascular circulating factors.
Laboratory and clinical evidence have demonstrated that atherosclerosis is not simply a disease of lipid deposits. Systemic inflammation also plays an important role in atherosclerosis development and progression and there is considerable evidence supporting the involvement of neutrophils in this inflammatory process.
Lipocalin-2 is known to be secreted by leukocytes primarily in the granules of human neutrophils. It acts through forming a complex with MMP-9, protecting the latter from degradation and thereby preserving MMP-9 enzymatic activity. MMP-9 and other members of the MMP family have been implicated in atherogenesis, and plaque rupture by degrading the vascular basement membrane, thereby increasing endothelial permeability and allowing more white blood cells and inflammatory cytokines to infiltrate the intima enhancing the role for lipocalin-2 in the pathogenesis of CAD.
In the view of the previous observations and postulations, our study aimed at assessing serum lipocalin-2 levels in patients with CAD and to investigate the association between circulating lipocalin-2 levels and disease severity.
This implied studying of serum levels of lipocalin-2 in 60 patients with CAD. According to the results of the coronary angiography those patients were further classified according to number of diseased vessels into 3 subgroups. 19 patients with 1 vessel disease, 24 patients with 2 vessel disease and 17 patients with 3 vessel disease. The control group consisted of 20 subjects with angiograms showing normal coronaries. The adopted assay method was ELISA for lipocalin-2.
Results of our study revealed that serum levels of lipocalin-2 were significantly higher in patients with CAD compared to control group. The high levels of lipocalin-2 are due to the fact that inflammation and neutrophils activation play a central role in atherogenesis and plaque rupture.
A remarkable finding in the present study is serum lipocalin-2 levels being significantly higher in patients with 3 vessel disease compared to those with 1 vessel disease and 2 vessel diseases. This augments the theory that the high levels of lipocalin-2 reflect the higher degree of inflammation among patients with severe CAD.
Our correlation analysis revealed a highly significant statistical positive correlation between lipocalin-2 and gensini score, supporting the association between circulating lipocalin-2 levels and CAD severity.
The significant increase in serum levels of lipocalin-2 that was present in all our patients’ groups, as well as the positive correlation between lipocalin-2 and gensini score reflecting CAD severity, allows us to conclude that inflammation has a pivotal role in the progression of CAD. Our data also suggest that lipocalin-2 is good indicator of the extent of the coronary atheromatous process.
In conclusion, the present study indicates clearly that increased level of lipocalin-2 is related to the extent of atherosclerosis in patients with CAD, supporting the role of inflammation in CAD development.
Atherosclerosis is defined as thickening of arterial wall as a result of the accumulation of calcium and fatty materials such as cholesterol and triglyceride leading to reduction of arterial wall elasticity. The buildup of an atheromatous plaque is a slow process, developed over a period of several years through a complex series of cellular events occurring within the arterial wall, and in response to a variety of local vascular circulating factors.
Laboratory and clinical evidence have demonstrated that atherosclerosis is not simply a disease of lipid deposits. Systemic inflammation also plays an important role in atherosclerosis development and progression and there is considerable evidence supporting the involvement of neutrophils in this inflammatory process.
Lipocalin-2 is known to be secreted by leukocytes primarily in the granules of human neutrophils. It acts through forming a complex with MMP-9, protecting the latter from degradation and thereby preserving MMP-9 enzymatic activity. MMP-9 and other members of the MMP family have been implicated in atherogenesis, and plaque rupture by degrading the vascular basement membrane, thereby increasing endothelial permeability and allowing more white blood cells and inflammatory cytokines to infiltrate the intima enhancing the role for lipocalin-2 in the pathogenesis of CAD.
In the view of the previous observations and postulations, our study aimed at assessing serum lipocalin-2 levels in patients with CAD and to investigate the association between circulating lipocalin-2 levels and disease severity.
This implied studying of serum levels of lipocalin-2 in 60 patients with CAD. According to the results of the coronary angiography those patients were further classified according to number of diseased vessels into 3 subgroups. 19 patients with 1 vessel disease, 24 patients with 2 vessel disease and 17 patients with 3 vessel disease. The control group consisted of 20 subjects with angiograms showing normal coronaries. The adopted assay method was ELISA for lipocalin-2.
Results of our study revealed that serum levels of lipocalin-2 were significantly higher in patients with CAD compared to control group. The high levels of lipocalin-2 are due to the fact that inflammation and neutrophils activation play a central role in atherogenesis and plaque rupture.
A remarkable finding in the present study is serum lipocalin-2 levels being significantly higher in patients with 3 vessel disease compared to those with 1 vessel disease and 2 vessel diseases. This augments the theory that the high levels of lipocalin-2 reflect the higher degree of inflammation among patients with severe CAD.
Our correlation analysis revealed a highly significant statistical positive correlation between lipocalin-2 and gensini score, supporting the association between circulating lipocalin-2 levels and CAD severity.
The significant increase in serum levels of lipocalin-2 that was present in all our patients’ groups, as well as the positive correlation between lipocalin-2 and gensini score reflecting CAD severity, allows us to conclude that inflammation has a pivotal role in the progression of CAD. Our data also suggest that lipocalin-2 is good indicator of the extent of the coronary atheromatous process.
In conclusion, the present study indicates clearly that increased level of lipocalin-2 is related to the extent of atherosclerosis in patients with CAD, supporting the role of inflammation in CAD development.
Other data
| Title | Clinical Utility of Serum Lipocalin-2 in Coronary Artery Disease | Other Titles | الاهميةالاكلينيكيةلقياسمستوىالليبوكالين 2 بالمصلفىمرضالشريانالتاجي | Authors | MarwaElazab Mahmoud | Issue Date | 2014 |
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