Finally, receiver operating characteristic curve analysis was used to determine predictive value endocan in isolated CAE. The optimal cutoff value for endocan was calculated as 3.2 ng/ml. The area under the curve was 0.860. At this cutoff value, the sensitivity and specificity of endocan were 79 and 76%, respectively. We also measured the power analysis, and we found that our result was 1, which provides a strong power (Fig. 3).
With the increase in the number of patients undergoing coronary angiography, we identify CAE in more patients. CAE is an independent predictor of mortality, and, in some studies, the mortality rate of patients with nonobstructive coronary artery aneurysms is similar to that of patients with multivessel disease 5,6. In a large cohort study on CAE, the 5-year mortality in patients with coronary artery aneurysm was reported as 26% in 1983 6. In contrast, two recent studies found significantly lower mortality rates in CAE patients. In the first study, the cardiovascular mortality rate was 2% after a mean follow-up of 49±21 months in 258 patients with CAE 15. The second study, which included 540 patients with CAE, reported 2.22% mortality after 36 months of follow-up 16. The decrease in mortality over time may be attributable to better management of CAE and the improvements in medicine. The pathophysiological mechanism of CAE has also become an important research topic because of high mortality rate. Although the etiology and pathophysiology of CAE are still unclear, some pathological mechanisms have been proposed. CAE is considered to be a large positive remodeling of the atherosclerotic coronary artery 17. The most emphasized mechanisms of this remodeling are the enzymatic degradation of the extracellular matrix and the thinning of the tunica media layer of the vessel caused by severe chronic inflammation 18. Markis et al. 7 examined ectatic layers by postmortem histopathological examination and suggested the destruction of vascular media layer in ectasia. Moreover, more than half of the CAE patients have CAD. However, excessive release of interstitial nitric oxide (NO) is suggested as another aspect of this pathology. Inflammatory cells are important factors in the production of NO by inducible NO synthase. Chronic exposure to NO may cause hyaline degeneration in the intima and media layers of the coronary arteries and may lead to abnormal coronary dilatation 19. In a recent study, plasma levels of vascular endothelial growth factor (VEGF) in isolated CAE patients were investigated, and a new insight into the molecular mechanisms of the widely isolated CAE was presented. Plasma levels of VEGF, matrix metalloproteinase-2 (MMP-2), tissue inhibitors of matrix metalloproteinase-1 (TIMP-1) and tissue inhibitors of MMP-2 (TIMP-2), as well as C-reactive protein (CRP), were investigated in a study 20. As a result of this study, VEGF levels in patients with diffuse isolated CAE were higher than those in patients with NCAs or obstructive CAD. MMP-2 and TIMP-1 levels were similar in these three groups, but TIMP-2 levels were lower in patients with diffuse isolated CAE than the other two groups. Although these studies had smaller samples sizes, more severe and extensive chronic inflammation in the coronary circulation in CAE patients suggests that a greater amount of vascular wall inflammation may have a role. hsCRP levels, a marker of systemic inflammation, are present in all atherosclerotic diseases and are associated with poor prognosis. Previous studies have shown that hsCRP levels are elevated in patients with CAE, which is seen as a derivative of atherosclerotic disease 16,21. CRP may cause endothelial dysfunction and medial breakdown by increasing monocyte adhesion to endothelial cells and secretion of MMPs 22. The prothrombotic effects of CRP were shown in humans 23 and transgenic mice. High hsCRP levels that were observed in our study support these data.
This study has several limitations. First, our research did not include a histopathological examination of obstructive CAD or ectatic segments. We have a relatively small number of patients, and further studies with larger sample sizes are warranted. Finally, further tests such as intravascular ultrasonography could not be used in the diagnosis of our control group; hence, the diagnosis of normal CAD was observational.
There are no conflicts of interest.
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