The Relation Between Endocan Levels and Subclinic Atherosclerosis.

Abstract

We read the article ‘‘The Relationship Between Serum Endocan Levels With the Presence of Slow Coronary Flow: A CrossSectional Study’’ by Kundi et al. They aimed to investigate the relation between endocan levels and slow coronary flow (SCF). They concluded that higher endocan levels were significantly and independently related to the presence of SCF. Slow coronary flow phenomenon is recently well known as an atherosclerotic process, which is triggered by increased inflammatory conditions. Indeed, various studies demonstrated the relation between SCF and inflammation. Furthermore, elevated levels of systemic inflammatory markers are related to SCF based on endothelial dysfunction. Endocan, a novel endothelial marker, was increased by many inflammatory diseases. In line with inflammation, we have reported that the elevated levels of endocan were described in some atherosclerotic processes. Hypertension is one of the most important fatal and nonfatal disease worldwide, and it is also associated with endothelial inflammation, endothelial injury, activation, and dysfunction caused by oxidative stress. Furthermore, diminished endocan levels by endocan antibody enhanced survival rate. Another cardiovascluar risk factor such as chronic kidney disease (CKD) can lead to endothelial dysfunction. Hence, Yilmaz et al have investigated the relation between endocan levels and CKD. They have showed that endocan levels were associated with all-cause mortality and cardiovascular events (CVEs) in patients with CKD, but plasma endocan concentrations also correlated positively with both markers of inflammation. Vasculitis related to endothelial dysfunction is considered to play a key role in pathogenesis of Behcet disease (BD). So we investigated endocan levels in patients with BD. Increased endocan levels were observed in these patients. Also, we have showed that serum endocan levels correlated positively with C-reactive protein, erythrocyte sedimentation rate, and activity of the disease. Serum levels of endocan were also higher in patients with systemic involvement. In other study, we investigated endocan levels in patients with psoriasis, which is associated with an increased risk of CVD. We showed higher serum levels of endocan in these patients. Additionally, serum endocan levels were correlated positively with cardiovascular risk and activity of the disease. In addition, some medications may change the endocan levels. We also reported antihypertensive therapy such as valsartan and amlodipine significantly diminished the endocan levels. There was a possibly significantly increased rate in these patients due to statin use. The potential effect of control of hyperlipidemia and pleiotropic effects of statin use on endocan levels would better be briefly discussed. Also, some of the oral antidiabetics may change endothelial dysfunction. In this context, medication should be considered. In conclusion, endocan is a novel indicator to evaluate the endothelial dysfunction in clinical practice, and without the above-mentioned conditions, endocan alone may not provide information to clinicians about inflammation in patients with SCF. It would have been better, if these factors were included in the recent text.