To the best of our knowledge, this is the first study to determine the close relationship between the serum endocan level and CHA2DS2-VASc score. Many studies have been conducted recently to investigate the relationship between cardiovascular diseases and endocan. It has been reported that in patients with acute myocardial infarction, an elevated level of endocan at the time of presentation to the hospital is an independent predictor of adverse cardiovascular outcomes, and it has also been independently associated with the severity of hypertensive coronary artery disease [13, 14]. Studies particularly focusing on the effects of cardiovascular diseases on the endothelium suggest that endocan may be a useful predictor of these diseases [15].
Risk factors, such as advancing age, hypertension, coronary heart disease, diabetes mellitus, valvular heart disease, heart failure, and hyperthyroidism cause structural changes in the heart resulting in the development of AF [16]. In fact, many conditions that cause vascular changes lead to the formation of AF, and several of these situations constitute the CHA2DS2-VASc score. On the other hand, many studies have shown that AF leads to endothelial dysfunction for many reasons, including increased shear stress, decreased nitric oxide bioavailability, increased oxidative stress, inflammation, and abnormalities of the renin-angiotensin system [17, 18]. As shown in a recently published meta-analysis, endocan released from endothelial cells increases in serum in disease that are components of the CHA2DS2-VASc score such as hypertension, diabetes, and coronary artery disease [19]. Similarly, we substantiated positive correlation between serum endocan level and CHA2DS2-VASc score in PAF patients.
Endothelial dysfunction mechanisms are closely related to the development of atrial cardiopathy [20]. It has been concluded that endothelial dysfunction, which is considered to develop as a result of AF, improves following the achievement of normal sinus rhythm [21, 22].
In addition, the detection of inflammatory infiltrates in the atrial and ventricular biopsies of patients with AF suggests that inflammation plays a role in AF [23]. Cox et al. reported that endocan played a significant role in endothelial dysfunction, since it regulated cell adhesion in inflammatory disorders [24]. Endothelial dysfunction and inflammatory damage mechanism caused by the components of the CHA2DS2-VASc score will lead to endocan release. Endothelial dysfunction, inflammatory damage seen in AF physiopathology, and indirect increased serum endocan level from components of the CHA2DS2-VASc score make it possible to observe a very close relationship between the CHA2DS2-VASc score and the endocan. In this study, a positive correlation was determined between endocan and the CHA2DS2-VASc score (≥ 2), an indicator of a high stroke risk, which includes a significant part of risk factors.
Chua et al. referred to the necessity of using biomarkers in AF and emphasized that markers, such as BNP and FGF-23 could be associated with AF [25]. There is not yet a biomarker predictive of thromboembolic complications. We determined a close relationship between CHA2DS2-VASc scores and endocan, which is an endothelium-specific marker. In addition, endocan was detected as an independent determinant of high CHA2DS2-VASc scores, which is an indicator of increased stroke risk in PAF in which many cardiovascular diseases may play a causative role.
The limitations of this study include the relatively small number of patients, observation nature of the study, and its lack of prospective validation. Also, the study is monocentric and does not comprise a large sample size.