{"title":"Increased serum resistin levels associated with isolated coronary artery ectasia.","authors":"Fatih Sivri, Ufuk Eryılmaz","doi":"10.5114/amsad/151954","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Coronary artery ectasia (CAE) is localized or diffuse enlargement of the coronary artery more than 1.5 times in diameter in comparison with the adjacent normal coronary artery. The etiology and pathophysiology of CAE are not fully elucidated. Resistin is a newly identified adipocyte secreted hormone belonging to a cysteine-rich protein family. Recently it has been found to be relevant to inflammation-related disease and correlated with serum C-reactive protein (CRP). This research aimed to investigate whether the resistin level has a role in CAE etiopathogenesis.</p><p><strong>Material and methods: </strong>A hundred and three patients with diagnosis of CAE and 122 with normal coronary anatomy (NCA) were included. Details of baseline clinical characteristics and angiographic findings were recorded. Other necessary biochemical parameters were measured with an autoanalyzer. Blood was collected and stored for serum resistin level analysis.</p><p><strong>Results: </strong>Serum resistin levels in CAE were higher than in the NCA group and were statistically significant (<i>p</i> = 0.001). Hypertension (OR = 1.006, 95% CI: 1.002-1.008, <i>p</i> = 0.025), tobacco use (OR = 1.089, 95% CI: 1.055-1.124, <i>p</i> < 0.001), serum resistin levels (OR = 2.431, 95% CI: 1.100-4.696, <i>p</i> = 0.01), hyperlipidemia (OR = 1.005, 95% CI: 1.000-1.014, p = 0.004), triglyceride (OR = 1.006, 95% CI: 1.001-1.010, <i>p</i> = 0.012) remained as independent factors for CAE. In the subgroup analysis of the CAE group, in patients with ectasia in three coronary arteries, resistin levels were significantly higher and statistically significant (<i>p</i> = 0.001). In ROC analysis, the sensitivity of serum resistin was 67.6% and specificity was 86.7% (AUC = 0.749, 95% CI: 0.621-0.877, <i>p</i> = 0.0001).</p><p><strong>Conclusions: </strong>Serum resistin level was significantly higher in CAE. In addition this study showed that serum resistin levels are directly proportional to the number of coronary arteries with ectasia. We think that this study will shed light on this subject and encourage further studies in this field.</p>","PeriodicalId":8317,"journal":{"name":"Archives of Medical Sciences. Atherosclerotic Diseases","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/64/e1/AMS-AD-7-151954.PMC9487800.pdf","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Medical Sciences. Atherosclerotic Diseases","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5114/amsad/151954","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Introduction: Coronary artery ectasia (CAE) is localized or diffuse enlargement of the coronary artery more than 1.5 times in diameter in comparison with the adjacent normal coronary artery. The etiology and pathophysiology of CAE are not fully elucidated. Resistin is a newly identified adipocyte secreted hormone belonging to a cysteine-rich protein family. Recently it has been found to be relevant to inflammation-related disease and correlated with serum C-reactive protein (CRP). This research aimed to investigate whether the resistin level has a role in CAE etiopathogenesis.
Material and methods: A hundred and three patients with diagnosis of CAE and 122 with normal coronary anatomy (NCA) were included. Details of baseline clinical characteristics and angiographic findings were recorded. Other necessary biochemical parameters were measured with an autoanalyzer. Blood was collected and stored for serum resistin level analysis.
Results: Serum resistin levels in CAE were higher than in the NCA group and were statistically significant (p = 0.001). Hypertension (OR = 1.006, 95% CI: 1.002-1.008, p = 0.025), tobacco use (OR = 1.089, 95% CI: 1.055-1.124, p < 0.001), serum resistin levels (OR = 2.431, 95% CI: 1.100-4.696, p = 0.01), hyperlipidemia (OR = 1.005, 95% CI: 1.000-1.014, p = 0.004), triglyceride (OR = 1.006, 95% CI: 1.001-1.010, p = 0.012) remained as independent factors for CAE. In the subgroup analysis of the CAE group, in patients with ectasia in three coronary arteries, resistin levels were significantly higher and statistically significant (p = 0.001). In ROC analysis, the sensitivity of serum resistin was 67.6% and specificity was 86.7% (AUC = 0.749, 95% CI: 0.621-0.877, p = 0.0001).
Conclusions: Serum resistin level was significantly higher in CAE. In addition this study showed that serum resistin levels are directly proportional to the number of coronary arteries with ectasia. We think that this study will shed light on this subject and encourage further studies in this field.