The association between serum serglycin level and coronary artery disease severity in patients with stable angina pectoris

Background: Serglycin plays a key role in the inflammatory status however the relationship between coronary artery disease (CAD) and serglycin is still unknown. Aim: In this study, we aimed to investigate association of serglycin levels with CAD severity in patients with stable angina pectoris (SAP). Methods: In total, 100 SAP patients diagnosed by coronary angiography and clinical manifestations, and 100 control subjects matched for age and sex were enrolled in this case-control study. Plasma levels of serglycin, high-sensitivity C-reactive protein (hsCRP), lipid profiles, and clinical parameters were assayed for all participants. The severity of coronary lesions was evaluated based on the SYNTAX score (SS) assessed by coronary angiography. Results: Positively correlated with the SS (r = 0.564, p < 0.001), the plasma serglycin level in the SAP group was higher than that in the control group (11.17 ± 1.82 vs. 19.28 ± 1.88 ng/mL, p < 0.001). The plasma serglycin level was an inde-pendent predictor for both SAP (odds ratio [OR] 1.037, 95% confidence interval [CI] 1.020–1.054, p < 0.001) and a high SS (OR = 1.087, 95% CI 1.051–1.124, p < 0.001) in a multivariate logistic regression model. In the receiver operating characteristic curve analysis, the plasma serglycin level was found to have a better predictive value for a high SS (area under the curve [AUC] 0.858, 95% CI 0.788–0.929, p < 0.001) compared with hsCRP (AUC 0.665, 95% CI 0.557–0.773, p = 0.006; Z = 2.94, p < 0.001), with an optimal cut-off value of 17.25 ng/mL (sensitivity 94.3%, specificity 68.2%). Conclusions: Plasma serglycin levels correlate with both the presence and severity of coronary stenosis in patients with SAP, suggesting that it could be a potential predictive marker of severe stenosis in SAP patients

The effect of serum IL-12/TGF-Beta1 ratio on extend of atherosclerosis

Amaç: Günümüzde kalp damar hastalıklarına bağlı ölümler gelişmiş ülkelerde tüm ölümlerin yaklaşık yarısından, gelişmekte olan ülkelerde ise dörtte birinden sorumludur. Aterosklerotik damar hastalığı gelişimine bakıldığında ise inflamasyonun önemli bir rol oynadığı görülmüştür. Bu nedenle proinflamatuar ve antiinflamatuar sitokinlerin aterosklerotik koroner arter hastalığı seyrine olan etkilerini değerlendirmek amacıyla, çalışmamızda; aterosklerotik koroner arter hastalığı oluşumuna zemin hazırladığı gösterilen hipertansiyon, hiperlipidemi, sigara içimi ve diyabetes mellitus gibi geleneksel risk faktörlerinin (medikal tedavi ile kontrol altında olsalar bile) serum okside LDL ve yd-CRP düzeylerini artırabildiğinin ve böylelikle oluştuğu kanıtlanması planlanan bu oksidatif ortamda, aterosklerotik sürecin seyrini ve aterosklerotik koroner arter hastalığı yaygınlığını IL-12 ve TGF-Beta1 arasındaki dengesizliğin belirleyebileceğinin gösterilmesi amaçlanmıştır. Yöntem: Aralık 2011-Aralık 2012 tarihleri arasında Gazi Üniversitesi Kardiyoloji Polikliniğine tipik vasıfta göğüs ağrısı nedeni ile başvuran, yapılan efor testi veya miyokard perfüzyon sintigrafisinde iskemi bulgusu izlenmesi üzerine koroner anjiografi uygulanan, 25 yaş üstünde ve aterosklerotik koroner arter hastalığı için en az bir geleneksel risk faktörüne sahip 80 hasta dahil edildi. Hastalarda mevcut geleneksel risk faktör(ler)inin medikal tedavi ile kontrol altında olması koşulu arandı ve akut koroner sendrom tablosundaki hastalar çalışmadan dışlandı. Bulgular: Hastalar; CASS 20 skorlarına göre ateroskleroz saptanmayanlar, ateroskleroz yaygınlığı düşük düzeyde olanlar ve ateroksleroz yaygınlığı yüksek düzeyde olanlar olmak üzere üç gruba ayrıldı. Hastaların bazal karakteristikleri ve demografik özellikleri açısından gruplar arasında anlamlı fark yoktu. Ateroskleroz yaygınlığı arttıkça ortalama serum okside LDL düzeylerinin, (73,6±3,24 / 144,4±4,45 / 243±9,3 ng/ml), ortalama serum yd-CRP düzeylerinin, (4,21±0,25 / 11,1±0,2 / 17,7±0,32 mg/lt) ve ortalama serum IL-12 düzeylerinin (3,33±0,15 / 9,70±0,22 / 23,60±0,46 pg/ml) arttığı; ortalama serum TGF-Beta1 düzeylerinin ise azaldığı (32,1±0,59 / 18±0,28 / 6,74±0,42 ng/ml) izlenmiş olup bu birliktelik istatistiksel olarak anlamlı bulunmuştur.(p<0,01) Sonuç: Medikal tedavi ile kontrol altında olsa dahi, geleneksel risk faktörlerinin serum okside LDL ve yd-CRP seviyelerini artırdığı gösterilmiştir. Bu belirteçlerin serum düzeylerinin, sahip olunan geleneksel risk faktörü sayısı ile ilişkisiz olduğu tespit edilmiştir. Okside LDL ve yd-CRP oluşumuyla/düzeylerinin artışıyla, oluştuğu kanıtlanmış olan bu oksidatif ve inflamatuar ortamda aterosklerotik koroner arter hastalığının gelişip gelişmeyeceğini, ilgili damar segmentinin intimasında bulunan baskın sitokinin belirlediği saptanmıştır. T helper hücrelerden salınan proinflamatuar sitokinler süreci aterojenik yöne sürüklerken Treg hücrelerinden salınan TGF-Beta1 ise süreci antiaterojenik yöne sürüklemiştir.Aim: Recently, the deaths related to cardiovascular diseases are responsible approximately half of all deaths in developed countries and quarter of all deaths in developing countries. Inflammation plays an important role in development of atherosclerotic vessel disease. So that; in our study, to examine the effect of proinflammatory and antiinflammatory cytokines on the progression of atherosclerotic coronary artery disease, firstly we aim to show that presence of traditionally risk factors (hypertension, diabetes mellitus, smoking and hiperlipidemia) that are under controlled by medical treatment can cause accretion of serum oxidized LDL and hs-CRP levels. Secondly we aim to show that, in this oxidative environment that is proved to be formed, disequilibrium between IL-12 and TGF-Beta1 can determine the progression of atherosclerosis and extent of atherosclerotic coronary artery disease. Method: Eighty patients, over twenty five years old, who applied between December 2011-December 2012 to Gazi University Hospital Cardiology Policlinic because of typically characterized chest pain and who have at least one traditionally risk factor and had positive exercise test or myocardial perfusion scintigraphy including evidence of ischemia and finally have been performed coronary angiography because of these reasons are included our study. Traditional risk factor(s) present in patients should be under controlled by medical therapy and patients who had acut coronary syndrome were excluded from this study. Findings: Patients were seperated into three groups according to their CASS 20 scores as patients had no atherosclerotic lesion, patients had low grade extend of atherosclerosis and patients had high grade extend of atherosclerosis. There was no significant differance between the groups in terms of characteristic and demographic properties. While the extend of atherosclerosis increased, average of serum oxidized LDL levels (73,6±3,24 / 144,4±4,45 / 243±9,3 ng/ml), average of serum hs-CRP levels (4,21±0,25 / 11,1±0,2 / 17,7±0,32 mg/lt) and average of serum IL-12 levels (3,33±0,15 / 9,70±0,22 / 23,60±0,46 pg/ml) increased too, average of serum TGF-Beta1 levels (32,1±0,59 / 18±0,28 / 6,74±0,42 ng/ml) decreased, contrastly. This synergy was statistically meaningful. Result: We have shown that even with medical treatment under control, presence of traditional risk factors can elevate serum oxidized LDL and hs-CRP levels and this accretion is compatible with extent of atherosclerotic coronary artery disease. In this way, presence of oxidative and inflammatory environment has been argued and we have shown that in this environment the dominant cytokine in related vessel intima designates the attendant of atherosclerosis. While the proinflammatory cytokines that are secreted by T helper cells are proatherogenic, the antiinflammatory cytokines, like TGF-Beta1 secreted by Treg cells, are antiatherogenic

Adropin and circadian variation of blood pressure

Background: Nocturnal hypertension and non-dipping pattern are often associated with endothelial dysfunction. Previous studies suggested that adropin, a novel secreted energy homeostasis protein, has the unique ability to regulate endothelial cell function. Aim: This study aims to investigate the association between absolute night-time blood pressure (BP) and circadian BP pat-tern with serum adropin and high-sensitivity C-reactive protein (hsCRP) levels in patients with newly diagnosed untreated arterial hypertension. Methods: Twenty-four-hour ambulatory BP monitoring was recorded in 100 hypertensives (50 dippers, 50 non-dippers) and 50 healthy controls. Serum levels of adropin and hsCRP were measured and recorded. Results: A strong correlation was found between night-time BP levels with adropin and hsCRP levels (p &lt; 0.001). On the other hand, the non-dipper group demonstrated lower adropin levels compared to the dipper and normotensive groups: non dipper group, 2580 ± 457 pg/mL; dipper group, 3298 ± 530 pg/mL; normotensive group, 3681 ± 411 pg/mL; p &lt; 0.001). HsCRP levels were significantly higher in the non-dipper group than in the two other groups (p = 0.017). In a multivariate logistic regression analysis, adropin (p = 0.012) and hsCRP (p = 0.039) were independently associated with a non-dipping pattern. Conclusions: Decreased adropin levels were found in the nocturnal hypertensive and non-dipper groups. Adropin and hsCRP were found to be independently associated with a non-dipping pattern. We suggest that decreased levels of adropin in non-dipper hypertensive patients might be associated with a longer duration of exposure to high BP. These results point to a possible future role of adropin in identifying hypertensive patients at higher risk of target organ damage

Association of rs10757274 and rs2383206 Polymorphisms on 9p21 locus with Coronary Artery Disease in Turkish Population

Background and Objectives: Genetic predisposition is an important risk factor for coronary artery disease (CAD). In this study, we aimed to evaluate the impact of rs10757274 and rs2383206 polymorphisms in chromosome 9p21 on presence and severity of CAD in a Turkish population. Subjects and Methods: A total of 646 patients who underwent coronary angiography were included in this study. Coronary vessel score and Gensini score were calculated to assess the angiographic severity of CAD. Alleles of AA, AG, and GG were determined for rs10757274 (polymorphism-1) and rs2383206 (polymorphism-2) polymorphisms located in chromosome 9p21 from the blood samples. Results: There was a significant difference between the alleles in polymorphism-1 in the presence of coronary artery disease (38.9% in AA, 48.0% in GG and 56.4% in AG, p=0.017). However, there was no difference between the alleles in polymorphism-2. According to vessel scores, there was a significant difference between the alleles in polymorphism-1 (AA 0.71 +/- 1.04, GG 0.88 +/- 1.07, AG 1.06 +/- 1.12, p=0.018). In polymorphism-2, vessel scores did not show a difference between the alleles. In polymorphism-1, there was a significant difference in Gensini score (p=0.041). Gensini scores did not differ between the alleles in polymorphism-2 (p>0.05 for all). In multivariate analyses, none of the alleles was an independent factor for presence of CAD. Conclusion: The presence of rs10757274 polymorphism including AG allele in chromosome 9p21 was related to CAD. However, this relationship was not independent of other cardiovascular risk factors