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Anatol J Cardiol: 22 (4)
Volume: 22  Issue: 4 - October 2019
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1.Metabolomics and many more…
Çetin Erol
PMID: 31584439  doi: 10.14744/AnatolJCardiol.2019.10  Page 159
Abstract | Full Text PDF

2.Intravascular ultrasound versus angiography-guided drug-eluting stent implantation in patients with complex coronary lesions: An updated meta-analysis of nine randomized clinical trials
Zhongguo Fan, Mengnan Xu, Yuanyuan Xiao, HuaLing Wang, Bing Xu, Shenghu He
PMID: 31584443  doi: 10.14744/AnatolJCardiol.2019.86598  Pages 160 - 167
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3.Precision medicine: The future of diagnostic approach to pulmonary hypertension?
Piotr Kedzierski, Adam Torbicki
PMID: 31584446  doi: 10.14744/AnatolJCardiol.2019.97820  Pages 168 - 171
Pulmonary hypertension (PH) is a common finding that can result from many different pathological conditions. Depending on the etiology, treatment may be quite different, but early diagnosis and correct classification of PH is difficult. With an aging population and recently suggested decreased pulmonary arterial pressure threshold defining PH, we are facing even more diagnostic uncertainties. A new approach to patients’ phenotyping is needed. Here we present available data and future perspectives on employing an in-depth analysis of the omics cascade to allow an earlier and more reliable diagnosis and classification of PH. Indeed, with the help of super-fast computing, it became possible to simultaneously consider the levels of thousands of potential biomarkers to find patterns specific for clinically suspected disease. The omics cascade is an invaluable source of information. However, while the genome can be perceived as providing possibilities, transcriptome–as carving them this is metabolome that may tell us “what is really going on” in an individual living organism. Metabolomics research requires blinded search for characteristic patterns of discreet changes in the levels of detectable metabolites. Since as many as 40,000 various substances are produced as a “side effect of staying alive”, metabolite profiling can be compared to fishing up for organized signals in a universe of chaos. Although difficult, such search for metabolic patterns that might lead to replacing the term biomarker by metabolic fingerprinting in the area of pulmonary circulation has already begun.

4.The better substitute for tricuspid valve replacement in patients with severe isolated tricuspid regurgitation
Weitao Liang, Honghua Yue, Tao Li, Xiaoli Qin, Yongjun Qian, Zhong Wu
PMID: 31584434  doi: 10.14744/AnatolJCardiol.2019.47381  Pages 172 - 176
Objective: The ideal alternative for tricuspid valve replacement (TVR) in patients with severe isolated tricuspid regurgitation remains unclear. The aim of the present study was to retrospectively investigate the outcomes of using bioprosthetic and mechanical valves at the tricuspid position.
Methods: A total of 98 consecutive patients without left-side cardiac disease or history of heart surgery who underwent first-time TVR between January 2010 and March 2017 at the West China Hospital, China were included in the study. Patient data, including all-cause death and need for tricuspid valve reoperation as the main end points, were retrospectively evaluated.
Results: A total of 76 patients were enrolled into the study. The mean follow-up period was 43.3±21.9 (10–87) months. The mean age of the patients was 45.7±13.4 years. The study comprised 32.9% of male patients. During the follow-up period, 4, 3, 12, and 3 cases of death, reoperation, prosthesis dysfunctions, and prosthesis-related thrombosis were noted, respectively. Biological and mechanical valves were used in 56.6% and 43.4% of the patients, respectively. However, there was no significant difference between mechanical and biological valves with respect to echocardiographic date and survival, reoperation, prosthetic valve dysfunction, and thromboembolism rate.
Conclusion: TVR is not a very high-risk procedure in patients with isolated tricuspid regurgitation, and the decision for prosthesis implantation in TVR should be made on an individual basis according to suitable clinical judgment.

5.Relationship of serum salusin beta levels with coronary slow flow
Aydın Akyüz, Fatma Aydın, Şeref Alpsoy, Demet Ozkaramanli Gur, Savas Guzel
PMID: 31584433  doi: 10.14744/AnatolJCardiol.2019.43247  Pages 177 - 184
Objective: The pathophysiology of coronary slow flow (CSF) has not been clarified. Salusin-β is released predominantly from the atheroma plaques and influences the pathophysiologic processes of atherosclerosis. Therefore, this study aimed to determine serum salusin-β levels in CSF and its correlation with CSF.
Methods: The study included 39 patients with CSF, and the control group (n=42) consisted of consecutive subjects with normal coronary arteriogram. We measured salusin-β and thrombolysis in myocardial infarction frame count (TFC).
Results: Age, body mass index (BMI), systolic blood pressure, diabetes, hyperlipidemia, and smoking rates were similar (p values>0.05) in both groups. High sensitive C-reactive protein (2.80±1.2 vs. 2.21±1.2 mg/dL, p=0.011), salusin-β [1205 (330–2092) vs. 162 (29–676), pg/ml, p<0.001], corrected TFC of left anterior descending coronary artery (29±9 vs. 19.7±3.7, p<0.001), circumflex artery TFC (25±10 vs. 15±3.2, p<0.001), right coronary artery TFC (28±7.1 vs. 13±3.3, p<0.001), and mean TFC (28±4.4 vs. 16±3.7, p<0.001) were significantly higher in the CSF group. In univariate and multivariate regression analysis, only BMI (unstandardized β±SE=0.178±0.08, p=0.036) and salusin-β levels (unstandardized β±SE=0.006±0.01, p<0.001) were determined as predictors of CSF. There was a good correlation between serum salusin-β and mean TFC values (r=0.564; p<0.001).
Conclusion: There is an association between serum salusin-β levels and CSF.

6.Assessment of subclinical atherosclerotic cardiovascular disease in patients with ankylosing spondylitis
Erdinç Hatipsoylu, İlker Şengül, Taciser Kaya, Altınay Göksel Karatepe, Seniz Akçay, Leyla Isayeva, Giray Bozkaya, Erhan Tatar
PMID: 31584431  doi: 10.14744/AnatolJCardiol.2019.13367  Pages 185 - 191
Objective: The aim of the present study was to compare patients with ankylosing spondylitis (AS) with healthy controls with respect to subclinical atherosclerotic cardiovascular disease (CVD).
Methods: A total of 44 patients with AS with no history of CVD, diabetes mellitus, hypertension, chronic kidney disease, and lipid-lowering drug use were compared with 40 age- and sex-matched healthy controls with respect to carotid intima-media thickness (CIMT) and pulse wave velocity (PWV), which are surrogate markers of subclinical atherosclerosis. Correlation analysis was also performed to examine the association between surrogate markers and disease activity with inflammation [Ankylosing spondylitis disease activity score with C-reactive protein (ASDAS-CRP)].
Results: In addition to age and sex, both groups were comparable with respect to cigarette smoking, body mass index, and high-density lipoprotein cholesterol (p=0.425, p=0.325, and p=0.103, respectively). The level of total cholesterol was significantly lower in patients with AS (p=0.002). Nonsteroidal anti-inflammatory drug and tumor necrosis factor alpha inhibitor use ratios in patients with AS were 79.5% and 65.9%, respectively. There was no significant difference between both groups regarding PWV and CIMT (p=0.788 and p=0.253, respectively). In patients with AS, there was a significant correlation between ASDAS-CRP and CIMT (r=0.315, p=0.038), but the correlation between ASDAS-CRP and PWV was not significant (r=−0.183, p=0.234).
Conclusion: The results of the present study could not provide sufficient evidence whether disease activity with inflammation caused subclinical atherosclerotic CVD in patients with AS without overt CVD. The increased atherosclerotic CVD risk is most probably multifactorial in patients with AS, but the extent of the contribution of disease activity with inflammation to increased atherosclerosis is controversial.

7.Subclinical atherosclerosis: A hidden threat for patients with ankylosing spondylitis
Wafa Hamdi, Kaouther Maatallah
PMID: 31584441  doi: 10.14744/AnatolJCardiol.2019.78703  Pages 192 - 193
Abstract | Full Text PDF

8.Frontal QRS-T angle is related with hemodynamic significance of coronary artery stenosis in patients with single vessel disease
Serkan Kahraman, Ali Kemal Kalkan, Ayse Beril Turkyilmaz, Arda Can Dogan, Yalcin Avci, Fatih Uzun, Mehmet Erturk
PMID: 31584447  doi: 10.14744/AnatolJCardiol.2019.99692  Pages 194 - 201
Objective: Fractional flow reserve (FFR) measurement is used to decide the hemodynamic significance of coronary artery lesion. QRS-T angle (QRSTa) is a novel marker of myocardial repolarization abnormality and is affected by obstructive coronary artery disease. The aim of the present study was to evaluate the association between QRSTa and coronary FFR measurement in patients with isolated left anterior descending (LAD) artery stenosis.
Methods: A total of 197 patients undergoing FFR measurement for isolated LAD artery stenosis were retrospectively enrolled in the present study. According to FFR value, patients were divided into two groups as 139 patients with normal FFR (>0.80, group 1) and 58 patients with low FFR (≤0.80, group 2). A 12-lead surface electrocardiography of all subjects that had been recorded before performing coronary angiography was evaluated to measure QRSTa, as well as baseline demographic and clinical variables.
Results: The mean age of group 2 was significantly higher than that of group 1 (61±11 and 64±11, p=0.044). While there were no differences in heart rate, QRS duration, and corrected QT interval between the two groups, QT interval [377 (359–397) and 379 (367–410), p=0.045] and frontal QRSTa [59 (10–120) and 86 (22–132), p<0.001] were higher in group 2. QT interval [odds ratio (OR)=1.046, 95% confidence interval (CI)=1.010–1.084, p=0.012] and frontal QRSTa (OR=1.025, 95% CI=1.010–1.041, p=0.001) were found to be independent predictors of low FFR value in multivariate logistic regression analysis.
Conclusion: In the present study, FFR measurement was demonstrated to be correlated with wide QRSTa as a noninvasive and easy method. Thus, we suggest that the results of FFR measurement as an invasive modality can be previously predicted with a simple electrocardiographic evaluation, such as QRSTa.

9.Mobitz type II, 2: 1 atrioventricular block mimicking as a convulsive seizure
Çağlar Kaya, Utku Zeybey, Meliha Akpınar, Gokay Taylan, Fatih Mehmet Uçar
PMID: 1584444  doi: 10.14744/AnatolJCardiol.2019.88646  Pages 202 - 203
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10.Unusual complication of carotid artery stenting as the result of a proximal emboli protection device (the Mo.Ma): Iatrogenic common carotid artery dissection
Fatih Gungoren, Feyzullah Besli, Zulkif Tanriverdi, Ozcan Kocaturk, Mustafa Begenc Tascanov
PMID: 31584432  doi: 10.14744/AnatolJCardiol.2019.33238  Pages 203 - 206
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11.Mitral valve and right ventricular thrombi possibly caused by heparin-induced thrombocytopenia
Ahmet Güner, Anıl Avcı, Abdulkadir Uslu, Semih Kalkan, Mehmet Özkan
PMID: 31584437  doi: 10.14744/AnatolJCardiol.2019.65712  Pages 206 - 209
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12.Angiogenin and osteopontin and coronary collateral circulation
Joob Beuy, Viroj Wiwanitkit
PMID: 31584435  doi: 10.14744/AnatolJCardiol.2019.53248  Page 210
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13.Author`s Reply
Kadri Murat Gurses, Muhammed Ulvi Yalcin, Duygu Kocyigit
PMID: 31584442  Pages 210 - 211
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14.Methodological problems in the measurement of interleukin-33 concentrations in patients with heart failure with a reduced ejection fraction
Berhan Keskin, İsmail Balaban, Seda Tanyeri, Özgür Yaşar Akbal, Ali Karagöz
PMID: 31584436  doi: 10.14744/AnatolJCardiol.2019.59387  Page 211
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15.Author`s Reply
Oliwia Anna Segiet, Ewa Romuk, Ewa Nowalany- Kozielska, Celina Wojciechowska, Adam Piecuch, Romuald Wojnicz
PMID: 31584445  Page 212
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16.Cangrelor bridging strategy for liver damage after mechanical chest compression
Alberto Francesco Cereda, Nuccia Morici, Paolo Aseni, Osvaldo Chiara
PMID: 31584440  doi: 10.14744/AnatolJCardiol.2019.78546  Pages E8 - E9
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17.Bilateral coronary artery–pulmonary artery fistulas with a giant coronary aneurysm
Qingyu Ji, Ruijuan Han, Kai Sun
PMID: 31584438  doi: 10.14744/AnatolJCardiol.2019.66562  Pages E9 - E10
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