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6. Fabry disease in cardiology: Diagnosis and therapeutic approaches [Kardiyolojide Fabry hastalığı: Tanı ve tedavi yaklaşımları]

Author

Çavuşoğlu, Y., Özpelit, E., Arslan, N., Demir, M., Kahveci, G., Onay, H., and Yıldırım, G.K.

Subjects
Fabry cardiomyopathy, Diagnosis, Therapy
Abstract

Fabry disease is a rare, progressive, X-linked inherited storage disorder due to absent or deficient of lysosomal alfa galactosidase A activity. Deficient activity of alfa-galactosidase A results in progressive accumulation of globotriaosylceramide in a variety of tissues and organs including myocardium, kidney and nerve system. This disorder predominantly affects males; however, female heterozygotes may also be affected with a less severe clinical picture. Classic Fabry disease is usually diagnosed in early age of childhood because of multiorgan involvement whereas cardiac and renal variants of Fabry are manifested in 30-50 years of age because of late onset of clinical picture in which other organs involvement are uncommon. Although Fabry is known as a very rare disease, its prevalence is reported to be higher in patients with ventricular hypertrophy, chronic kidney disease and cryptogenic stroke. From the cardiology point of view, the most important key finding of the disease is unexplained ventricular hypertrophy. However, in clinical practice, ventricular hypertrophy is usually thought to be due to hypertrophic cardiomyopathy in the absence of hypertension or aortic stenosis and Fabry disease is often undiagnosed or overlooked. Early diagnosis and enzyme replacement therapy have been shown to significantly improve prognosis. The aim of this paper is to provide a comprehensive review including epidemiology, prognosis, clinical presentation, diagnosis and therapeutic approaches of cardiac variant of Fabry based on the available data in the literature. © 2020 Türk Kardiyoloji Derneği

Published
2020

7. Turkish Cardiology Association Consensus report: COVID-19 pandemic and cardiovascular diseases (May 13, 2020)

Author

Aytekin, Vedat; Ergönül, Mehmet Önder (ORCID 0000-0003-1935-9235 & YÖK ID 110398); Ural, Dilek (ORCID 0000-0001-6419-0323 & YÖK ID 1057), Aktoz, M.; Altay, H.; Aslanger, E.; Atalar, E.; Atar, İ.; Baykan, A.O.; Barçın, C.; Barış, N.; Boyacı, A.; Çavuşoğlu, Y.; Çelik, A.; Çinier, G.; Değertekin, M.; Demircan, S.; Ertürk, M.; Erol, M.K.; Görenek, B.; Gürsoy, M.O.; Hünük, B.; Kahveci, G.; Karabay, C.Y.; Karaca, I.; Kayıkçıoğlu, M.; Keskin, M.; Kılıç, T.; KılıçkıranAvcı, B.; Kırma, C.; Kocabaş, U.; Kocakaya, D.; Küçükoğlu, S.; Mutlu, B.; Nalbantgil, S.; Okuyan, E.; Okyay, K.; KaptanÖzen, D.; Özgül, S.; Özpelit, E.; Pirat, B.; Sert, S.; Sinan, Ü.Y.; Şener, Y.Z.; Tatlı, E.; Tekkeşin, A.İ.; Tutar, E.; Yıldırımtürk, Ö.; Yıldızeli, B., School of Medicine, Aytekin, Vedat; Ergönül, Mehmet Önder (ORCID 0000-0003-1935-9235 & YÖK ID 110398); Ural, Dilek (ORCID 0000-0001-6419-0323 & YÖK ID 1057), Aktoz, M.; Altay, H.; Aslanger, E.; Atalar, E.; Atar, İ.; Baykan, A.O.; Barçın, C.; Barış, N.; Boyacı, A.; Çavuşoğlu, Y.; Çelik, A.; Çinier, G.; Değertekin, M.; Demircan, S.; Ertürk, M.; Erol, M.K.; Görenek, B.; Gürsoy, M.O.; Hünük, B.; Kahveci, G.; Karabay, C.Y.; Karaca, I.; Kayıkçıoğlu, M.; Keskin, M.; Kılıç, T.; KılıçkıranAvcı, B.; Kırma, C.; Kocabaş, U.; Kocakaya, D.; Küçükoğlu, S.; Mutlu, B.; Nalbantgil, S.; Okuyan, E.; Okyay, K.; KaptanÖzen, D.; Özgül, S.; Özpelit, E.; Pirat, B.; Sert, S.; Sinan, Ü.Y.; Şener, Y.Z.; Tatlı, E.; Tekkeşin, A.İ.; Tutar, E.; Yıldırımtürk, Ö.; Yıldızeli, B., and School of Medicine

Abstract

In December 2019, in the city of Wuhan, in the Hubei province of China, treatment-resistant cases of pneumonia emerged and spread rapidly for reasons unknown. A new strain of coronavirus (severe acute respiratory syndrome coronavirus-2 [SARS-CoV-2]) was identified and caused the first pandemic of the 21st century. The virus was officially detected in our country on March 11, 2020, and the number of cases increased rapidly; the virus was isolated in 670 patients within 10 days. The rapid increase in the number of patients has required our physicians to learn to protect both the public and themselves when treating patients with this highly infectious disease. The group most affected by the outbreak and with the highest mortality rate is elderly patients with known cardiovascular disease. Therefore, it is necessary for cardiology specialists to take an active role in combating the epidemic. The aim of this article is to make a brief assessment of current information regarding the management of cardiovascular patients affected by COVID-19 and to provide practical suggestions to cardiology specialists about problems and questions they have frequently encountered. / Aralık 2019’da, Çin’in Hubei eyaletindeki Wuhan şehrinde, nedeni bilinmeyen, tedaviye dirençli pnömoni olguları ile ortaya çıkan ve devamında hızla yayılarak XXI. yüzyılın ilk pandemisine neden olan yeni koronavirüsün (severe acute respiratory syndrome koranavirüs-2 [SARS-CoV-2]) 11 Mart 2020 tarihinde ülkemizde de resmi olarak saptanmasının ardından olgu sayısı hızla artmış ve 10 gün içerisinde 670 hastada virüs izole edilmiştir. Hasta sayısındaki hızlı artış, hekimlerimizin bir yandan etkilenen hastalara müdahale ederken diğer yandan toplumu ve kendilerini korumayı öğrenmelerini gerektirmektedir. Salgından en çok etkilenen ve ölüm oranı en yüksek seyreden grup, bilinen kalp ve damar hastalıkları olan yaşlılardır. Bu nedenle, kardiyoloji uzmanlarının salgınla mücadelede aktif görev almaları kaçınılmazdır. Bu, NA

Published
2020

16. Determinants of high sensitivity troponin T concentration in chronic stable patients with heart failure: Ischemic heart failure versus non-ischemic dilated cardiomyopathy

Author

Bakal, R.B., Hatipoglu, S., Kahveci, G., Omaygenc, M.O., Unkun, T., Akgun, T., Ozdemir, N., Bakal, R.B., Hatipoglu, S., Kahveci, G., Omaygenc, M.O., Unkun, T., Akgun, T., Ozdemir, N., and Yeditepe Üniversitesi

Subjects
Echocardiography, Myocardial mechanics, cardiovascular system, Heart failure, High sensitivity troponin T, cardiovascular diseases
Abstract

Background: Cardiac troponin T is a marker of myocardial injury, especially when measured by means of the high-sensitivity assay (hs-cTnT). The echocardiographic and clinical predictors of hs-cTnT may be different in ischemic heart failure (IHF) and non-ischemic dilated cardiomyopathy (DCM). Methods: Sixty consecutive patients (19 female, 41 male; mean age 56.3 ± 13.9 years) with stable congestive heart failure (33 patient with IHF and 27 patients with DCM), with New York Heart Association functional class I-II symptoms, and left ventricular ejection fraction < 40% were included. Results: In patients with IHF peak early mitral inflow velocity (E), E/peak early diastolic mitral annular tissue Doppler velocity (Em) lateral, peak systolic mitral annular tissue Doppler velocity (Sm) lateral and logBNP were univariate predictors of hs-cTnT above median. But only E/Em lateral was an independent predictor of hs-cTnT above median (p = 0.04, HR: 1.2, CI: 1-1.4). In patients with DCM; left atrial volume index, male sex, Sm lateral and global longitudinal strain (LV-GLS) were included in multivariate model and LV-GLS was detected to be an independent predictor for hs-cTnT above median (p < 0.05, HR: 0.7, CI: 0.4-1.0). Conclusions: While LV-GLS is an independent predictor of hs-cTnT concentrations in patients with DCM, E/Em lateral predicted hs-TnT concentrations in patients with IHF. © 2014 Via Medica.

Published
2014

17. P1088Match and mismatch between opening area and resistance in mild and moderate rheumatic mitral stenosisP1089When should cardiovascular magnetic resonance imaging be considered in patients with chronic aortic or mitral regurgitation?P1090Echocardiographic characteristics of aortic valve fenestration with aortic regurgitation for aortic valve repairP1091Aortic regurgitation assessment by 3D transesophageal echocardiography vena contracta area: usefulness and comparison with 2D methods.P1092Characterising cardiomyopathy in mitral regurgitation due to barlow disease: role of CMRP1093Compensatory peripheral increase in artero-venous o2 difference to severe functional mitral regurgitation in heart failureP1094Prognostic impact of concomitant atrioventricular valve regurgitation in patients undergoing transcatheter aortic valve implantationP1095Morphological characterization of vegetations by real-time three-dimensional transesophageal echocardiography in infective endocarditis: prognostic impactP1096Relation between causative pathogen and echocardiographic findings in patients with infective endocarditis: is there an association and is it clinically relevant?P1097Aortic and mitral valve infective endocarditis: different clinical and echocardiographic features and peculiar complication ratesP1098Vegetation size relevance and impact on prognosis in patients with infective endocarditisP1099Causes of death on the valvular heart disease surveillance list- a 5 year auditP1100Left ventricular non-compaction and idiopathic dilated cardiomyopathy: the significant diagnostic value of longitudinal strainP1101The role of echocardiography in the management of diuretics withdrawal in patients with chronic heart failure and severely reduced ejection fraction: a prospective cohort studyP1102Outcomes in paediatric new onset left ventricle dysfunction and dilatation: differences between post-myocarditis and DCMP1103De novo mitral regurgitation as a cause of heart failure exacerbation in hypertrophic cardiomyopathyP1104Correlation of conventional and new echocardiograhic parameters with sudden cardiac death risk score in patients with hypertrophic cardiomyopathyP1105Inverse correlation between myocardial fibrosis and left ventricular function in rheumatic mitral stenosis: a preliminary study with cardiac magnetic resonanceP1106Left ventricular diastolic dysfunction and cardiac sympathetic derangement in patients with Anderson-Fabry disease: a 2D speckle tracking echocardiography and cardiac 123I-MIBG studyP1107Left ventricular hypertrophy and mild cognitive impairment as markers for target organ damage in hypertensive patients with multiple risk factorsP1108Subclinical left ventricular dysfunction in asymptomatic type 1 diabetic childrenP1109Minimal differences shown by echocardiography and NT-proBNP level distinguishing cardiotoxic effect related to breast cancer therapy in patients with or without HER2 expression.P1110Speed of recovery of left ventricular function is not related to the prognosis of takotsubo cardiomyopathy - a portuguese multicenter studyP1111Myocardial dysfunction in Takotsubo cardiomyopathy - more than meets the eye?P1112Obstructive sleep apnea and echocardiographic parameters

Author

El-Dosouky, I., primary, Polte, CL., primary, Okubo, T., primary, Gonzalez Gomez, A., primary, Liu, B., primary, Generati, G., primary, Drakopoulou, M., primary, Olmos, C., primary, Trifunovic, D., primary, Ilhao Moreira, R., primary, Morgan, HP., primary, Bosseau, C., primary, Romano, G., primary, Argiolas, A., primary, Kuperstein, R., primary, Koyuncu, A., primary, Sahara, E., primary, Spinelli, L., primary, Yaneva-Sirakova, T., primary, Ben Said, R., primary, Nowakowska, MA., primary, Ruivo, C., primary, Neves Pestana, G., primary, Wiligorska, N., primary, Gao, SA., additional, Lagerstrand, KM., additional, Johnsson, ÅA, additional, Bech-Hanssen, O., additional, Mahara, K., additional, Yamamoto, H., additional, Shitan, H., additional, Abe, K., additional, Terada, M., additional, Saito, M., additional, Nagatomo, Y., additional, Takanashi, S., additional, Del Val, D., additional, Monteagudo, JM., additional, Fernandez-Golfin, C., additional, Hinojar, R., additional, Garcia, A., additional, Marco, A., additional, Casas, E., additional, Jimenez-Nacher, JJ., additional, Zamorano, JL., additional, Baig, S., additional, Hayer, M., additional, Edwards, N., additional, Steeds, R., additional, Bandera, F., additional, Alfonzetti, E., additional, Guazzi, M., additional, Toutouzas, K., additional, Stathogiannis, K., additional, Michelongona, A., additional, Latsios, G., additional, Synetos, A., additional, Lazaros, G., additional, Brili, S., additional, Tsiamis, E., additional, Tousoulis, D., additional, Islas, F., additional, Ferrera, C., additional, Sanchez-Enrique, C., additional, Freitas-Ferraz, A., additional, Mahia, P., additional, Marcos-Alberca, P., additional, Tirado, G., additional, Perez De Isla, L., additional, Vilacosta, I., additional, Marinkovic, J., additional, Obrenovic- Kircanski, B., additional, Ivanovic, B., additional, Kalimanovska-Ostric, D., additional, Stevanovic, G., additional, Petrovic, M., additional, Boricic-Kostic, M., additional, Petrovic, O., additional, Tutos, V., additional, Petrovic, I., additional, Petrovic, J., additional, Draganic, G., additional, Stepanovic, J., additional, Vujisic-Tesic, B., additional, Coutinho Cruz, M., additional, Moura Branco, L., additional, Galrinho, A., additional, Coutinho Miranda, L., additional, Almeida Morais, L., additional, Modas Daniel, P., additional, Rodrigues, I., additional, Fragata, J., additional, Cruz Ferreira, R., additional, Timoteo, AT., additional, Viveiros Monteiro, S., additional, Aguiar Rosa, S., additional, Nana, M., additional, Constantin, C., additional, Tarando, F., additional, Galli, E., additional, Rousseau, C., additional, Hubert, A., additional, Leclercq, C., additional, Donal, E., additional, Vitale, G., additional, Agnese, V., additional, Mina', C., additional, Magro, S., additional, Falletta, C., additional, Di Gesaro, G., additional, Bellavia, D., additional, Clemenza, F., additional, Elena Reffo, ER., additional, Ornella Milanesi, OM., additional, Klempfner, R., additional, Ben-Zekry, S., additional, Maor, E., additional, Raanani, E., additional, Ofek, E., additional, Freimark, D., additional, Arad, M., additional, Oflar, E., additional, Ciftci, S., additional, Ungan, I., additional, Caglar, FM., additional, Ocal, L., additional, Kilicgedik, A., additional, Toprak, C., additional, Kahveci, G., additional, Atmadikoesoemah, C., additional, Kasim, M., additional, Pellegrino, T., additional, Pisani, A., additional, Giudice, CA., additional, Riccio, E., additional, Imbriaco, M., additional, Cuocolo, A., additional, Trimarco, B., additional, Tarnovska-Kadreva, R., additional, Traykov, L., additional, Vassilev, D., additional, Vladimirova, L., additional, Shumkova, M., additional, Gruev, I., additional, Zairi, I., additional, Mzoughi, K., additional, Ben Moussa, F., additional, Kammoun, S., additional, Fennira, S., additional, Kraiem, S., additional, Chrzanowski, L., additional, Frynas-Jonczyk, K., additional, Wdowiak-Okrojek, K., additional, Wejner-Mik, P., additional, Lipiec, P., additional, Krakowska, M., additional, Potemski, P., additional, Plonska-Gosciniak, E., additional, Kasprzak, JD., additional, Marques, N., additional, Domingues, K., additional, Lourenco, C., additional, Santos, R., additional, Gomes, C., additional, Abreu, L., additional, Reis, L., additional, Moz, M., additional, Azevedo, O., additional, Tavares-Silva, M., additional, Sousa, C., additional, Pinto, R., additional, Ribeiro, V., additional, Vasconcelos, M., additional, Bernardo-Almeida, P., additional, Macedo, F., additional, Maciel, MJ., additional, Wiligorska, D., additional, Talarowska, P., additional, Segiet, A., additional, Mozenska, O., additional, and Kosior, DA., additional

Published
2016
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18. Extent of left ventricular hypertrophy is related to interatrial conduction delay in hypertensive patients

Author

Bakal, R.B., Hatipoglu, S., Kahveci, G., Omaygenc, M.O., Dogan, C., Izgi, C., Ozdemir, N., Bakal, R.B., Hatipoglu, S., Kahveci, G., Omaygenc, M.O., Dogan, C., Izgi, C., Ozdemir, N., and Yeditepe Üniversitesi

Subjects
Interatrial conduction delay, Hypertension, cardiovascular system, Left ventricular hypertrophy, cardiovascular diseases, Atrial fibrillation, Left ventricular mass
Abstract

The aim of this study was to investigate the relationship between left ventricular mass (LVM) and interatrial conduction delay (CD) measured by tissue Doppler echocardiography. In enrolled 66 hypertensive patients, positive correlation between interatrial CD and LVM index (r = 0.32) was detected. Meanwhile, intra-atrial CD was correlated to early diastolic tissue Doppler mitral annular velocity measured from septum (r = 0.34), tricuspid annular velocity (r = 0.29), and left atrial volume index (r = 0.26). By using stepwise linear regression analysis, LVM index was determined as an independent predictor of interatrial CD. © 2013 Informa Healthcare USA, Inc.

Published
2013

20. Enfektif endokarditli hastalarda D-dimer düzeyinin sistemik emboliyle ilişkisi

Author

Bakal, R.B., Karakoyun, S., Kahveci, G., Özveren, O., Omaygenç, O., Akpinar, S.H., Özdemir, N., Bakal, R.B., Karakoyun, S., Kahveci, G., Özveren, O., Omaygenç, O., Akpinar, S.H., Özdemir, N., and Yeditepe Üniversitesi

Subjects
Endocarditis, D-dimer, Embolism/blood, Bacterial/etiology/therapy, Blood coagulation
Abstract

Objectives: The aim of this study was to investigate the value of plasma D-dimer (DD) levels for predicting systemic embolism in patients with infective endocarditis (IE). Study design: A total of 42 patients (mean age: 46±16 years; 78% males) with IE were included. Clinical, laboratory and echocardiographic fndings of the patients were evaluated. Results: Increased plasma DD levels were determined in 13 patients with systemic embolism (p=0.016). Moreover, when patients were divided in two groups as DD >500 ng/dl and DD 500 ng/dl group (p=0.036). Receiver operating characteristics (ROC) curve analysis was performed to detect the best cut-off value of DD in the prediction of systemic embolism. DD >425 ng/dl yielded an area under the curve (AUC) value of 0.735 (95% CI 0.560-0.909, p=0.016). DD >425 ng/dl demonstrated a sensitivity of 77% and specifcity of 62% for the prediction of clinical embolism. Hematocrit (r=-0.31, p=0.045), platelet count (r=-0.40, p=0.009), albumin (r=-0.37, p=0.026), and globulin (r=0.38, p=0.028) levels were correlated with DD levels. Conclusion: Plasma DD levels are increased in patients with IE who suffered from clinically signifcant systemic embolism. Further studies are needed to determine the predictive value of DD levels for clinically silent systemic embolism. © 2013 Türk Kardiyoloji Dernegi.

Published
2013

21. Impact of bicuspid aortic valve on complications and death in infective endocarditis of native aortic valves

Author

Kahveci, G., Bayrak, F., Pala, S., Mutlu, B., Kahveci, G., Bayrak, F., Pala, S., Mutlu, B., and Yeditepe Üniversitesi

Subjects
Retrospective studies, congenital, hereditary, and neonatal diseases and abnormalities, Aortic valve/abnormalities/pathology/ultrasonography, Endocarditis, bacterial/complications/mortality/pathology/ultrasonography, Risk factors, Hospital mortality, cardiovascular system, Aortic valve insufficiency/classification/diagnosis, Heart diseases/complications, Heart defects/congenital, cardiovascular diseases, Heart valve diseases/ classification/complications/congenital/pathology, Echocardiography/methods
Abstract

We retrospectively investigated the impact of bicuspid aortic valve on the prognosis of patients who had definite infective endocarditis of the native aortic valve. Of 51 patients, a bicuspid aortic valve was present in 22 (43%); the other 29 had tricuspid aortic valves. On average, the patients who had bicuspid valves were younger than those who had tricuspid valves. Patients with a tricuspid valve had larger left atrial diameters and were more likely to have severe mitral regurgitation. Periannular complications, which we detected in 19 patients (37%), were much more common in the patients who had a bicuspid valve (64% vs 17%, P=0.001). The presence of a bicuspid valve was the only significant independent predictor of periannular complications. The in-hospital mortality rate in the bicuspid group was lower than that in the tricuspid group; however, this figure did not reach statistical significance (9% vs 24%, P=0.15). In multivariate analysis, left atrial diameter was the only independent predictor associated with an increased risk of death (hazard ratio, 2.19; 95% confidence interval, 1.1-4.5; P=0.031). In our study, patients with infective endocarditis in a bicuspid aortic valve were younger and had a higher incidence of periannular complications. Although a worse prognosis has been reported previously, we found that infective endocarditis in a native bicuspid aortic valve is not likely to increase the risk of death in comparison with infective endocarditis in native tricuspid aortic valves. © 2009 by the Texas Heart® Institute.

Published
2009

22. Importance of left atrial size in predicting adverse clinical events in hypertrophic cardiomyopathy

Author

Kahveci, G., Bayrak, F., Mutlu, B., Başaran, Y., Kahveci, G., Bayrak, F., Mutlu, B., Başaran, Y., and Yeditepe Üniversitesi

Subjects
Atrial function, left, Risk factors, Echocardiography, Heart atria, cardiovascular system, cardiovascular diseases, Prognosis, Cardiomyopathy, hypertrophic
Abstract

Objectives: This study sought to investigate the role of left atrial diameter in predicting adverse clinical events in patients with hypertrophic cardiomyopathy (HCM). Study design: The study prospectively included 83 consecutive patients (45 males, 38 females; mean age 47±17 years) with HCM. Admission transthoracic echocardiograms were obtained. Left atrial diameter was measured at end-systole from the parasternal long-axis view and left atrial diameter index (LADI) was derived (left atrial diameter/body surface area). Clinical endpoints were defined as cardiovascular death and/or worsening heart failure symptoms. The mean follow-up period was 622±366 days (range 14 to 1142 days). Results: Adverse clinical events were seen in 27 patients (32.5%), including two deaths and deterioration in NYHA functional class (n=25). Based on the median LADI of 2.5 cm/m 2, patients whose LADI was ?2.5 cm/m 2 had a higher value of log NT-proBNP, increased maximal wall thickness, and higher rates of adverse events, advanced NYHA functional class, significant mitral regurgitation, and left ventricular outflow tract obstruction. In ROC analysis, the cutoff value of 2.2 cm/m 2 for LADI predicted adverse events with 89% sensitivity, 34% specificity, 84% negative and 38% positive predictive values. Kaplan-Meier analysis showed that patients with LADI

Published
2008

23. Prognostic Value of N-Terminal Pro-B-Type Natriuretic Peptide in Patients With Active Infective Endocarditis

Author

Kahveci, G., Bayrak, F., Mutlu, B., Bitigen, A., Karaahmet, T., Sonmez, K., Basaran, Y., Kahveci, G., Bayrak, F., Mutlu, B., Bitigen, A., Karaahmet, T., Sonmez, K., Basaran, Y., and Yeditepe Üniversitesi

Subjects
cardiovascular system, cardiovascular diseases
Abstract

Our aim was to determine whether N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) and cardiac troponin I (cTnI) levels are valuable for predicting prognosis in patients with infective endocarditis (IE). We analyzed measured plasma NT-pro-BNP levels at admission in 45 patients with definite IE. The primary end point was early surgery or in-hospital death. The other data recorded were baseline clinical, echocardiographic, and laboratory parameters. Thirty patients underwent early surgery, and 9 died in hospital. Univariate analysis revealed that log NT-pro-BNP, cTnI ?0.03 ng/ml, New York Heart Association functional class III to IV symptoms, left atrial diameter, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and severe valvular regurgitation were associated with increased risk of reaching the primary end point. Cox proportional hazard regression analysis identified log NT-pro-BNP (hazard ratio 1.5; 95% confidence interval 1.2 to 1.9, p

Published
2007

27. Oral Abstract session * Imaging in structural interventions: 13/12/2013, 08:30-10:00 * Location: Bursa

Author

Kalcik, M., primary, Gursoy, M., additional, Astarcioglu, M., additional, Gokdeniz, T., additional, Karakoyun, S., additional, Cakal, B., additional, Yesin, M., additional, Kahveci, G., additional, Yildiz, M., additional, Ozkan, M., additional, Cresti, A., additional, Cesareo, F., additional, Guerrini, F., additional, Capati, E., additional, Miracapillo, G., additional, Severi, S., additional, Ternacle, J., additional, Lellouche, N., additional, Gallet, R., additional, Deux, J.-F., additional, Dubois-Rande, J.-L., additional, Teiger, E., additional, Lim, P., additional, Polizzi, V., additional, Pino, P., additional, Luzi, G., additional, Fiorilli, R., additional, Buffa, V., additional, Visconti, C., additional, Bellavia, D., additional, Violini, R., additional, Musumeci, F., additional, Saura Espin, D., additional, Oliva Sandoval, M., additional, Gonzalez Carrillo, J., additional, Caballero Jimenez, L., additional, Espinosa Garcia, M., additional, Garcia Navarro, M., additional, Lopez Ruiz, M., additional, Valdes Chavarri, M., additional, and De La Morena Valenzuela, G., additional

Published
2013
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30. Prosthetic meCHAnical mitral ring clot: clinical implication of utility of Serial real time three dimensional transesophageal Echocardiography in the evaluation of THRombus evolution (CHASE-THR trial)

Author

Gursoy, M. O., primary, Karakoyun, S., additional, Kalcik, M., additional, Bayram, Z., additional, Cakal, B., additional, Yesin, M., additional, Kahveci, G., additional, Eksi Duran, N., additional, Yildiz, M., additional, and Ozkan, M., additional

Published
2013
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33. Poster Session: Right ventricular systolic function

Author

Altman, M., primary, Bergerot, C., additional, Thibault, H., additional, Aussoleil, A., additional, Skuldadt Davidsen, E., additional, Barthelet, M., additional, Derumeaux, G. A., additional, Grapsa, J., additional, Zimbarra Cabrita, I., additional, Afilalo, J., additional, Paschou, S., additional, Dawson, D., additional, Durighel, G., additional, O'regan, D., additional, Howard, L., additional, Gibbs, J., additional, Nihoyannopoulos, P., additional, Morenate Navio, M., additional, Mesa Rubio, M., additional, Ortega, M. D., additional, Ruiz Ortiz, M., additional, Castillo Bernal, F., additional, Del Pino, C. L., additional, Toledano, F., additional, Alvarez-Ossorio, M. P., additional, Ojeda Pineda, S., additional, Lezo Cruz-Conde, J. S. D., additional, Jasaityte, R., additional, Claus, P., additional, Teske, A., additional, Herbots, L., additional, Verheyden, B., additional, Rademakers, F., additional, D'hooge, J., additional, Tocchetti, C. G., additional, Coppola, C., additional, Rea, D., additional, Quintavalle, C., additional, Guarino, L., additional, Castaldo, N., additional, De Lorenzo, C., additional, Condorelli, G., additional, Arra, C., additional, Maurea, N., additional, Voilliot, D., additional, Huttin, O., additional, Camara, Y., additional, Djaballah, W., additional, Carillo, S., additional, Zinzius, P., additional, Sellal, J., additional, Angioi, M., additional, Juilliere, Y., additional, Selton-Suty, C., additional, Dobrowolski, P., additional, Klisiewicz, A., additional, Florczak, E., additional, Prejbisz, A., additional, Szwench, E., additional, Rybicka, J., additional, Januszewicz, A., additional, Hoffman, P., additional, Jurado Roman, A., additional, De Dios Perez, S., additional, De Nicolas, J. M. M., additional, Diaz Anton, B., additional, Rubio Alonso, B., additional, Martin Asenjo, R., additional, Mayordomo Gomez, S., additional, Villagraz Tecedor, L., additional, Blazquez, L., additional, De Meneses, R. T., additional, Bernard, A., additional, Hernandez, A. 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additional, Unger, P., additional, Mornos, C., additional, Cozma, D., additional, Ionac, A., additional, Mornos, A., additional, Valcovici, M., additional, Pescariu, S., additional, Petrescu, L., additional, Hu, K., additional, Liu, D., additional, Niemann, M., additional, Herrmann, S., additional, Cikes, M., additional, Stoerk, S., additional, Knop, S., additional, Ertl, G., additional, Bijnens, B., additional, Weidemann, F., additional, De Knegt, M., additional, Biering-Sorensen, T., additional, Sogaard, P., additional, Sivertsen, J., additional, Jensen, J., additional, Mogelvang, R., additional, Lam, W., additional, Tang, M., additional, Chan, K., additional, Yang, Y., additional, Fang, F., additional, Sun, J., additional, Yu, C., additional, Lam, Y., additional, Panoulas, V., additional, Sulemane, S., additional, Bratsas, A., additional, Konstantinou, K., additional, Francone, M., additional, Schau, T., additional, Seifert, M., additional, Ridjab, D., additional, Schoep, M., 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additional, Van Camp, G., additional, and Cosyns, B., additional

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2012
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34. Poster Session 1: Thursday 8 December 2011, 08:30-12:30 * Location: Poster Area

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Vijayan, S., primary, Khanji, M., additional, Ionescu, A., additional, Vijayan, S., additional, Podoleanu, C., additional, Frigy, A., additional, Ugri, A., additional, Varga, A., additional, Podoleanu, D., additional, Incze, A., additional, Carasca, E., additional, Dobreanu, D., additional, Mjolstad, O., additional, Dalen, H., additional, Graven, T., additional, Kleinau, J., additional, Hagen, B., additional, Fu, H., additional, Liu, T., additional, Li, J., additional, Liu, C., additional, Zhou, C., additional, Li, G., additional, Bordese, R., additional, Capriolo, M., additional, Brero, D., additional, Salvetti, I., additional, Cannillo, M., additional, Antolini, M., additional, Grosso Marra, W., additional, Frea, S., additional, Morello, M., additional, Gaita, F., additional, Maffessanti, F., additional, Caiani, E., additional, Muraru, D., additional, Tuveri, F., additional, Dal Bianco, L., additional, Badano, L., additional, Majid, A., additional, Soesanto, A., additional, Ario Suryo Kuncoro, B., additional, Sukmawan, R., additional, Ganesja, M. H., additional, Benedek, T., additional, Chitu, M., additional, Beata, J., additional, Suciu, Z., additional, Kovacs, I., additional, Bucur, O., additional, Benedek, I., additional, Hrynkiewicz-Szymanska, A., additional, Szymanski, F., additional, Karpinski, G., additional, Filipiak, K., additional, Radunovic, Z., additional, Lande Wekre, L., additional, Steine, K., additional, Bech-Hanssen, O., additional, Rundqvist, B., additional, Lindgren, F., additional, Selimovic, N., additional, Jedrzychowska-Baraniak, J., additional, Jozwa, R., additional, Larysz, B., additional, Kasprzak, J., additional, Ripp, T., additional, Mordovin, V., additional, Ripp, E., additional, Ciobanu, A., additional, Dulgheru, R., additional, Dragoi, R., additional, Magda, S., additional, Florescu, M., additional, Mihaila, S., additional, Rimbas, R., additional, Cinteza, M., additional, Vinereanu, D., additional, Benavides-Vallve, C., additional, Pelacho, B., additional, Iglesias, O., additional, Castano, S., additional, Munoz-Barrutia, A., additional, Prosper, F., additional, Ortiz De Solorzano, C., additional, Manouras, A., additional, Sahlen, A., additional, Winter, R., additional, Vardas, P., additional, Brodin, L., additional, Sarvari, S. I., additional, Haugaa, K. H., additional, Zahid, W., additional, Bendz, B., additional, Aaberge, L., additional, Edvardsen, T., additional, Di Bella, G., additional, Pedri, S., additional, Donato, R., additional, Madaffari, A., additional, Zito, C., additional, Stapf, D., additional, Schreckenberg, M., additional, Carerj, S., additional, Yoshikawa, H., additional, Suzuki, M., additional, Kusunose, Y., additional, Hashimoto, G., additional, Otsuka, T., additional, Nakamura, M., additional, Sugi, K., additional, Grapsa, J., additional, Dawson, D., additional, Gin-Sing, W., additional, Howard, L., additional, Gibbs, J., additional, Nihoyannopoulos, P., additional, Smith, B., additional, Coulter, T., additional, Rendon, A., additional, Gorissen, W., additional, Shiran, A., additional, Asmer, I., additional, Adawi, S., additional, Ganaeem, M., additional, Shehadeh, J., additional, Cameli, M., additional, Lisi, M., additional, Righini, F., additional, Maccherini, M., additional, Sani, G., additional, Galderisi, M., additional, Mondillo, S., additional, Kalimanovska-Ostric, D., additional, Nastasovic, T., additional, Jovanovic, I., additional, Milakovic, B., additional, Dostanic, M., additional, Stosic, M., additional, Sasic, I., additional, Sveen, K., additional, Nerdrum, T., additional, Hanssen, K., additional, Dahl-Jorgensen, K., additional, Holte, E., additional, Vegsundvaag, J., additional, Hole, T., additional, Hegbom, K., additional, Wiseth, R., additional, Ikonomidis, I., additional, Lekakis, J., additional, Tritakis, V., additional, Papadakis, I., additional, Kadoglou, N., additional, Tzortzis, S., additional, Trivilou, P., additional, Koukoulis, C., additional, Paraskevaidis, I., additional, Anastasiou-Nana, M., additional, Smedsrud, M. 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D., additional, Lee, J., additional, Shin, S., additional, Woo, S., additional, Kim, D., additional, Park, K., additional, Kwan, J., additional, Tsang, W., additional, Chandra, S., additional, Weinert, L., additional, Gayat, E., additional, Djelassi, M., additional, Balbach, T., additional, Mor-Avi, V., additional, Lang, R., additional, De Meester, P., additional, Van De Bruaene, A., additional, Delcroix, M., additional, Budts, W., additional, Abid, L., additional, Frikha, Z., additional, Makni, K., additional, Rekik, H., additional, Znazen, A., additional, Mourad, H., additional, Kammoun, S., additional, Sargento, L., additional, Satendra, M., additional, Sousa, C., additional, Lopes, S., additional, Longo, S., additional, Lousada, N., additional, Palma Reis, R., additional, Fouad, D., additional, Shams Eldeen, R., additional, Beladan, C., additional, Calin, A., additional, Voinea, F., additional, Enache, R., additional, Jurcut, R., additional, Coman, I., additional, Ghionea, M., additional, Djordjevic-Dikic, A., additional, Petrovic, O., additional, Boricic, M., additional, Giga, V., additional, Pisciella, L., additional, Lanzillo, C., additional, Minati, M., additional, Caselli, S., additional, Di Roma, M., additional, Fratini, S., additional, Romano, S., additional, Calo', L., additional, Lioy, E., additional, Penco, M., additional, Finocchiaro, G., additional, Pinamonti, B., additional, Merlo, M., additional, Barbati, G., additional, Sinagra, G., additional, Dilenarda, A., additional, Comenale Pinto, S., additional, Ancona, R., additional, Caso, P., additional, Cavallaro, C., additional, Vecchione, F., additional, D'onofrio, A., additional, Fero', M., additional, Calabro', R., additional, Gustafsson, S., additional, Ihse, E., additional, Henein, M., additional, Westermark, P., additional, Suhr, O., additional, Lindqvist, P., additional, Oliva Sandoval, M., additional, Gonzalez Carrillo, M., additional, Garcia Navarro, M., additional, Garcia-Molina Saez, E., additional, Sabater Molina, M., additional, Saura Espin, D., additional, Lacunza Ruiz, J., additional, Gimeno Blanes, J., additional, De La Morena Valenzuela, G., additional, Valdes Chavarri, M., additional, Prinz, C., additional, Faber, L., additional, Horstkotte, D., additional, Hoetz, H., additional, Voigt, J., additional, Gandara, F., additional, Correia, M., additional, Rosario, I., additional, Fonseca, C., additional, Arroja, I., additional, Aleixo, A., additional, Martins, A., additional, Radulescu, L., additional, Dan Radulescu, D., additional, Parv Andreea, P., additional, Duncea Caius, D., additional, Ciuleanu T, C., additional, Mitrea Paulina, M., additional, Cali Quaglia, F., additional, Ribezzo, M., additional, Boffini, M., additional, Rinaldi, M., additional, Maceira Gonzalez, A. M., additional, Cosin-Sales, J., additional, Dalli, E., additional, Diago, J., additional, Aguilar, J., additional, Ruvira, J., additional, Goncalves, S., additional, Gomes, A., additional, Pinto, F., additional, Tsai, W.-C., additional, Liu, Y.-W., additional, Shih, J.-Y., additional, Huang, Y.-Y., additional, Chen, J.-Y., additional, Tsai, L.-M., additional, Chen, J.-H., additional, Ribeiro, S., additional, Doroteia, D., additional, Santos, L., additional, David, C., additional, Vinhas De Sousa, G., additional, Almeida, A., additional, Iwase, M., additional, Itou, Y., additional, Yasukochi, S., additional, Shiino, K., additional, Inuzuka, H., additional, Sugimoto, K., additional, Ozaki, Y., additional, Gieszczyk-Strozik, K., additional, Sikora-Puz, A., additional, Mizia, M., additional, Lasota, B., additional, Chmiel, A., additional, Lis-Swiety, A., additional, Michna, J., additional, Brzezinska-Wcislo, L., additional, Mizia-Stec, K., additional, Gasior, Z., additional, Luijendijk, P., additional, De Bruin-Bon, H., additional, Zwiers, C., additional, Vriend, J., additional, Van Den Brink, R., additional, Mulder, B., additional, Bouma, B., additional, Brigido, S., additional, Gianfagna, P., additional, Proclemer, A., additional, Plicht, B., additional, Kahlert, P., additional, Kaelsch, H., additional, Buck, T., additional, Erbel, R., additional, Konorza, T., additional, Yoon, H., additional, Kim, K., additional, Ahn, Y., additional, Jeong, M., additional, Cho, J., additional, Park, J., additional, Kang, J., additional, Rha, W., additional, Jansen Klomp, W. W., additional, Brandon Bravo Bruinsma, G., additional, Van 'T Hof, A., additional, Spanjersberg, S., additional, Nierich, A., additional, Bombardini, T., additional, Gherardi, S., additional, Picano, E., additional, Ciarka, A., additional, Herbots, L., additional, Eroglu, E., additional, Van Cleemput, J., additional, Droogne, W., additional, Jasityte, R., additional, Meyns, B., additional, D'hooge, J., additional, Vanhaecke, J., additional, Al Barjas, M., additional, Iskreva, R., additional, Morris, R., additional, Davar, J., additional, Zhao, Y., additional, Holmgren, A., additional, Morner, S., additional, Stepanovic, J., additional, Beleslin, B., additional, Nedeljkovic, M., additional, Mazic, S., additional, Stojanov, V., additional, Piatkowski, R., additional, Kochanowski, J., additional, Scislo, P., additional, Grabowski, M., additional, Marchel, M., additional, Roik, M., additional, Kosior, D., additional, Opolski, G., additional, Tomaszewski, A., additional, Kutarski, A., additional, Tomaszewski, M., additional, Eibel, S., additional, Hasheminejad, E., additional, Mukherjee, C., additional, Tschernich, H., additional, Ender, J., additional, Delithanasis, I., additional, Celutkiene, J., additional, Kenny, C., additional, Monaghan, M., additional, Van Den Oord, S., additional, Ten Kate, G., additional, Akkus, Z., additional, Renaud, G., additional, Sijbrands, E., additional, Ten Cate, F., additional, De Jong, N., additional, Bosch, J., additional, Van Der Steen, A., additional, Schinkel, A., additional, Lisowska, A., additional, Knapp, M., additional, Tycinska, A., additional, Sawicki, R., additional, Kralisz, P., additional, Sobkowicz, B., additional, Chang, S.-A., additional, Lee, S.-C., additional, Kim, E.-Y., additional, Hahm, S.-H., additional, Ahn, G.-T., additional, Sohn, M.-K., additional, Park, S.-J., additional, Choi, J.-O., additional, Park, S.-W., additional, Oh, J.-K., additional, Gursoy, M. O., additional, Gokdeniz, T., additional, Astarcioglu, M., additional, Bayram, Z., additional, Cakal, B., additional, Karakoyun, S., additional, Kalcik, M., additional, Kahveci, G., additional, Yildiz, M., additional, Ozkan, M., additional, Skidan, V., additional, Borowski, A., additional, Park, M., additional, Thomas, J., additional, Ranjbar, S., additional, Hassantash, S., additional, Karvandi, M., additional, Foroughi, M., additional, Davidsen, E. S., additional, Cramariuc, D., additional, Bleie, O., additional, Gerdts, E., additional, Matre, K., additional, Cusma' Piccione, M., additional, Bagnato, G., additional, Mohammed, M., additional, Piluso, S., additional, Oreto, L., additional, Bitter, T., additional, Carvalho, S., additional, Canada, M., additional, Santisteban Sanchez De Puerta, M., additional, Mesa Rubio, M. D., additional, Ruiz Ortiz, M., additional, Delgado Ortega, M., additional, Pena Pena, M. L., additional, Puentes Chiachio, M., additional, Suarez De Lezo Cruz-Conde, J., additional, Pan Alvarez-Ossorio, M., additional, Mazuelos Bellido, F., additional, Suarez De Lezo Herreros De Tejada, J., additional, Altekin, E., additional, Yanikoglu, A., additional, Karakas, S., additional, Oncel, C., additional, Akdemir, B., additional, Belgi Yildirim, A., additional, Cilli, A., additional, Yilmaz, H., additional, Lenartowska, L., additional, Furdal, M., additional, Knysz, B., additional, Konieczny, A., additional, Lewczuk, J., additional, Severino, S., additional, Cavallaro, M., additional, Coppola, M., additional, Motoki, H., additional, To, A., additional, Bhargava, M., additional, Wazni, O., additional, Marwick, T., additional, Klein, A., additional, Sinkovskaya, E., additional, Horton, S., additional, Abuhamad, A., additional, Mingo Santos, S., additional, Monivas Palomero, V., additional, Beltran Correas, B., additional, Mitroi, C., additional, Gutierrez Landaluce, C., additional, Garcia Lunar, I., additional, Gonzalez Mirelis, J., additional, Cavero, M., additional, Segovia Cubero, J., additional, Alonso Pulpon, L., additional, Gurel, E., additional, Karaahmet, T., additional, Tigen, K., additional, Kirma, C., additional, Dundar, C., additional, Pala, S., additional, Isiklar, I., additional, Cevik, C., additional, Kilicgedik, A., additional, Basaran, Y., additional, Brambatti, M., additional, Romandini, A., additional, Barbarossa, A., additional, Molini, S., additional, Urbinati, A., additional, Giovagnoli, A., additional, Cipolletta, L., additional, Capucci, A., additional, Park, S., additional, Choi, E., additional, Ahn, C., additional, Hong, S., additional, Kim, M., additional, Lim, D., additional, Shim, W., additional, Xie, J., additional, Fang, F., additional, Zhang, Q., additional, Chan, J., additional, Yip, G., additional, Sanderson, J., additional, Lam, Y., additional, Yan, B., additional, Yu, C., additional, Jorge Perez, P., additional, De La Rosa Hernandez, A., additional, Hernandez Garcia, C., additional, Duque Garcia, A., additional, Barragan Acea, A., additional, Arroyo Ucar, E., additional, Jimenez Rivera, J., additional, Lacalzada Almeida, J., additional, Laynez Cerdena, I., additional, Carminati, C., additional, Capoulade, R., additional, Larose, E., additional, Clavel, M., additional, Dumesnil, J., additional, Arsenault, M., additional, Bedard, E., additional, Mathieu, P., additional, Pibarot, P., additional, Gargani, L., additional, Baldi, G., additional, Forfori, F., additional, Caramella, D., additional, D'errico, L., additional, Abramo, A., additional, Sicari, R., additional, Giunta, F., additional, Lee, W.-N., additional, Larrat, B., additional, Messas, E., additional, Pernot, M., additional, Tanter, M., additional, Velagic, V., additional, Cikes, M., additional, Matasic, R., additional, Skorak, I., additional, Samardzic, J., additional, Puljevic, D., additional, Lovric Bencic, M., additional, Biocina, B., additional, Milicic, D., additional, Roosens, B., additional, Bala, G., additional, Droogmans, S., additional, Hostens, J., additional, Somja, J., additional, Delvenne, E., additional, Schiettecatte, J., additional, Lahoutte, T., additional, Van Camp, G., additional, Cosyns, B., additional, Ghosh, A., additional, Hardy, R., additional, Chaturvedi, N., additional, Deanfield, J., additional, Pellerin, D., additional, Kuh, D., additional, Hughes, A., additional, Malmgren, A., additional, Dencker, M., additional, Stagmo, M., additional, Gudmundsson, P., additional, Seo, Y., additional, Ishizu, T., additional, Aonuma, K., additional, Schuuring, M. J., additional, Vis, J., additional, Van Dijk, A., additional, Van Melle, J., additional, Pieper, P., additional, Vliegen, H., additional, Sieswerda, G., additional, Foukarakis, E., additional, Pitarokilis, A., additional, Kafarakis, P., additional, Kiritsi, A., additional, Klironomos, E., additional, Manousakis, A., additional, Fragiadaki, X., additional, Papadakis, E., additional, and Dermitzakis, A., additional

Published
2011
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39. Usefulness of surface electrocardiogram in predicting the clinical course of patients with hypertrophic cardiomyopathy.

Author

Bayrak F, Kahveci G, Mutlu B, Degertekin M, Demirtas E, Bayrak, Fatih, Kahveci, Gökhan, Mutlu, Bülent, Değertekin, Muzaffer, and Demirtaş, Ertan

Abstract

Objective: Few data exist regarding the prognostic value of QT dispersion in hypertrophic cardiomyopathy (HCM). In this study, we prospectively investigated the association between baseline QT dispersion and clinical course of HCM. Methods: Overall, 101 patients with asymmetric septal hypertrophy (59 men, mean age 45+/-16 years, range 13-74 years) were included in the study and were followed up for 595+/-367 days for clinical endpoints defined as cardiac death and hospitalization due to worsening in heart failure symptoms. QRS duration, QT interval, and JT interval were manually measured on 12-lead electrocardiogram (ECG). QT dispersion and corrected QT dispersion were calculated accordingly. The ECG findings of the patients with and without clinical endpoints were compared. Results: Twenty-nine patients experienced clinical endpoints (3 sudden deaths, 26 hospitalizations due to worsening heart failure). The measurements of QT, JT and QRS intervals were all comparable between the two groups (p>0.05 for all). QT dispersion and corrected QT dispersion were significantly different between patients with and without clinical endpoints (64+/-30 ms vs. 83+/-18 ms and 71+/-33 ms vs. 90+/-18 ms, respectively, p=0.001 for both). Corrected QT dispersion >80 ms detected patients with clinical endpoints with sensitivity and specificity of 79% and 75%, respectively. Patients with corrected QT dispersion <80 ms were significantly free of clinical endpoints. Conclusion: In conclusion, for patients with hypertrophic cardiomyopathy, measurement of baseline corrected QT dispersion from surface ECG may be used to identify those at risk for clinical deterioration at long-term follow-up. [ABSTRACT FROM AUTHOR]

Published
2007

40. Genetic analysis of the Ir×4 gene in hypertrophic cardiomyopathy

Author

Bayrak, F., Bayrak, E.K., Mutlu, B., Kahveci, G., Ünaltuna, N.E., Bayrak, F., Bayrak, E.K., Mutlu, B., Kahveci, G., Ünaltuna, N.E., and Yeditepe Üniversitesi

Subjects
Genetic, Genotype, Hypertrophic/genetics, Cardiomyopathy, Genetic screening, Polymorphism
Abstract

Objectives: The Ir×4 gene is predominantly expressed in cardiac ventricles. It has been demonstrated in animal studies that disruption of the Ir×4 gene caused inhibition of chamber-specific expression of myosin heavy chain genes, resulting in abnormal ventricular gene expression and cardiac hypertrophy. In this study, we aimed to investigate a possible association between mutations in the Ir×4 gene and hypertrophic cardiomyopathy (HC). Study design: The study included 68 patients (32 females, 36 males; mean age 49 years; range 17 to 74 years) with HC and 67 healthy controls (33 females, 34 males; mean age 45 years; range 20 to 88 years). All the patients were evaluated with a detailed history, physical examination, 12-lead electrocardiography, and transthoracic echocardiography. DNA samples of all the subjects were extracted. Genomic DNA fragments were amplified by polymerase chain reaction and screened by single-strand conformation polymorphism analysis. DNA sequences were determined through an automated sequencing system. Results: All exons in the Ir×x4 gene were examined. No mutations were detected associated with HC. Four polymorphisms were identified including G355>A, A381>G, G1203>A, and C1431>T. Compared with patients having the GA and GG genotyes, patients with the AA genotype of A381>G polymorphism were found to have a higher maximal left ventricle outflow tract gradient (p=0.03), prolonged corrected QT dispersion (p=0.05), and albeit not statistically significant, increased septal thickness (p=0.07). Conclusion: This is the first human study investigating the association between the Ir×4 gene and HC. Polymorphism A381>G of the Ir×4 gene may have a modifier, effect on septal thickness, resulting in increased corrected QT dispersion and higher outflow gradients.

45. 114 Validation of N Terminal pro brain natriuretic peptide levels for monitoring clinical course and assesing mortality in patients with idiopathic dilated cardiomyopathy

Author

Mutlu, B., Tigen, K., Kahveci, G., Karaahmet, T., Türkyýlmaz, E., Bayrak, F., Fotbolcu, H., and Ba∂aran, Y.

Subjects
NATRIURETIC peptides, CARDIOMYOPATHIES
Abstract

An abstract of the study "Validation of N Terminal Pro Brain Natriuretic Peptide Levels for Monitoring Clinical Course and Assesing Mortality in Patients With Idiopathic Dilated Cardiomyopathy," by B. Mutlu and colleagues is presented.

Published
2004
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46. Oral Abstract session * Imaging in structural interventions: 13/12/2013, 08:30-10:00 * Location: Bursa

Author

Kalcik, M, Gursoy, MO, Astarcioglu, MA, Gokdeniz, T, Karakoyun, S, Cakal, B, Yesin, M, Kahveci, G, Yildiz, M, Ozkan, M, Cresti, A, Cesareo, F, Guerrini, F, Capati, E, Miracapillo, G, Severi, S, Ternacle, J, Lellouche, N, Gallet, R, Deux, J-F, Dubois-Rande, J-L, Teiger, E, Lim, P, Polizzi, V, Pino, PG, Luzi, G, Fiorilli, R, Buffa, V, Visconti, C, Bellavia, D, Violini, R, Musumeci, F, Saura Espin, D, Oliva Sandoval, MJ, Gonzalez Carrillo, J, Caballero Jimenez, L, Espinosa Garcia, MD, Garcia Navarro, M, Lopez Ruiz, M, Valdes Chavarri, M, and De La Morena Valenzuela, G

Abstract

Purpose: Paravalvular leak (PVL) is not an uncommon complication of valve surgery. PVL severity, size, shape and morphology are important factors in determining subsequent clinical presentation and the severity of heart failure. Symptoms may be due to hemolytic anemia as a result of hemolysis. RT-3D TEE is superior over 2D TEE as it provides additional information about the complex 3D anatomy. Methods: The study was comprised of 108 patients with severe mitral PVLs. The PVLs were visualized using two dimensional transesophageal echocardiography (2D TEE) and subsequent real time three dimensional transesophageal echocardiography (RT-3D TEE). The relationship between echocardiographic findings and development of hemolysis were studied. The presence and severity of hemolysis was assessed on the basis of serum lactic dehydrogenase, blood hemoglobin, bilirubin and reticulocyte levels. Results: The study group included mechanical (n= 98) and bioprosthetic valves (n= 10). The most common PVL localizations were anterolateral commisure, posteromedial commissures and posterolateral region. The mean PVL width measured by 2D TEE was 3.2 ± 1.5 (range; 2-7) mm and the mean width of defect measured by 3D TEE was 3.1 ± 1.7 (range; 2-7) mm (p= 0.6). The mean length of defect measured by 3D TEE was 12.5 ± 7 (range; 4-22) mm. The mean area of severe PVLs was 35 ± 25 mm2 (range; 8-100). Fifty-six patients (52 %) PVLs were oval/round shaped whereas 34 (31 %) were cresentric, 11 (10 %) were slit-like and 5 (5 %) were slope-tunnel shaped. Two posteriorly-localized defects (2 %) were not clearly visualized by RT-3D TEE. Nine cresentic-shaped (8%) and 4 slit-like shaped (% 4) PVLs were ‘multi-fenestrated’. Besides, 74 % of the cresentic shaped leaks had irregular borders (n=25). The oval / round, tunnel-like and slit-like defects had regular borders. The patients were followed-up for 4 ± 0.8 years. Hemolysis was observed in 65 (60 %) patients. The patients with cresentic and irregular defects had significantly higher severity of hemolysis compared to the others (p=0.02). The size of the defect did not correlate with severity of hemolysis. Conclusions: RT-3D TEE permits detailed structural evaluation of paravalvular leak shape which may contribute to the severity of hemolysis.

Published
2013
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47. Hipertrofik kardiyomiyopatide BOP geni varyasyonlari

Author

Çağrı Güleç, Nihan Erginel Ünaltuna, Neslihan Abaci, Fatih Bayrak, Gökhan Kahveci, Evrim Kömürcü Bayrak, Abaci, N., Güleç, C., Bayrak, F., Kömürcü-Bayrak, E., Kahveci, G., Erginel-Ünaltuna, N., and Yeditepe Üniversitesi

Subjects
Clinical heterogeneity, Adult, Male, medicine.medical_specialty, Adolescent, Chromosomes, Human, Pair 21, CD8 Antigens, Muscle Proteins, Single-nucleotide polymorphism, Bioinformatics, Mice, Exon, Modifying gene, Reference Values, Internal medicine, Genetic variation, Genotype, medicine, Animals, Humans, BOP, Aged, business.industry, Haplotype, Hypertrophic cardiomyopathy, Genetic Variation, Proteins, RNA-Binding Proteins, Electroencephalography, Single-strand conformation polymorphism, Cardiomyopathy, Hypertrophic, Middle Aged, medicine.disease, Null allele, Molecular biology, DNA-Binding Proteins, Cross-Sectional Studies, QT dispersion, Mutation, Cardiology, Female, Cardiology and Cardiovascular Medicine, business, Chickens, Echocardiography, Transesophageal, Transcription Factors
Abstract

Objective: The observation that Bop null allele mice show underdeveloped right ventricle and excessive development of left ventricle, suggests the possible relationship between human BOP gene and hypertrophic cardiomyopathy (HCMP). In our study, we investigated this possible relationship between BOP gene variations and QT dispersion, a noninvasive arrhythmic risk marker for HCMP. Methods: This cross-sectional study consisted of 50 patients clinically diagnosed with HCMP and 60 healthy subjects. Exonic regions of BOP gene were amplified by polymerase chain reaction and amplified exonic regions were analyzed by Single-Strand Conformation Polymorphisms (SSCP). The samples with different migration patterns were sequenced through an automated sequencing system. Continuous variables were compared by unpaired t-test for independent samples or Mann-Whitney U test. Genotype-disease relationship was tested by Chi-square test. Results: The nucleotide substitutions G275>A and C965>A in exon 2 and 7 were determined only in HCMP group. The G707>C, C710>T, T761>C, T1217>C SNPs in exon 6 and 9 are also found in the control group. Significant differences were found between two groups (p=0.002 and p

Published
2010

48. Clinical Significance of High-Density Lipoprotein Cholesterol in Left-Sided Infective Endocarditis

Author

Kursat Tigen, Yusuf Gurel, Yelda Basaran, Bülent Mutlu, Tansu Karaahmet, Fatih Bayrak, Gökhan Kahveci, Kahveci, G., Bayrak, F., Mutlu, B., Gurel, Y.E., Karaahmet, T., Tigen, K., Basaran, Y., and Yeditepe Üniversitesi

Subjects
Male, medicine.medical_specialty, Sensitivity and Specificity, Severity of Illness Index, Gastroenterology, chemistry.chemical_compound, High-density lipoprotein, Predictive Value of Tests, Serum HDL cholesterol level, Internal medicine, medicine, Left sided infective endocarditis, Humans, Clinical significance, In patient, Serum Albumin, Triglycerides, Retrospective Studies, Endocarditis, Cholesterol, business.industry, Middle Aged, Prognosis, medicine.disease, Hospitalization, Lipoproteins, LDL, Cross-Sectional Studies, Endocrinology, chemistry, Case-Control Studies, Creatinine, Infective endocarditis, Cardiology, Female, lipids (amino acids, peptides, and proteins), Lipoproteins, HDL, Cardiology and Cardiovascular Medicine, business, Lipoprotein
Abstract

Decreased serum levels of high-density lipoprotein (HDL) cholesterol have been shown to be of prognostic significance in patients with severe infectious diseases. Serum HDL cholesterol levels were therefore investigated as a possible parameter for the prediction of clinical outcomes in patients with left-sided infective endocarditis (IE). Fifty-four patients with IE with available admission serum HDL cholesterol levels were included in the study. A clinical outcome was defined as a complicated course during hospitalization. Forty-two patients had complicated courses during their in-hospital stays. The median serum HDL cholesterol level was significantly lower in patients with IE (n = 54) than healthy controls (n = 26) (26 vs 47 mg/dl, p

Published
2008

49. Ventricular pre-excitation and cardiac hypertrophy mimicking hypertrophic cardiomyopathy in a Turkish family with a novel PRKAG2 mutation

Author

Bülent Mutlu, Yelda Basaran, Evrim Komurcu-Bayrak, Nihan Erginel-Unaltuna, Fatih Bayrak, Gökhan Kahveci, Bayrak, F, Komurcu-Bayrak, E, Mutju, B, Kahveci, G, Basaran, Y, Erginel-Unaltuna, N, and Yeditepe Üniversitesi

Subjects
Adult, Male, medicine.medical_specialty, Pre-Excitation Syndromes, Adolescent, Turkey, Cardiomyopathy, Ventricular outflow tract obstruction, Cardiomegaly, AMP-Activated Protein Kinases, Protein Serine-Threonine Kinases, White People, Diagnosis, Differential, Multienzyme Complexes, Ventricular hypertrophy, Right ventricular hypertrophy, Internal medicine, Cardiomyopathy, Hypertrophic, Familial, medicine, Humans, Missense mutation, genetics, Genetic Predisposition to Disease, business.industry, Hypertrophic cardiomyopathy, ventricular pre-excitation, Middle Aged, medicine.disease, Pedigree, Case-Control Studies, Heart failure, Mutation, Mutation (genetic algorithm), cardiovascular system, Cardiology, Female, medicine.symptom, Cardiology and Cardiovascular Medicine, business, cardiomyopathy
Abstract

Background: Mutations in PRKAG2, the gene for the gamma 2 regulatory subunit of AMP-activated protein kinase, cause cardiac hypertrophy and electrophysiological abnormalities. We identified a novel mutation in PRKAG2 causing familial ventricular pre-excitation and severe cardiac hypertrophy. Methods and results: We studied 30 members of one family and 120 healthy controls. Molecular analysis of PRKAG2 gene revealed one missense mutation in exon 14 which was confirmed by restriction enzyme digestion. We identified a G to A transition, resulting in a Glu506Lys substitution in the PRKAG2 gene in 8 of the family members, who all had cardiac hypertrophy and ventricular pre-excitation. High incidence of right ventricular hypertrophy and left ventricular outflow tract obstruction are other prominent features of this novel PRKAG2 mutation. Family members without mutation had no cardiac disease. The 120 unrelated healthy individuals did not show this mutation. Conclusions: Coexistence of unexplained ventricular hypertrophy and pre-excitation should prompt the diagnosis of PRKAG2 mutations and these patients should be referred for genetic analysis. The possible alteration of AMP-activated protein kinase activity due to genetic defects in PRKAG2 may serve as a template for developing more specific therapies in the treatment of patients with this mutation. (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.

Published
2006

50. Determinants of Elevated NT-proBNP Levels in Patients With Hypertrophic Cardiomyopathy: An Echocardiographic Study

Author

Fatih Bayrak, Yelda Basaran, Bülent Mutlu, Gökhan Kahveci, Kahveci, G., Bayrak, F., Mutlu, B., Basaran, Y., and Yeditepe Üniversitesi

Subjects
Pulmonary and Respiratory Medicine, Adult, Male, medicine.medical_specialty, Diastole, Cardiomyopathy, Ventricular outflow tract obstruction, Doppler echocardiography, Cohort Studies, Ventricular Dysfunction, Left, Internal medicine, Natriuretic Peptide, Brain, medicine, Humans, cardiovascular diseases, Mitral regurgitation, Ejection fraction, medicine.diagnostic_test, business.industry, Hypertrophic cardiomyopathy, Cardiomyopathy, Hypertrophic, Middle Aged, medicine.disease, Echocardiography, Doppler, Peptide Fragments, NT-proBNP, Left atrium, Cardiology, cardiovascular system, Female, medicine.symptom, Cardiology and Cardiovascular Medicine, Isovolumic relaxation time, business, hormones, hormone substitutes, and hormone antagonists
Abstract

Background: The purpose of this study was to explore the relationship between plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) and extensive echocardiographic variables in patients with hypertrophic cardiomyopathy (HCM). Methods: We evaluated plasma NT-proBNP levels in 88 patients with HCM and examined the plasma NT-proBNP levels' relationships with echocardiographic indexes. Echocardiographic variables were analysed using univariate and multivariate logistic regression to identify predictors of NT-proBNP elevation. Results: Several echocardiographic variables predicted NT-proBNP elevation, including left atrial dimension index (LADI), left ventricular maximal wall thickness (MWT), left ventricular posterior wall thickness, severe mitral regurgitation, mitral septal and lateral tissue Doppler velocities, and mitral septal E/Ea ratio. Left ventricular ejection fraction, left ventricular dimensions, mitral early flow propagation velocity, isovolumic relaxation time, and left ventricular outflow tract obstruction were not significant predictors of NT-proBNP in this group of patients. With multivariate analysis LADI (HR 5.0; 95% CI 1.5-17.1, p = 0.01) and MWT (HR 4.0; 95% CI 1.2-13.2, p = 0.022) emerged as independent determinants of NT-proBNP elevation. Conclusions: In HCM plasma NT-proBNP is prominently increased. LADI and MWT are independent predictors of elevated levels. These data indicate that NT-proBNP elevations are mainly determined by diastolic load in HCM. © 2008 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand.

Published
2009

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