Mustafa Yurtdaş

Dr. Mustafa Yurtdaş

Balıkesir Sevgi Hospital
orcid

Research Focus & Metrics

Academic Career Length

21Years (2006-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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22 January 2014 in Echocardiography
Verified
Journal Article
Closed access
PDF file
MYMustafa Yurtdaş
Mustafa Yurtdaş
YYYalin T. Yaylali
Yalin T. Yaylali
YKYüksel Kaya
Yüksel Kaya
MÖMahmut Özdemir
Mahmut Özdemir
IÖİlKer Özkan
İlKer Özkan
NANesim Aladağ
Nesim Aladağ

15 April 2012 in Cardiology Journal
Verified
Journal Article
Open access
MYMustafa Yurtdaş
Mustafa Yurtdaş
OGOktay Gülen
Oktay Gülen
Coronary artery anomalies that take place during fetal development are determined in approximately 1.3% of coronary angiograms. The right coronary artery originating from the left coronary system is an extremely rare variation of the single coronary artery anomaly in which the prognosis is usually benign provided that the anomalous vessel dose not pass between the aorta and the pulmonary artery. Anomalous right coronary artery anomaly has been rarely associated with other congenital cardiovascular anomalies such as transposition of the great vessels and tetralogy of Fallot. To date, a few attempts at classification have been made for coronary artery anomalies, but none of them seems comprehensive or practical for clinicians. The clinical significance of coronary anomalies is usually determined by underlying anatomic features of the wrong coronary origin and/or coronary atherosclerosis. Although coronary angiography is an important diagnostic method, new non-invasive methods such as coronary computed tomography angiography and cardiac magnetic resonance imaging have important roles to play in characterizing this coronary anomaly. It should be noted that the management strategy of these patients may vary based on clinical presentation, anatomical details and additional findings.

1 January 2012 in Korean Circulation Journal
Verified
Journal Article
Open access
PDF file
MYMustafa Yurtdaş
Mustafa Yurtdaş
MAMehmet Kasım Aydın
Mehmet Kasım Aydın
Yurtdaş M, et al. Korean Circ J. 2012 Sep;42(9):641-645. https://doi.org/10.4070/kcj.2012.42.9.641

12 June 2020 in Clinical and Experimental Hypertension
Verified
Journal Article
Closed access
MÖMahmut Özdemir
Mahmut Özdemir
MYMustafa Yurtdaş
Mustafa Yurtdaş
RARamazan Asoğlu
Ramazan Asoğlu
TYTarik Yildirim
Tarik Yildirim
NANesim Aladağ
Nesim Aladağ
EAEmin Asoğlu
Emin Asoğlu
The exaggerated morning blood pressure surge (MS) is a risk factor for cardiovascular diseases. Inflammation is associated with the pathogenesis of hypertension. We aimed to investigate the associa...

1 January 2016 in Arquivos Brasileiros de Cardiologia
Verified
Journal Article
Open access
YYYalin Tolga Yaylali
Yalin Tolga Yaylali
ASAhmet Saricopur
Ahmet Saricopur
MYMustafa Yurtdaş
Mustafa Yurtdaş
HSHande Senol
Hande Senol
GGGamze Gokoz-Dogu
Gamze Gokoz-Dogu
Atrial electromechanical delay (EMD) is used to predict atrial fibrillation, measured by echocardiography. The aim of this study was to assess atrial EMD and mechanical function after anthracycline-containing chemotherapy. Fifty-three patients with breast cancer (48 ± 8 years old) who received 240 mg/m2of Adriamycin, 2400 mg/m2 of cyclophosphamide, and 960 mg/m2 of paclitaxel were included in this retrospective study, as were 42 healthy subjects (47 ± 9 years old). Echocardiographic measurements were performed 11 ± 7 months (median 9 months) after treatment with anthracyclines. Left intra-atrial EMD (11.4 ± 6.0 vs. 8.1 ± 4.9, p=0.008) and inter-atrial EMD (19.7 ± 7.4 vs. 14.7 ± 6.5, p=0.001) were prolonged; LA passive emptying volume and fraction were decreased (p=0.0001 and p=0.0001); LA active emptying volume and fraction were increased (p=0.0001 and p=0.0001); Mitral A velocity (0.8 ± 0.2 vs. 0.6 ± 0.2, p=0.0001) and mitral E-wave deceleration time (201.2 ± 35.6 vs. 163.7 ± 21.8, p=0.0001) were increased; Mitral E/A ratio (1.0 ± 0.3 vs. 1.3 ± 0.3, p=0.0001) and mitral Em (0.09 ± 0.03 vs. 0.11 ± 0.03, p=0.001) were decreased; Mitral Am (0.11 ± 0.02 vs. 0.09 ± 0.02, p=0.0001) and mitral E/Em ratio (8.8 ± 3.2 vs. 7.6 ± 2.6, p=0.017) were increased in the patients. In patients with breast cancer after anthracycline therapy: Left intra-atrial, inter-atrial electromechanical intervals were prolonged. Diastolic function was impaired. Impaired left ventricular relaxation and left atrial electrical conduction could be contributing to the development of atrial arrhythmias. Atraso eletromecânico atrial (AEA) é utilizado para prever fibrilação atrial, medido pela ecocardiografia. O propósito deste estudo era verificar o AEA e a função mecânica após quimioterapia com antraciclinas. Cinquenta e três pacientes com câncer de mama (48 ± 8 anos) que receberam 240 mg/m2 de adriamicina, 2400 mg/m2 de ciclofosfamida, e 960 mg/m2 de paclitaxel foram incluídas neste estudo retrospectivo, além de 42 indivíduos saudáveis (47 ± 9 anos). Medidas ecocardiográficas foram realizadas por aproximadamente 11 ± 7 meses (média de 9 meses) após tratamento com antraciclinas. AEA esquerdo intra-atrial (11,4 ± 6,0 vs. 8,1 ± 4,9, p=0,008) e AEA interarterial (19,7 ± 7,4 vs. 14,7 ± 6,5, p=0,001) foram prolongados; Volume de esvaziamento passivo e fracionamento de AE diminuíram (p=0,0001 e p=0,0001); Volume de esvaziamento ativo e fracionamento de AE (p=0,0001 e p=0,0001); Tempo de aceleração mitral A (0,8 ± 0,2 vs. 0,6 ± 0,2, p=0,0001) e de desaceleração de onda-E mitral (201,2 ± 35,6 vs. 163,7 ± 21,8, p=0,0001) aumentarão; Razão mitral E/A (1,0 ± 0,3 vs. 1,3 ± 0,3, p=0,0001) e mitral Em (0,09 ± 0,03 vs. 0,11 ± 0,03, p=0,001) diminuíram; Razão mitral Am (0,11 ± 0,02 vs. 0,09 ± 0,02, p=0,0001) e mitral E/Em (8,8 ± 3,2 vs. 7,6 ± 2,6, p=0,017) aumentaram nos pacientes. Em pacientes com câncer de mama após terapia com antraciclina: intervalos eletromecânicos intra-atriais esquerdos, intra-atriais foram prolongados. A função diastólica foi prejudicada. O relaxamento ventricular esquerdo foi prejudicado, e a condução elétrica atrial esquerda pode estar contribuindo para o desenvolvimento de arritmias atriais.

1 January 2009 in International Heart Journal
Verified
Journal Article
Closed access
MAMehmet Necdet Akkus
Mehmet Necdet Akkus
GPGurbuz Polat
Gurbuz Polat
MYMustafa Yurtdaş
Mustafa Yurtdaş
BABurak Akcay
Burak Akcay
NENeslihan Ercetin
Neslihan Ercetin
NSNehir Sucu
Nehir Sucu
Scarce data exist on the relationship of C-reactive protein (CRP) or plasminogen activator inhibitor-1 (PAI-1) to the occurrence of heart failure (HF) or cardiogenic shock (CS) after acute myocardial infarction (AMI) and on the relationship between these biomarkers and mortality in CS patients. Thus, we compared high-sensitivity CRP and PAI-1 antigen plasma levels on admission among 3 age- and gender-matched AMI patients groups (consisting of 60 patients with CS, 60 with HF, and 60 without HF on admission), after determining that PAI-1 levels did not vary significantly diurnally in these groups by comparing the data among subgroups which were divided according to admission time within the groups. For CS patients, we also conducted regression analyses to examine the relations of these biomarkers to mortality. CRP levels both in CS (P < 0.001) and HF (P < 0.05) patients were significantly higher compared to those without HF, PAI-1 levels in CS patients were significantly higher compared to both those with (P < 0.05) and without HF (P > 0.01), and CRP and PAI-1 were independent predictors of in-hospital (Odds ratio [OR] = 6.12, 95% confidence intervals [95%CI] = 1.47-25.54 and OR = 5.92, 95%CI = 1.31-26.77, respectively) and 1-year mortality (OR = 5.53, 95%CI = 1.21-25.17 and OR = 5.48, 95%CI = 1.09-27.52, respectively) in CS patients. In conclusion, at admission, CRP is associated with the occurrence of CS and HF and PAI-1 is associated with the occurrence of CS after AMI, and they are of prognostic value in CS complicating AMI.