Yurdaer Dönmez

Dr. Yurdaer Dönmez

orcid

Research Focus & Metrics

Academic Career Length

24Years (2003-Present)

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

Representative Publications

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1 January 2004 in Japanese Heart Journal
Verified
Journal Article
Closed access
YDYurdaer Dönmez
Yurdaer Dönmez
MKMehmet Kanadasi
Mehmet Kanadasi
KTKahraman Tanriverdi
Kahraman Tanriverdi
MDMesut Demir
Mesut Demir
MDMustafa Demirtas
Mustafa Demirtas
FBFikri Baslamisli
Fikri Baslamisli
Several studies claim that prothrombin 20210GA and factor V Leiden mutations are related to arterial thrombosis. We investigated the frequencies of these mutations and their significance in the development of early atherosclerosis in acute myocardial infarction (AMI) patients younger than 55 years of age. We investigated 96 patients with AMI and 77 control subjects. The diagnosis of AMI was established by typical chest pain and ST elevations on the presentation electrocardiogram and characteristic cardiac enzyme elevations. None of the control subjects had evidence of cardiovascular disease. DNA samples were isolated from all subjects and prothrombin 20210GA and factor V Leiden mutations were determined by the RealTime PCR technique with the aid of a Light Cycler device. The prevalence of factor V Leiden mutation was 6.3% and 5.2% in the patient and control groups, respectively (OR 0.6 [95% CI 0.1- 3.9], P = 0.6), whereas the prevalence of prothrombin G20210A mutation was 4.2% and 2.6% in the patient and control groups, respectively (OR 2.8 [95% CI 0.2 - 32.2], P = 0.4). None of the patients had both mutations. Prothrombin 20210GA and factor V Leiden mutations are not significant risk factors for the development of myocardial infarction in patients less than 55 years old in Southern Turkey.

29 September 2006 in Heart and Vessels
Verified
Journal Article
Closed access
PDF file
MKMehmet Kanadaşı
Mehmet Kanadaşı
MÇMurat Çaylı
Murat Çaylı
MDMustafa Demirtaş
Mustafa Demirtaş
TITamer İnAl
Tamer İnAl
MDMesut Demir
Mesut Demir
MŞMustafa Şan
Mustafa Şan

1 November 2005 in Acta Cardiologica
Verified
Journal Article
Closed access
MKMehmet Kanadaşi
Mehmet Kanadaşi
OAOnur Akpinar
Onur Akpinar
MÇMurat Çayli
Murat Çayli
YDYurdaer Dönmez
Yurdaer Dönmez
EAEsmeray Acartürk
Esmeray Acartürk
Although cardiac dilatation and systolic dysfunction have been well documented as a late manifestation, there are conflicting reports regarding the diastolic dysfunction, by using traditional echocardiographic methods in patients with sickle cell anaemia (SCA). The aim of this study was to investigate left ventricular diastolic function in SCA patients without congestive heart failure by using pulsed wave tissue Doppler imaging (TDI). Thirty-one patients (18 men and 13 women, mean age: 26.4 +/- 8.5 years) with homozygous SCA without congestive heart failure and 31 healthy control subjects (19 men and 12 women, mean age: 26.5 +/- 7.6 years) were enrolled in the study. All patients and the controls underwent echocardiographic examination. Left ventricular diastolic function was evaluated by using both traditional pulsed wave Doppler (PWD) and TDI. The cardiac chamber dimensions, wall thicknesses, E and A transmitral peak diastolic velocities, systolic (Sm), early (Em) and late (Am) diastolic myocardial velocities were significantly increased in the patients compared to the controls. Diastolic dysfunction was found in 7 (22.6%) and 3 (9.7%) patients by PWD and TDI, respectively. Of the 7 patients with diastolic abnormalities, 4 patients with a restrictive pattern by PWD were found to be normal by TDI. Our results show that left ventricular diastolic dysfunction is not a frequent finding in patients with SCA without congestive heart failure and TDI is a more reliable and easy method to evaluate diastolic function. Patients with a restrictive pattern found by PWD should be reevaluated by using TDI.

1 March 2007 in Cardiovascular Pathology
Verified
Journal Article
Closed access
MDMesut Demir
Mesut Demir
EAEsmeray Acartürk
Esmeray Acartürk
TITamer İnal
Tamer İnal
GAGülen Attila
Gülen Attila
YDYurdaer Dönmez
Yurdaer Dönmez
MÇMurat Çaylı
Murat Çaylı


1 October 2007 in Angiology
Verified
Journal Article
Closed access
MDMesut Demir
Mesut Demir
MKMehmet Kanadaşı
Mehmet Kanadaşı
OAOnur Akpınar
Onur Akpınar
YDYurdaer Dönmez
Yurdaer Dönmez
MAMahir Avkaroğulları
Mahir Avkaroğulları
MDMustafa Demirtaş
Mustafa Demirtaş
Cardiac troponin T (cTnT), a highly sensitive and specific indicator of myocardial cell death, may be elevated in congestive heart failure (CHF). The aims of this study were to test the hypothesis that decompensated CHF may be associated with an increase in cTnT release and to correlate between cTnT levels and patient outcomes. The authors studied 55 patients aged between 38 and 86 years (30 women and 25 men) who were hospitalized for CHF. Left ventricular ejection fraction (EF) was calculated by using modified Simpson's rule by echocardiography. cTnT levels were assessed. Troponin T ≥0.1 ng/mL was considered as positive. All patients were contacted by phone annually during the next 3 years, and their history of subsequent hospital admissions and current health status were recorded. cTnT was negative in 44 (80%) and positive in 11 (20%) patients. EF was significantly lower and NYHA was higher in cTnT-positive patients. During the 3-year follow-up period, 25 patients died from CHF. The mortality rate was 8/11 (72.7%) among cTnT-positive patients, whereas the mortality rate was 17/44 (38.6%) among cTnT-negative patients. There were significant relationships among positivity of cTnT, NYHA, EF, and mortality rate. Multivariate regression analysis yielded an independent relationship between positivity of cTnT, NYHA classification, and mortality rate. The percent of hospital admissions due to CHF was also higher in patients with cTnT positive (63.6% versus, 27.3%, p <0.05). In conclusion, this study shows that cTnT positivity is an independent risk factor in predicting the long-term mortality and morbidity rate in patients with CHF. Patients with worsening CHF may possibly be identified early on the basis of their elevated serum cTnT levels.