Objective: Nicotine, one of the most dangerous substances in tobacco, can pass the placenta and affect the fetal hemodynamics. The aim of this study was to evaluate the protective effects of melatonin on hearts of nicotine exposed newborn rats whose mothers received nicotine.
Methods: This is an experimental, randomized, controlled study. Study groups were composed of five groups of rats; high-dose nicotine (HDN), HDN+melatonin (HDNM), low-dose nicotine (LDN), LDN+melatonin (LDNM), control. Myocardial and plasma malondialdehyde (MDA), nitric oxide(NO), glutathione peroxidase (GSHPx) and superoxide dismutase (SOD) were analyzed and myocardial tissue was examined histopathologically. Comparisons of groups were done with Kruskal-Wallis one way analysis test. All pairwise multiple comparisons and the comparisons between control and other groups were done with Dunn’s nonparametric multiple comparison test.
Results: Plasma and tissue MDA levels among groups were different (p=0.001 for plasma MDA and p=0.001 for tissue MDA). Plasma MDA levels of HDN, HDNM, LDN, and tissue MDA levels of HDN and LDN were significantly higher than in control group (p<0.05 for plasma MDA and for tissue MDA). Plasma and tissue NO levels among groups were also different (p=0.011 for plasma NO and p=0.001 for tissue NO). Plasma NO of LDN group was higher than of LDNM group, and plasma NO of LDNM group was lower than in control group (p<0.05). Tissue NO levels of HDN and LDN groups were higher than of control group (p<0.05). There was no difference between plasma GSHPx levels among groups (p=0.221) but statistically significant different was detected between tissue GSHPx levels among groups (p=0.001). Tissue GSHPx level was found lower in HDN group than in control group (p<0.05). Tissue GSHPx level of LDNM group was higher than of LDN group, and tissue GSHPx level of HDNM group was higher than of HDN group (p<0.05). A difference was found between plasma and tissue SOD among groups (p=0.005 for plasma SOD and p=0.001 for tissue SOD). Plasma SOD of LDN group was significantly lower than of HDNM and LDNM groups (p<0.05). Tissue SOD analyzes revealed lower levels in HDN and LDN groups than in control group (p<0.05). Severe cardiomyopathy was determined in HDN and LDN groups (p<0.05).
Conclusion: Nicotine exposure depletes myocardial antioxidant enzymes and increases free radicals and lipid peroxidation products. Melatonin particularly prevents the nicotine-induced cardiac injury as an antioxidant

Objective: Eight different learning algorithms used for creating artificial neural network (ANN) models and the different ANN models in the prediction of coronary artery disease (CAD) are introduced.
Methods: This work was carried out as a retrospective case-control study. Overall, 124 consecutive patients who had been diagnosed with CAD by coronary angiography (at least 1 coronary stenosis > 50% in major epicardial arteries) were enrolled in the work. Angiographically, the 113 people (group 2) with normal coronary arteries were taken as control subjects. Multi-layered perceptrons ANN architecture were applied. The ANN models trained with different learning algorithms were performed in 237 records, divided into training (n=171) and testing (n=66) data sets. The performance of prediction was evaluated by sensitivity, specificity and accuracy values based on standard definitions.
Results: The results have demonstrated that ANN models trained with eight different learning algorithms are promising because of high (greater than 71%) sensitivity, specificity and accuracy values in the prediction of CAD. Accuracy, sensitivity and specificity values varied between 83.63% - 100%, 86.46% - 100% and 74.67% - 100% for training, respectively. For testing, the values were more than 71% for sensitivity, 76% for specificity and 81% for accuracy.
Conclusions: It may be proposed that the use of different learning algorithms other than backpropagation and larger sample sizes can improve the performance of prediction. The proposed ANN models trained with these learning algorithms could be used a promising approach for predicting CAD without the need for invasive diagnostic methods and could help in the prognostic clinical decision.

Objective: Despite impressive advances in therapeutics in the last years, acute heart failure (AHF) remains a major cause of cardiovascular morbidity and mortality. Patients hospitalized because of heart failure (HF), irrespective of left ventricular systolic function, represent a high-risk population with limited short-term prognosis. A substantial component of HF-related mortality occurs during a hospital stay. In this study, we aimed to determine the factors impacting on in-hospital mortality in patients with AHF.
Methods: During a 15-month period (December 2005-March 2007), 85 consecutive patients with (mean age: 64±8 years, male: 54%) an episode of AHF were included in this study. The effect of demographic, clinical, electrocardiographic, and echocardiographic characteristics, laboratory findings on in-hospital mortality were evaluated retrospectively.
Results: Of 85 patients 24.7% of patients had new-onset HF. Coronary artery disease (61%) was the most common underlying disease. The 44.7% of patients had hypertension, 37.6% had diabetes mellitus, 21% had chronic renal failure and 16.4% had chronic obstructive pulmonary disease. Left ventricular ejection fraction was 35±7%. In-hospital mortality rate was found as 11.7% (10 patients).The major cause of mortality was the progression of HF to cardiogenic shock in 60% of deaths. In comparison with surviving patients in terms of the clinical, demographic, electrocardiographic, and laboratory characteristics and left and right ventricular functions, patients died during hospitalization had higher blood urea nitrogen (45±20 mg/dl vs. 36±12 mg/dl, p=0.04), higher creatinine level (2.2±0.8 mg/dl vs. 1.1±0.5 mg/dl, p=0.001), and wider QRS duration (130±13 ms vs. 116±18 ms, p=0.04) whereas they had lower plasma sodium level (128±5 mmol/l vs. 135±9 mmol/l, p=0.02) and systolic blood pressure (p=0.01). Logistic regression analysis revealed that plasma creatinine level (OR 1.5, 95% CI 1.2 to 2.1, p=0.01), blood urea nitrogen (OR 2.1, 95% CI 1.8 to 3.1, p=0.001), plasma sodium level (OR 1.3, 95% CI 1.1 to 1.7, p=0.02), and systolic blood pressure (OR 2.2, 95% CI 1.9 to 2.8, p=0.01) were the independent predictors of in-hospital mortality.
Conclusion: In-hospital mortality increases in patients who had lower systolic blood pressure, lower plasma sodium level, and renal dysfunction on admission.

Objective: We studied all English-written peer-reviewed reports on drug-induced Torsades de Pointes (TdP) in patients aged 80 years or more in order to characterize the clinical circumstances leading to this serious complication.
Methods: Our literature search yielded 24 reports on 25 patients aged 80-95 years with drug-induced TdP. We systematically reviewed each report and recorded the non-modifiable risk factors for drug-induced TdP (i.e., female sex and structural heart disease) as well as preventable clinical circumstances, which might have been associated with drug-induced TdP.
Results: The most prevalent risk factors for drug-induced TdP were non-modifiable risk factors: 22 (88%) patients were female patients and 19 (76%) patients had structural heart disease. Overall, 16 (64%) patients were female patients with structural heart disease. The literature did not report any elderly male patients without structural heart disease. Among the preventable clinical circumstances, which might have been associated with drug-induced TdP, the most prevalent were: administrating QT prolonging agents despite long QT interval (n=11; 44%) and co-administration of two or more QT prolonging agents (n=9; 36%). The most prevalent QT prolonging agents found to trigger TdP were macrolides and quinolones (n=9; 36%). All but three patients had at least one or more preventable clinical circumstances, which might have been associated with drug-induced TdP.
Conclusion: Physicians should be more aware of the risk for drug-induced TdP in patients aged 80 years or more while administrating QT prolonging agents despite long QT interval and co- administrating two or more QT prolonging agents, specifically in elderly female patients with structural heart disease.

Objective: Hypoxia is one of the major concerns in aviation. Clinical hypoxia has been shown to increase QT dispersion (QTd). We aimed to examine QTd during hypobaric chamber training to observe the effect of hypobaric hypoxia on QT dispersion.
Methods: A total of 38 healthy male aviators volunteered to take part in this longitudinal study. Subjects' electrocardiograms were recorded by 12-lead digital Holter device before, during, and after hypobaric exposure at simulated altitude of 30,000ft. Data from 23 of the subjects, aged 27.91±6.02 years (range 22–39) was used. QT intervals were measured manually. QT dispersion and heart rate adjusted QTd (QTcd) were calculated for each subject. Statistical significance of changes in parameters was analyzed using the Friedman test. Comparison of pre-post exposure clusters was made using Dunn’s test.
Results: QT dispersion values were as following: prehypoxic 64.09±8.39 ms, hypoxic 50.35±11.06 ms and posthypoxic 59.83±9.06 ms (Median: 64, 50, 60; Mean rank: 2.65, 1.28, 2.07) (p=0.0001 for prehypoxic–hypoxic, p=0.046-prehypoxic-posthypoxic, and p=0.002 for posthypoxic-hypoxic). Heart rate values were as following: prehypoxic 74.09±6.43 beats/min, hypoxic 127.1±17.39 beats/min, and posthypoxic 95.17±11.35 beats/min (Median: 75, 122, 92; Mean rank: 1, 3, 2) (p=0.0001 for prehypoxic–hypoxic, prehypoxic–posthypoxic, and posthypoxic–hypoxic). The change in QTd and HR during hypobaric chamber exposure was statistically significant but, the change in QTcd was not (p<0.001, p<0.001, p>0.1, respectively).
Conclusion: From the findings of present study, it is not possible to directly comment on the validity of QTd in revealing arrhythmogenic predisposition of healthy subjects exposed to hypobaric hypoxia. The relationship between QT dispersion and hypobaric hypoxic exposure is not clear, particularly when QTd is corrected for the increased heart rate. QT dispersion measurement has not been proven a reliable and practical method to show arrhythmia predisposition during a hypobaric hypoxic exposure in healthy individuals.

Objective: To investigate systolic and diastolic ventricular functions, aortic elastic properties and the presence of pericardial effusion in familial Mediterranean fever (FMF) patients.
Methods: A case-controlled, cross-sectional study was performed on 44 FMF patients and 27 controls. Subjects with hypertension, diabetes mellitus and hyperlipidemia were excluded. Left and right ventricular functions were measured using echocardiography including two-dimensional, M-mode, and conventional Doppler as well as pulsed wave tissue Doppler imaging (TDI). Aortic elasticity was analyzed using M-mode tracing guided by the two-dimensional echocardiography. Statistical analysis was performed using Mann Whitney U, Spearman rho correlation and Fisher's exact tests.
Results: Age, sex, body mass index, smoking status and lipids were comparable in patients and controls (p>0.05). None of the subjects had pericarditis and/or pericardial effusion. Aortic wall properties were similar between groups (p>0.05). The TDI parameters of mitral lateral annulus revealed significantly lower Em/Am ratios in patients compared to controls [1.77 (0.6-3.4) vs. 1.79 (0.9-4.8), p=0.02]. Mitral flow propagation velocity was significantly lower in patients than healthy subjects [63 (39-100) vs. 74 (40-94) cm/s, p=0.008]. Tricuspid annular plane systolic excursion (TAPSE) was significantly reduced in FMF group than in controls [2 (1.3-2.5) vs. 2.5 (1.7-3.2) cm; p<0.001]. Eight of the patients and one control had impaired TAPSE (<2 cm; p=0.025). There was no difference regarding right ventricular diastolic dysfunction (RVDD) as assessed by using standard Doppler echocardiography (p>0.05). However, pronounced RVDD was observed in FMF patients documented by TDI (Em/Am<1; 19 patients vs. 0 controls, p<0.001).
Conclusion: Subclinical myocardial involvement is present in a cohort of relatively young FMF patients who were also free of classical cardiovascular risk factors. Pericardium and aorta seem to be spared during attack free periods of FMF.

Objective: Pulmonary arterial hypertension (PAH) is a term used to define a variety of progressive conditions that have in common, increased pulmonary vascular resistance leading to right heart failure and death. There has been considerable decrease in mortality and morbidity with the advances in PAH treatment over the past decade. However, since there is no epidemiologic study in Turkey, the prevalence of PAH and its importance is not known yet. This study aimed to evaluate the diagnostic clinical experience of Ege University Medical School Cardiology Department with PAH patients.
Methods: We evaluated the diagnostic approach to patients referred to our department with the diagnosis of PAH since 2000 by retrospective analysis method.
Results: The diagnosis of pulmonary hypertension was definite in 70 patients (mean age 47±16 years, 61% women). Etiology from most prevalent to least was as following: congenital heart diseases (27%), chronic thromboembolic pulmonary hypertension (24%), connective tissue diseases-scleroderma (14%), idiopathic PAH (8%), diastolic dysfunction (3%), pulmonary disease (3%), pulmonary veno-occlusive disease (2%), hepatopulmonary hypertension (1%), and HIV-infection associated PAH (1%). At diagnosis, 68% of patients were in NYHA functional class-III or IV. Six-minute walk test was 263±127m. Mean pulmonary artery pressure was 65±20 mmHg. The prognostic marker pro-BNP (brain natriuretic peptid) level was 3208±4145 pg/ml.
Conclusion: Our practice shows that PAH is diagnosed late in the course of the disease in Turkey. This can be overcome with structured management in designated centers with multidisciplinary team-working in a shared care approach. There is also an urgent need for an epidemiological registry in order to determine the burden of PAH in Turkey and increase the awareness of doctors.

Objective: Spontaneous dissection of the abdominal aorta should be considered as a vascular surgical emergency. We report here our experience with this rare pathology.
Methods: At our hospital, we operated on 200 patients for abdominal aortic aneurysm over a 4-year period, and aortic dissection was the underlying pathology in eight of them. Diagnosis was based on history, imaging study findings and visualization at surgery.
Results: The mean size of the aorta at the time of diagnosis was 5.5 ± 0.4 cm. Aortic dissection was complicated by acute ischemia of lower limb and paraplegia in 1 patient and four patients were admitted to hospital with severe abdominal and back pain. Two patients with contained rupture were admitted with hemodynamic collapse and shock. One of the patients who presented with abdominal pain experienced also sudden onset paraplegia. The diagnosis of dissecting abdominal aortic aneurysm was established incidentally in the remaining 2 patients. All patients were treated using open techniques with paramedian transperitoneal incision. We performed aorto-bifemoral bypass operation procedure in all patients; there was no post-operative mortality in our series. One patient had to be reoperated because of bleeding during early postoperative period. One patient required transient dialysis at early postoperative period because of transient rise of serum creatinine level.
Conclusion: The surgical treatment of spontaneous abdominal aortic dissection is usually associated with low morbidity and mortality rates. However, the clinical form of presentation of acute abdominal aortic dissection is usually nonspecific, and diagnosis requires a high index of suspicion.

Objective: Atheromatous plaques in the ascending aorta are major risk factors for strokes caused by macroembolization after coronary artery surgery. Detection of plaque formations and changes in the surgical strategy are very important. This study was planned to compare value direct palpation and multislice computerized tomography to establish aortic plaques and to establish clinical predictors of aortic calcification.
Methods: Fifty-four patients who underwent coronary bypass surgery were included in this prospective and diagnostic study. Proximal portion of each patient’s aorta was evaluated with multislice computerized tomography and was compared with direct palpation. The efficacy of intraoperative palpation to predict calcifications was studied with ROC analysis and the predictors of aortic plaque formation were analyzed using logistic regression analysis.
Results: Atheromatous plaques were detected with palpation in four patients (7.4%), and with multislice tomography in six patients (11.1%). The aortic instrumentation was changed in two patients (3.7%) and strategy was changed in one patient (1.8%).According to the ROC analysis, when multislice computerized tomography was taken as the reference, intraoperative direct palpation was 67% sensitive and 100% specific to predict aortic plaques. Logistic regression analysis of the risk factors showed that the older age was the only significant risk factor (OR – 1.3, 95% CI -1.114-1.568, p=0.001) for plaque formation in the aorta. Neither stroke nor other neurological disorders have been observed during the study.
Conclusions: It can be stated that multislice computerized tomography is more effective to show aortic plaques, but it is not sufficient. Multislice tomography may give additional information about the ascending aorta and the opportunity to visualize the aortic arch. It can be preferred in patients with aortic aneurysm or dissection.

The present review addresses the issues related to innovative contributions in biotechnology and their potential role in stem cell research at present and in the future. We can expect that future developments and applications in biotechnological sciences and industry will effect the direction of emerging cellular therapies. The use of these advances may offer a unique opportunity to investigate the mechanisms related to the journey from embryonic cells or bone-marrow derived stem/progenitor cells to cardiomyocytes or endothelial cells and the molecular regulators of cell differentiation.