The aim of this study was to investigate the effect of periodontal inflammation on oxidative stress in patients with atherosclerosis by considering serum and saliva total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI). In the study, there were 4 groups, with 20 individuals in each group. These groups consisted of individuals who had periodontitis with atherosclerosis (group A-P), were periodontally healthy with atherosclerosis (group A-C), were systemically healthy with periodontitis (group P), and were systemically and periodontally healthy (group C). Clinical periodontal parameters were recorded. PISA values were calculated. Atherosclerosis severity was determined by the Gensini score. The ratio of TAS/TOS resulting in the OSI levels of the serum and saliva samples was examined biochemically. Group A-P serum TAS and group C saliva OSI values were lower than those of the other groups (p < 0.05). Group A-P serum TOS and OSI values were higher than those of the other groups (p < 0.05). Groups A-C and P serum TOS and OSI values were higher than those of group C (p < 0.05). In the multivariate linear regression analysis, group A-P and PISA values were independently associated with serum TOS and OSI values (p < 0.05). Group A-P, group P, and PISA values were independently associated with saliva OSI values (p < 0.05). Periodontitis and atherosclerosis may have systemic oxidative stress-increasing effects. The coexistence of periodontitis and atherosclerosis increases oxidative stress beyond that seen in either condition alone. Periodontitis can be associated with increased systemic TOS and OSI values in patients with atherosclerosis. Oxidative status is affected more severely when periodontitis and atherosclerosis coexist rather than when either exists alone. Periodontitis can cause increasing effect on serum TOS and OSI and decreasing effect on TAS in patients with atherosclerosis. The increase in oxidative stress markers with the presence of periodontal disease in patients with atherosclerosis emphasizes that controlling periodontal diseases, a treatable disease, may contribute to the prognosis of atherosclerosis.

Objective: The aim of this study was to evaluate the effects of periodontitis on oxidative stress parameters by investigating serum and gingival crevicular fluid (GCF) total antioxidant capacity (TAOC), total oxidant status (TOS), and oxidative stress index (OSI) values in patients with rheumatic heart valve disease (RHVD). Materials and methods: The study population comprised 76 patients, who were divided into four groups: chronic periodontitis with RVHD (RV-CP), periodontally healthy with RVHD (RV-C), systemically healthy with chronic periodontitis (CP), and systemically and periodontally healthy (C). Demographic, periodontal, and echocardiographic parameters were measured. Serum and GCF oxidative stress parameters were evaluated based on the OSI. Results: Similar serum oxidative stress parameters were found in all study groups (P >= 0.05). The GCF TAOC values of the C group were significantly higher than those of the other groups (P = 0.001). The GCF OSI values of the C group were significantly lower than those of the other groups (P = 0.001). The GCF TOS and OSI values of the RV-CP group were significantly higher than those of the CP and C groups (P = 0.001). The GCF TOS value of the RV-C group was significantly higher than those of the CP and C groups (P = 0.001). Conclusions: Altered local oxidative stress profile was associated with the presence of periodontitis. Rheumatic heart valve disease may increase oxidative stress in individuals with chronic periodontitis.

Objective: There are many factors associated with chorda tendinea rupture. The present study aims to investigate the role of Interleukin-6 (IL-6), total antioxidant activity (TAA), total oxidant activity (TOA) and tumor necrosis factor alpha (TNF-alpha) levels on the development of the mitral valve chordae tendinea rupture. Methods: Our study consisted of 30 patients with mitral chordae rupture, 30 patients with severe rheumatic mitral regurgitation, and 20 healthy participants who were admitted to our polyclinic unit. The participants do not have a previously known comorbid disease. After transthoracic echocardiography, their diagnoses were confirmed by the transesophageal echocardiography. Plasma IL-6, TAA-TOA and TNF-alpha level of all patients were measured and their oxidative stress index (OSI) was calculated. Results: Compared to the rheumatic severe mitral insufficiency patients and control group, TOA-OSI levels in the chordae rupture group were significantly higher (p=0.038 and p=0.019, respectively). The TNF-alpha levels in the rheumatic severe mitral insufficiency group were determined as statistically and significantly higher than the chordae rupture group (p=0.028). Conclusion: We have put forth that there is a significant relationship between the chordae rupture levels and oxidative stress levels (TOA-OSI) for the first time in our study. According to the results of our study, high oxidative stress might be accepted as a risk factor for chordae rupture. In addition, it has been observed that the TNF-alpha level in the rheumatic severe mitral insufficiency group have been higher than those in the chordae rupture group. It seems, these data support the role of inflammation in the rheumatic severe mitral insufficiency development.

Objective: Heart failure (HF) has a high prevalence and mortality rate in elderly patients; however, there are few studies that have focused on patients older than 80 years. The aim of this study is to describe and compare the age-specific demographics and clinical features of Turkish elderly patients with HF who were admitted to cardiology clinics. Methods: The Epidemiology of Cardiovascular Disease in Elderly Turkish population (ELDER-TURK) study was conducted in 73 centers in Turkey, and it recruited a total of 5694 patients aged 65 years or older. In this study, the clinical profile of the patients who were aged 80 years or older and those between 65 and 79 years with HF were described and compared based on the ejection fraction (EF)-related classification: HFrEF and HFpEF (is considered as EF: >= 50%). Results: A total of 1098 patients (male, 47.5%; mean age, 83.5 +/- 3.1 years) aged 80 years and 4596 patients (male, 50.2 %; mean age, 71.1 +/- 4.31 years) aged 65-79 years were enrolled in this study. The prevalence of HF was 39.8% for patients who were >= 80 years and 27.1% for patients 65-79 years old. For patients aged >= 80 years with HF, the prevalence rate was 67% for hypertension (HT), 25.6% for diabetes mellitus (DM), 54.3% for coronary artery disease (CAD), and 42.3% for atrial fibrilation. Female proportion was lower in the HFrEF group (p=0.019). The prevalence of HT and DM was higher in the HFpEF group (p<0.01), whereas CAD had a higher prevalence in the HFrEF group (p=0.02). Among patients aged 65-79 years, 43.9% (548) had HFpEF, and 56.1% (700) had HFrEF. In this group of patients aged 65-79 years with HFrEF, the prevalence of DM was significantly higher than in patients aged >= 80 years with HFrEF (p<0.01). Conclusion: HF is common in elderly Turkish population, and its frequency increases significantly with age. Females, diabetics, and hypertensives are more likely to have HFpEF, whereas CAD patients are more likely to have HFrEF.

Herein we share, to our knowledge for the first time, a a case of valproic acid use complicated by symptomatic atrio-ventricular conduction block episodes on Holter monitoring. Symptomatic atrio-ventricular block episodes should be considered as an unusual side effect of valproic acid despite normal blood therapeutic level. Before consideration of pacemaker implantation in such cases, valproic acid usage should be investigated, and dose reduction should be attempted.

Obstructive sleep apnoea syndrome is an important health problem which may cause or worsen systemic diseases. Chronic intermittent hypoxia during repetitive airflow cessations may cause endothelial dysfunction. Sleep apnoea is also shown to be associated with hypercoagulability which may be due to decreased nitric oxide levels and impaired vasodilatation. Endothelial dysfunction, increased systemic inflammation, sympathetic nervous system activation, increased oxidative stress and dysglycaemia may all contribute to cardiovascular processes such as hypertension, arrhythmia, stroke, heart failure and coronary artery disease in patients with obstructive sleep apnoea. Treatment approaches in patients with obstructive sleep apnoea mainly focus on maintaining upper airway patency either with positive airway pressure devices or upper airway appliances. Strategies involving positive airway pressure therapy are associated with decreased morbidity and mortality. Obstructive sleep apnoea should be suspected as an underlying mechanism in patients with cardiovascular disease and warrants appropriate treatment.

Answer for impact of exercise on improving exercise capacity, quality of life or abnormal physiology that develops with mitral valve stenosis is lacking. Studies for identifying which patient subgroup might benefit the most and the optimal level of exercise needed to decrease symptoms need to be performed. Lack of research on this topic led us to speculate and propose potential effect and benefit of exercise training on rheumatic mitral stenosis. First, we report a fully asymptomatic adult patient with severe mitral valve stenosis complicated with pulmonary hypertension who is a heavy trainer performing isometric and isotonic exercises regularly for long time (approximately twenty years) (Fig. 1). Second, we discuss potential role and benefit of chronic training on exercise capacity, quality of life and improving abnormal physiology that develops in mitral stenosis.

The relationship between patients and physicians has maintained its importance throughout human history because of special features of the medical profession. This relationship engendered true loyalty of patients to their physicians as well as serious legal conflicts. Medical malpractice has gained importance among physicians and ignited discussion because of new articles added to the Turkish Penal Code in 2005. In a very short time, the penalties mandated had a chilling, negative effect on doctors, resulting in loss of affection for the profession, hesitation to intervene, and burnout syndrome. Cardiologists work in an environment where the line between life and death is very thin. The aim of the present study was to raise awareness and avoid possible grievances by informing them of their responsibilities under the law.

Myocardial dysfunction, pericarditis, arrhythmias and acute coronary syndromes (ACS) are reported as advers effect of 5-Fluorouracil (5-FU). A 43 year-old man admitted to hospital with a chest pain one hour. He had no history of cardiac disease, and also had no any cardiovasculer risk factors. The patient had history of colon carcinoma. One day ago, 5-FU was given as chemotherapy regimen at oncology department. There was ST segment elevation on anterior and inferior derivations. He was initially managed as an acute coronary syndrome and emergency coronary angiography was then performed and it was normal. While introvenous nitroglycerin, the chest pain disappeared and ECG elevation regressed. Cardiac markers were within the normal ranges. There was no any wall motion abnormality on echocardiography. He was accepted vasospastic angina according to 5-FU and discharged after one day. Consequently, after 5-FU therapy, acute coronary syndrome may become. Frequently, it is associated with vasospasm especially patients with no cardiac history, and it response to vasodilator therapy well.

A 47-year-old woman was admitted to the hospital with progressive exertional dyspnea and palpitation for two years. She suffered from dyspnea limiting her daily ordinary activity during the last 6 months. Her medical history was unremarkable. Her physical examination revealed that blood pressure was 100/80 mm Hg, heart rate was 82/min and regularly, respiratory rate was 32/min, O2 saturation while breathing room air was 95%. Holosystolic murmur 3/6 was heard at the lower sternal border. Breath sounds were decreased over the right hemithorax on auscultation. Increased jugular venous distention and lower extremity edema were noted. Chest X-ray showed diminished vasculature on right upper and middle lung zones (Fig. 1). Echocardiography showed enlarged and depressed right ventricle, moderate degree tricuspid regurgitation and severe pulmonary hypertension (PH) (estimated maximal systolic pulmonary arterial pressure 110 mm Hg). Left ventricle systolic and diastolic functions were normal. Respiratory function test was compatible with mild obstructive pattern. Right heart catheterization was performed and revealed that mean pulmonary artery pressure was 63 mm Hg, pulmonary vascular resistance was 16 Wood unit, and pulmonary capillary wedge pressure was 12 mm Hg. Also we further investigated the patient in terms of causes of PH including HIV, portal hypertension, and rheumatologic, hematologic and metabolic disease and all of them were ruled out. Taken together, the diagnosis of idiopathic pulmonary arterial hypertension (PAH) was made. We commence bosentan increased up to 125 mg bid then according her symptoms we added Tadalafil 40 mg qd.

The patient was a 39-year-old female with recurrent paroxysmal, regular narrow QRS complex tachycardia. Atrioventricular nodal reentrant tachycardia (AVNRT) was induced. The cryo-ablation attempts (-80°C, 240 second) were performed in the inferior-posterior triangle of Koch. We observed several junctional beats during cryo-ablation. After successful cryo-ablation, AVNRT induction was repeatedly checked during a waiting period of 30 minutes without recurrence. In our case we demonstrated that junctional beats can be observed during cryo-ablation. We believe this to be the first description of junctional beats occurring during cryo-ablation of AVNRT.

Atrial fibrillation (AF) is the most frequently observed arrhythmia in clinical practice. Many causative factors have been identified from well-known structural heart disease to less understood triggers. Both sympathetic and parasympathetic (vagal) stimuli are able to trigger paroxysms of AF. Vagally mediated AF is especially observed in young healthy subjects and especially during nights when the heart rate is considerably slow. Tachycardia induced AF is demonstrated and the possible mechanisms are explained. However, a case of bradycardia induced AF, thus far, hasn't been reported. Here we present a case of AF induced by severe bradycardia which was triggered by concomitant use of beta-blockers and diltiazem.

The aim of this study is to investigate possible factors influencing glomerular filtration rate (GFR) in obstructive sleep apnea (OSA).

The patient was a 68-year-old female with recurrent paroxysmal, regular narrow QRS complex tachycardia. We observed complete VA conduction block, during tachycardia in our patient. A characteristic feature of our patient is the noticeable irregular atrial and ventricular rates. We considered that possible mechanism of this tachycardia was atrioventricular nodal reentrant tachycardia (AVNRT) with retrograde complete type block in the upper common pathway.

BACKGROUND AND AIM OF STUDY: Rheumatic valvular heart disease, which remains a common health problem in developing countries, has numerous consequences on the heart chambers and circulation. The study aim was to investigate the effects of chronic rheumatic valve disease on the diameters of the descending aorta (DA) and inferior vena cava (IVC).METHODS: A total of 88 patients with echocardiographically documented rheumatic valvular heart disease and 112 healthy controls were enrolled into the study. All patients underwent detailed echocardiographic examinations, while their height and body weight were recorded and adjusted to their body surface area.RESULTS: The most common involvement was mitral valve disease, followed by aortic valve disease and tricuspid valve disease. The mean diameter of the DA (indexed to BSA) was 1.79 ± 0.49 cm for patients and 1.53 ± 0.41 for controls (p <0.001). The mean diameter of the IVC (indexed to BSA) was 1.69 ± 0.73 for patients and 1.38 ± 0.35 cm for controls (p <0.001). There was a significant positive correlation between mitral valve mean gradient and IVC diameter (p = 0.01, r = 0.18). There were also strong associations between the mitral valve area and the diameters of the DA (p = 0.001, r = -0.239) and IVC (p <0.001, r = -0.246).CONCLUSION: Rheumatic valve disease, especially mitral stenosis, was closely related to remodeling of the great vessels.

Objectives: Atrial fibrillation (AF) is one of the most common causes of preventable ischemic stroke and is related to increased cardiovascular morbidity and mortality. There is a lack of data in Turkey on the use of new oral anticoagulants (NOACs), and time in therapeutic INR range (TTR) in vitamin K antagonist users and AF management modality. In this multi-center trial, we aimed to analyze, follow and evaluate the epidemiological data in non-valvular AF patients. Study design: Four thousand one hundred consecutive adult patients from 42 centers with at least one AF attack identified on electrocardiography will be included in the study. Patients with rheumatic mitral valve stenosis and prosthetic valve disease will be excluded from the study. At the end of one year, the patients will be evaluated in terms of major cardiac end points (death, transient ischemic attack, stroke, systemic thromboembolism, major bleeding and hospitalization). Results: First results are expected in June 2015. Data about major cardiovascular end-points will be available in January 2016. Conclusion: The rates and kind of oral anticoagulant use, TTR in vitamin K antagonist users and main management modality applied in non-valvular AF patients will be determined by AFTER-2 study. In addition, the rate of major adverse events (MACEs) and the independent predictors of these MACEs will be detected (AFTER-2 Study ClinicalTrials.gov number, NCT02354456.).

BackgroundWe aimed to analyze ventricular repolarization in neurocardiogenic syncope (NCS) patients by using T-peak-T-end interval, T-peak-T-end/QT ratio, T-peak-T-end/QTc ratio and corrected QT interval (QTc), QT dispersion (QTd), QT index (QTI) and corrected QT interval index (QTcI) comparing with the corrected JT dispersion (JTcd), and corrected JT (JTc) and the corrected JT interval index (JTcI), by inspecting ventricular activation until termination of repolarization. These parameters are used as an index of potential ventricular arrhythmogenesis.MethodsWe have studied patients with head-up tilt table test (HUTT) (+) (33 patients; mean age: 28 11 years) and HUTT (-) as control group (33 patients; mean age: 30 11 years). In all patients, T-peak-T-end interval, T-peak-T-end/QT ratio, T-peak-T-end/QTc ratio, QT, QTd, QTI, QTc, QTcI, JTd, JTc, and JTcI were measured on electrocardiogram.ResultsThe following parameters were statistically significant between groups: QTd (22.72 +/- 17.54 msn; 11.21 +/- 13.40 msn; P = 0.004), QTc (424.27 +/- 33.75 msn; 403.66 +/- 38.08 msn; P = 0.023), QTcI (114.09 +/- 14, 29%; 106.71 +/- 15.33%, P = 0.047), and QTI (100.72 +/- 7.19%; 97.14 +/- 7.13%, P = 0.046). Furthermore, T-peak-T-end interval was significantly prolonged in the study group (93.78 +/- 20.27 msn; 81.21 +/- 11.66 msn; P = 0.003). T-peak-T-end/QT ratio was significantly higher in the study group (0.24 +/- 0.04 msn; 0.22 +/- 0.04 msn; P = 0.030). T-peak-T-end/QTc ratio was significantly higher in the study group (0.22 +/- 0.04 msn; 0.20 +/- 0.03 msn; P = 0.015). The JTc and JTd were also significantly higher in the study group ([103.00 +/- 9, 72%; 95.44 +/- 10.26%, P = 0.003], [27.57 +/- 16.01 msn; 10.45 +/- 16.08 msn; P < 0.001], respectively).ConclusionsElectrocardiographic ventricular repolarization parameters including T-peak-T-end interval, T-peak-T-end/QT ratio, T-peak-T-end/QTc ratio, QTc, QTd, QTI, QTcI, JTc, JTd, and JTI are prolonged in NCS.