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WOS: 000462345900002, PubMed ID: 30860204, Natriuretic peptides have long been introduced into clinical practice. These biomarkers have certainly been shown to provide useful information in the diagnosis, prognosis and risk stratification in heart failure and also may have a role in the guidance of heart failure therapy. Although, there are some limitations in using of these markers such as lack of specificity, aging, renal dysfunction or obesity, among the huge number of candidates for heart failure biomarkers, only natriuretic peptides are currently widely used in daily clinical practice in heart failure. Recent heart failure guidelines recognize natriuretic peptides as an essential tool in the new diagnostic and therapeutic algorithms. Furthermore, natriuretic peptides are not only used in the diagnosis or prognosis of heart failure, but also these biomarkers are referred to have some potential role in primary prevention, cardio-oncology, advanced heart failure, assessment of response to cardiac resynchronization therapy, pulmonary arterial hypertension, acute coronary syndromes, atrial fibrillation and valvular heart disease. In this article, natriuretic peptides have been reviewed for their updated information and new recommendations in heart failure and also potential role of these biomarkers in the management of various clinical conditions have been addressed in the form of expert opinion based on the available data in the literature.

[Abstract] This article updates the Heart Failure Association of the European Society of Cardiology (ESC) 2007 classification of advanced heart failure and describes new diagnostic and treatment options for these patients. Recognizing the patient with advanced heart failure is critical to facilitate timely referral to advanced heart failure centres. Unplanned visits for heart failure decompensation, malignant arrhythmias, co‐morbidities, and the 2016 ESC guidelines criteria for the diagnosis of heart failure with preserved ejection fraction are included in this updated definition. Standard treatment is, by definition, insufficient in these patients. Inotropic therapy may be used as a bridge strategy, but it is only a palliative measure when used on its own, because of the lack of outcomes data. Major progress has occurred with short‐term mechanical circulatory support devices for immediate management of cardiogenic shock and long‐term mechanical circulatory support for either a bridge to transplantation or as destination therapy. Heart transplantation remains the treatment of choice for patients without contraindications. Some patients will not be candidates for advanced heart failure therapies. For these patients, who are often elderly with multiple co‐morbidities, management of advanced heart failure to reduce symptoms and improve quality of life should be emphasized. Robust evidence from prospective studies is lacking for most therapies for advanced heart failure. There is an urgent need to develop evidence‐based treatment algorithms to prolong life when possible and in accordance with patient preferences, increase life quality, and reduce the burden of hospitalization in this vulnerable patient population.

WOS: 000385271000002, Heart failure is a progressive disease. A considerable portion of patients reach an advanced or terminal phase later or sooner, despite all of the developments in diagnosis, management, and follow-up and alternatives which can slow the disease process. As well as the palliative care of the patient in the terminal phase, definite recognition of the patient with advanced disease is vital for the consideration of therapeutic options in this patient population. Overall management and care of patients with heart failure obligates a collaboration of multiple disciplines. In addition, patients with advanced heart failure should be managed by a "heart team", as indicated by the guideline recommendations, since it requires a close communication and collaboration among cardiologists, cardiovascular surgeons, and other medical staff who are responsible for taking care of these patients. In Turkey, we have experienced physicians for managing patients with advanced heart failure. However, we are unlikely to be sufficient in the distribution of the centers and equal accessibility for all patients to therapeutic options. Hence, we still have more to do for the referral of eligible patients and patient circulation issues. This consensus report is developed to strengthen the connection between experienced and certified centers and the centers which take care of heart failure patients independent of the disease phase and other healthcare staff to increase awareness and to provide updated information for the current conditions of Turkey.

Objective: Germline mutations in the bone morphogenetic protein receptor type-2 (BMPR2) gene are considered to be a major risk factor for pulmonary arterial hypertension (PAH). BMPR2 mutations have been reported in 10%-20% of idiopathic PAH and in 80% of familial PAH cases. the aim of this study was to evaluate the frequency of mutations in the serine/threonine kinase domain of the BMPR2 gene in a group of patients from a single PAH referral center in Turkey.Methods: This cross-sectional study used a DNA-sequencing method to investigate BMPR2 mutations in the serine-threonine-kinase domain in 43 patients diagnosed with PAH [8 with idiopathic PAH and 35 with congenital heart disease (CHD)] from a single PAH referral center. Patients were included if they had a hemodynamically measured mean pulmonary arterial pressure of >25 mm Hg with a mean pulmonary capillary wedge pressure of A)], in one patient with idiopathic PAH in exon 8 of the BMPR2 gene. the mutation was detected in a 27-year-old female with a remarkable family history for PAH. She had a favorable response to endothelin receptor antagonists. No mutations were detected in the exons 5-11 of the BMPR2 gene in the PAH-CHD group.Conclusion: A missense mutation was detected in only one of the eight patients with idiopathic PAH. the BMPR2 missense mutation rate of 12.5% in this cohort of Turkish patients with idiopathic PAH was similar to that seen in European registries. the index patient was a young female with a family history remarkable for PAH; she had a good long-term response to PAH-specific treatment, probably due to the early initiation of the treatment. Genetic screening of families affected by PAH might have great value in identifying the disease at an early stage.

Objective: Allograft rejection is still an important cause of morbidity and mortality after heart transplantation (HTx). Many techniques in cardiac magnetic resonance imaging (CMR) were investigated to diagnose acute cellular rejection (ACR). However, there is not enough information about late gadolinium enhancement (LGE) in the myocardium and ACR.Methods: We prospectively analyzed our consecutive 41 heart transplant recipients who were admitted for routine endomyocardial biopsies. CMR was performed maximum 6 h before the scheduled endomyocardial biopsy. Correlation between LGE in the myocardium and ACR was investigated.Results: Twenty-seven patients showed no rejection, and nine of them had LGE in the myocardium. Fourteen patients had LGE in the left ventricle (LV), and two patients had LGE also in the right ventricle (RV). There was no correlation between LGE and ACR (p=0.879). There was no difference in the left ventricular ejection fraction (LVEF), right ventricular fractional area change (RVFAC), and cardiac ischemic time between the groups (p=0.825, p=0.370, and p=0.419, respectively). LGE in the myocardium could be due to previous rejection episodes; therefore, all patients were retrospectively searched for previous rejection grades and number of episodes. Thirty-eight of the 41 patients had a history of one ACR episode, but none of them had a statistically significant correlation with LGE (for grade 1R, p=0.964 and grade 3R, p=1) There was also no correlation between number of rejection episodes history and LGE.Conclusion: LGE is not suitable to detect ACR in heart transplant patients. LGE and the history of ACR have no correlation.

WOS: 000273266400002, PubMed ID: 19965312, Acute heart failure syndrome is a heterogeneous group, which requires distinct therapeutic approaches. Diuretics and/or vasodilators for patients with high blood pressure and inotropic agents for patients with low left ventricular ejection fraction and evidence of hypoperfusion are kept in the forefront. Early initiation of therapy along with accurate and early diagnosis in acute heart failure reduces mortality and morbidity significantly. Therefore, it is critically important to develop algorithms, which could easily be followed by all physicians. In this paper, in parallelism with heart failure guidelines and utilizing data of the clinical studies, performed by colleagues of our country in this area, therapeutic algorithms compatible with the conditions of our country are suggested for distinct clinical presentations of acute heart failure. (Anadolu Kardiyol Derg 2009; 9: 436-46)

3rd World Heart Failure Congress -- NOV 29-DEC 02, 2012 -- -- Istanbul, TURKEY, WOS: 000311698200190, …

3rd World Heart Failure Congress -- NOV 29-DEC 02, 2012 -- -- Istanbul, TURKEY, WOS: 000311698200070, …

[Özet Yok]

WOS: 000253867900004, PubMed ID: 17347068, Objective: Myocardial bridge (MB) is a congenital anomaly characterized by narrowing during systole of some of the epicardial coronary arterial segments running in the myocardium. Although, it is considered as a benign anomaly, it may lead to such complications as acute myocardial infarction, ventricular tachycardia, syncope, atrioventricular block and sudden cardiac death. In this study, we aimed to investigate demographic, clinical and angiographic characteristics of the patients with MB found on coronary angiography. Methods: The present study included 71 patients with MB found on coronary angiographies performed in our institution between January 1999 and September 2003. Based on the findings on angiography, the patients were subdivided into group A (n=41) and group B (n=30). The patients in the group A had no atherosclerotic lesion and the patients in the group B had coronary artery disease in addition to MB. Angiographic, demographic and clinical characteristics of both groups were compared. Results: There were no differences between two groups in distribution of gender and risk factors of coronary artery diseases whereas mean age of the patients in the group A was lower (47 +/- 5 years vs 55 +/- 11 years, p = 0.01). Frequency of two or more risk factors for coronary artery disease in a particular patient was significantly higher in the group B (55% vs 30%, p = 0.03). Myocardial bridge was located at proximal or mid segments of left anterior descending artery (LAD) in 40 patients whereas its presence in both LAD and right coronary artery was found only in one patient in group A. Mean bridging percent was 43 +/- 27% in group A. Localization of MB was LAD in 29 patients of group B, which was significantly higher than in group A (p

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