Background: Nonbacterial thrombotic endocarditis is characterized by the presence of organized thrombi on cardiac valves, often associated with hypercoagulable states. There is a paucity of data regarding the predictors of mortality in patients with nonbacterial thrombotic endocarditis. Our primary aim was to identify predictors of in-hospital mortality in patients with nonbacterial thrombotic endocarditis.

Methods: A systematic literature review of all published cases and case series was performed until May 2018 according to Preferred Reporting Items for Systematic Review and Meta-analyses statement guidelines. We applied random forest machine learning model to identify predictors of in-patient mortality in patients with nonbacterial thrombotic endocarditis.

Results: Our search generated a total of 163 patients (mean age, 46 ± 17 years; women, 69%) with newly diagnosed nonbacterial thrombotic endocarditis. The in-hospital mortality rate in the study cohort was 30%. Among the patients who died in the hospital, initial presentation of pulmonary embolism (12.2 vs. 2.6%), splenic (38.7 vs. 10.5%), and renal (40.8 vs. 9.6%) infarcts were higher compared to patients alive at the time of discharge. Higher rates of malignancy (71.4 vs. 39.4%, P =.0003) and lower rates of antiphospholipid syndrome (8.1 vs. 48.2%, P =.0001) were noted in deceased patients. Random forest machine learning analysis showed that older age, presence of antiphospholipid syndrome, splenic infarct, renal infarct, peripheral thromboembolism, pulmonary embolism, myocardial infarction, and mitral valve regurgitation were significantly associated with increased risk of in-hospital mortality.

Conclusion: Patients admitted with nonbacterial thrombotic endocarditis have a high rate of in-hospital mortality. Factors including older age, presence of antiphospholipid syndrome, splenic/renal infarct, lower limb thromboembolism, pulmonary embolism, myocardial infarction, and mitral valve regurgitation were significantly associated with increased risk of in-hospital mortality in patients with nonbacterial thrombotic endocarditis.

Background: The endothelium is crucial for the control of vascular homeostasis and plays a role in angiogenesis. Leptin, a protein released mainly by adipose tissue, plays a key role in the regulation of energy balance and angiogenesis. We aimed to investigate the changes of endothelial nitric oxide synthetase expression on human umbilical vein endothelial cells wound healing model after leptin treatment.

Methods: In this study, 5 groups were planned as Group 1: control (untreated), Group 2: treated with 0.1 ng/mL leptin, Group 3: treated with 1 ng/mL leptin, Group 4: treated with 10 ng/mL leptin, and Group 5: treated with 100 ng/mL leptin. Closure rates of wound areas were calculated by the Image J program after 24 hours of leptin treatment. The WST-1 assay was used to calculate the cell viability. Immunocytochemical analysis was performed for endothelial nitric oxide synthase expression and H-Score was calculated.

Results: The closure rates of wound areas were calculated as 80.24%, 89.73%, 87.40%, 90.73%, and 93.70%, respectively. When all groups treated with leptin were compared with the control group, there was a statistically significant difference (P <.05). The WST-1 results showed that the most increasing levels of viable cells were found in the groups treated with 0.1 ng/mL leptin and 100 ng/mL leptin when compared to the control group. H-Score values of each group were calculated as 284.8 ± 15.22, 288.6 ± 8.41, 291 ± 8.16, 295.2 ± 11.60, and 308.8 ± 4.32, respectively. The difference between the control group and the group treated with 100 ng/mL leptin was statistically significant (P <.05).

Conclusions: Endothelial nitric oxide synthase expression in human umbilical vein endothelial cells increased depending on the leptin dose and the highest increase was in the group treated with 100 ng/mL leptin.

Background: The use of prosthetic valves and intracardiac devices has steadily increased in recent years. In this group of patients with prosthetic valves or intracardiac devices, infective endocarditis could not be easily diagnosed, and in general, infective endocarditis can be missed in many patients. The purpose of this study was to evaluate the diagnostic performance of clinical, laboratory, and imaging parameters in a group of patients with pre-diagnosis of infective endocarditis.

Methods: Ninety-four patients diagnosed with prosthetic valve or intracardiac device endocarditis during 2008-2019 were included in the study. The patients’ data were evaluated according to modified Duke criteria, and the data of the patients who were diagnosed with and without a definitive infective endocarditis were compared accordingly.

Results: Values of procalcitonin (P <.001), leukocytes (P =.004), C-reactive protein (P <.001), sedimentation (P <.001), and maximal vegetation size (P =.012) were found to be significant in the diagnosis of IE. Criteria to determine definitive IE included a C-reactive protein level of 105 mg/dL or higher, 77% sensitivity, 75% specificity, 60% positive predictive value, and 87% negative predictive value. In particular, a C-reactive protein level of ≥105 mg/dL was found to positively indicate the diagnosis of definitive infective endocarditis by 10 times (odds ratio = 10; 95% CI: 3.6-27.8, P <.001). In a multiple logistic regression
analysis, the C-reactive protein level was found to be the best independent predictor of definitive infective endocarditis in this population.

Conclusion: In cases of prosthetic valve and intracardiac devices endocarditis where prediagnosis
is difficult to confirm, measuring C-reactive protein levels is a reliable, strong, and simple parameter for definitive infective endocarditis diagnosis.

Background: Considering that ectopic fat accumulation in various organs, especially the heart and liver, is a cardiometabolic risk factor, the need for easily accessible markers of ectopic fat accumulation is inevitable. The main starting point of the study is based on the hypothesis of predicting cardiovascular disease risk through the link that can be established between the liver–spleen ratio, which is one of the strong indicators of hepatosteatosis, and epicardial adipose tissue volume.

Methods: This was a retrospective study. The records of 283 consecutive patients who underwent coronary computed tomography angiography in our Radiology Department were reviewed retrospectively from our hospital’s system. All patients’ epicardial adipose tissue volume and liver–spleen ratio were calculated using appropriate criteria on non-contrast computed tomography images. Additionally, the Coronary Artery Disease–Reporting and Data System was calculated on contrast computed tomography images. The participating patients were divided into groups according to the liver–spleen ratio and Coronary Artery Disease–Reporting and Data System score.

Results: We found that while there was a negative correlation between the liver–spleen ratio and epicardial adipose tissue volume in the hepatosteatosis group, this relationship was not observed in the non-steatosis group. In addition, we observed that the family history of cardiovascular disease and the frequency of cardiovascular disease were higher in the hepatosteatosis group than in the other group, and there was a correlation between cardiovascular disease and the liver–spleen ratio. Also, we found that age and liver–spleen ratio values were found to be independent predictors of coronary artery disease.

Conclusion: In our study, we found that the frequency of cardiovascular disease was lower in patients with a high liver–spleen ratio. We also demonstrated in the study that the liver–spleen ratio, which indicates a low level of epicardial adipose tissue volume accumulation, is an independent predictor of cardiovascular disease. In addition, the use of liver–spleen ratio, which is more valuable than liver attenuation in predicting hepatic steatosis, may be more useful in evaluating the risk of hepatosteatosis-related cardiovascular disease.

Background: In this study, we investigated whether left atrial functions evaluated by speckle tracking echocardiography, classic echocardiographic and clinic parameters predict appropriate Implantable Cardioverter Defibrillator (ICD) shock in patients who underwent ICD implantation for hypertrophic cardiomyopathy.

Methods: Totally 87 patients who received ICD implantation for primary or secondary prevention were included in the study. Patients’ clinical, elect rocardiographic, 2 dimension classic, and speckle tracking echocardiographic data were collected. Left atrial functions were assessed by speckle tracking echocardiography. Left atrial strain just before mitral valve opening was taken as peak atrial longitudinal strain. Appropriate ICD therapy was defined as cardioversion or defibrillation due to ventricular tachycardia or fibrillation. Patients were divided into 2 groups as occurrence or absence of appropriate ICD therapy during follow-up (mean, 50.2 ± 9.3 months). Patients with an European Society of Cardiology (ESC) risk score >6% were considered high-risk patients.

Results: A total of 24 (27.5 %) patients were observed to have an appropriate ICD therapy. In patients on whom appropriate ICD therapy was performed, a higher Sudden Cardiac Death risk Score and decreased peak atrial longitudinal strain and global longitudinal
peak strain were observed. In patients with high ESC risk score (> 6%), in Cox regression analysis, peak atrial longitudinal strain (odds ratio: 0.806, P =.008), Sudden Cardiac Death risk score (odds ratio: 1.114, P =.03) and global longitudinal peak strain (odds ratio: 1.263, P =.02) were found to be independent predictors of occurrence of appropriate ICD therapy.

Conclusion: Easily measurable peak atrial longitudinal strain may provide additional information in predicting ventricular arrhythmias or deciding on prophylactic medical treatment to prevent ventricular arrhythmias or reduce the frequency of appropriate shock in high-risk patients with ICD implanted.

Background: In this single-center study, we evaluated efficacy and safety issues and predictors of survival in patients with idiopathic and congenital heart disease-associated pulmonary arterial hypertension who were under macitentan therapies.

Method: Our study retrospectively evaluated 221 patients with pulmonary arterial hypertension enrolled in our single-center study, and mono, dual, and triple macitentan therapies were noted in 30, 115, and 76 patients, respectively. The longitudinal changes in clinical, neurohumoral, and echocardiographic measures of pulmonary arterial hypertension were evaluated. The Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management, Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management 2.0, and Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management Lite 2 scores  at baseline, Swedish PAH Registry, Comparative Prospective Registry of Newly Initiated Therapies for Pulmonary Hypertension registry, and French Pulmonary Hypertension Network registry risk status both at baseline and first control were assessed.

Result: The median follow-up period was 1068 [415-2245] days. Macitentan was associated with significant improvements in functional class, 6-minute walk distance, N-terminal pro-brain natriuretic peptide (NT-proBNP), and echocardiographic measures without any deterioration of hemoglobin or hepatic enzymes. The low-risk scores with each model at baseline and/or first control are related to significantly better survival. Age, gender, and log-NT-proBNP in time-fixed and idiopathic pulmonary arterial hyper-tension, and log-NT-proBNP in time-dependent Cox proportional hazard regression analyses were independent predictors of mortality.

Conclusion: Mono- or sequential combination macitentan therapies were associated with sustained benefits in functional class, 6-minute walk distance, NT-proBNP, and echocardiographic measures in patients with idiopathic pulmonary arterial hypertension and con-genital heart disease-associated pulmonary arterial hypertension, and low-risk scores at baseline and/or first controls can be translated to better survival.