PurposeThe aim of this study was to assess whether nebivolol treatment could have beneficial effects in the prevention of anthracyclines-induced cardiotoxicity.Patients and methodsOur prospective study included 60 women, mean age 52.6±13 years, with HER2 negative breast cancer, scheduled to undergo treatment with doxorubicin. The patients were randomly divided into two groups: the treatment group (n=30) which received nebivolol 5 mg once daily for the duration of chemotherapy and the control group (n=30) without treatment with nebivolol. Cytostatic treatment was performed with doxorubicin 70 mg/m2 administered intravenously every 21 days for six cycles. The average cumulative dose of doxorubicin was 520±8 mg/m2. Echocardiography was performed immediately before and after six cycles of doxorubicin therapy.ResultsWe found no significant differences between the two groups regarding baseline clinical and echocardiographic parameters. The two groups reached a similar cumulative dose of doxorubicin. No patient died during the study. None of the patients withdrew from chemotherapy. After six cycles of doxorubicin therapy, the left ventricular (LV) ejection fraction, shortening fraction, and LV diameters changed, but not significantly. Tissue Doppler imaging (TDI) detected in the control group a significant decrease of myocardial velocities, indicating a LV diastolic dysfunction. In the same group, speckle tracking imaging (STI) revealed a statistically significant alteration of the ventricular deformation, which means a decrease in LV systolic function. In the nebivolol treatment group, no significant alterations in the LV systolic and diastolic function were observed.ConclusionThe results of this study show the benefit of new echocardiographic imaging methods such as TDI and STI in the screening of early cardiac dysfunction induced by cytostatic treatment. Nebivolol treatment prevented the occurrence of anthracyclines-induced cardiomyopathy in the short term. In order to confirm these preliminary results, larger studies with a longer follow-up period are required.

BackgroundThe purpose of this retrospective study was to evaluate the prognostic impact of systolic blood pressure (SBP) and heart rate (HR) on in-hospital mortality in ST-segment elevation acute myocardial infarction (STEMI) patients, after primary percutaneous intervention (PCI).Patients and methodsThe study included 294 patients admitted for STEMI. They were divided into five groups according to the SBP at admission: group I, <105 mmHg; group II, 105–125 mmHg; group III, 126–140 mmHg; group IV, 141–158 mmHg; and group V, ≥159 mmHg. Increased HR was defined as ≥80 beats per minute (bpm). In-hospital death was defined as all-cause death during admission and classified into cardiac and noncardiac death.ResultsAmong the 294 patients admitted for STEMI, 218 (74%) were men. The mean age was 62±17 years. In-hospital mortality rate was 6% (n=18), with 11 (3.7%) deaths having cardiac causes. The highest mortality was registered in group I (n=9, 16%, P=0.018). Compared to the other groups, group I patients were older (P=0.033), more often smokers (P=0.026), and had a history of myocardial infarction (P=0.003), systemic hypertension (P=0.023), diabetes (P=0.041), or chronic kidney disease (P=0.0200). They more often had a HR ≥80 bpm (P=0.028) and a Killip class 3 or 4 at admission (P=0.020). The peak creatine phosphokinase-MB level was significantly higher in this group (P=0.005), while the angiographic findings more often identified as culprit lesions were the right coronary artery (P=0.005), the left main trunk (P=0.040), or a multivessel coronary artery disease (P=0.044). Multivariate analysis showed that group I patients had a significantly higher risk for both all-cause death (P=0.006) and cardiac death (P=0.003). Patients with HR ≥80 bpm also had higher mortality rates (P=0.0272 for general mortality and P=0.0280 for cardiac mortality).ConclusionThe present study suggests that SBP <105 mmHg and HR ≥80 bpm at admission of STEMI patients are associated with a higher risk of in-hospital death, even after primary PCI.

This study aimed to assess the serum levels of intracellular adhesion molecule (sICAM-1), and vascular cell adhesion molecule (sVCAM-1), in the first psychotic episode schizophrenia (SZ) patients, before and after six months of antipsychotic treatment. Patients and Methods: The study included 50 patients with a first hospitalization for SZ and 50 healthy control subjects that were patient-matched regarding age, gender, body mass index and smoking status. The evaluation included the presence of cardiovascular risk factors, measurements of systolic and diastolic blood pressure, body mass index, smoking status, anklebrachial index, carotid intima-media thickness, and echocardiography. The Brief Psychiatric Rating Scale (BPRS) score was calculated for the patients. The plasma levels of fasting glucose, total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, sICAM-1 and sVCAM-1 were determined at baseline in all subjects and after six months of antipsychotic treatment. Thirty patients (60%) were treated with olanzapine and 20 (40%) with risperidone. Results: The average age of patients experiencing their first episode of SZ was 29.7±6.6 years, and 23 (46%) were men. The initial sICAM-1 levels of the patients were lower than those of the control group (P<0.0001), and increased after treatment (P=0.02), but remained lower than in the healthy controls (P=0.026). The initial levels of sVCAM-1 levels were higher in the patients (P<0.0001) and decreased after treatment (P<0.0001) to values that were similar to those of the control group (P=0.39). The only independent predictor of a baseline BPRS over 120 was the baseline sVCAM-1 level (P<0.0001). Antipsychotic treatment induced significant decreases in BPRS score (P<0.0001), in systolic (P=0.005) and diastolic (P<0.0001) blood pressure, in HDLc (P=0.02), as well as significant increases in blood glucose (P<0.01) and LDL-c (P<0.001), with no differences between olanzapine and risperidone. Conclusion: In the patients experiencing an FEP of SZ, the levels of sICAM-1 were lower, while the levels of sVCAM-1 were higher than in the healthy control subjects. The antipsychotics used in the treatment of schizophrenia increased sICAM-1 and decreased sVCAM. The baseline level of sVCAM-1 was an independent predictor of a BPRS score >120 at baseline.

BackgroundThrombospondin-1 (TSP-1) is a matricellular functional protein of the extracellular matrix. As it is not constitutively present extracellularly, its secretion is enhanced in several situations, namely injury, chronic pathology, tissue remodeling, angiogenesis, and aging. Over the last decade, TSP-1 has been reported to be involved in complex and opposing biological effects on vasculature in the context of NO signaling. Several studies have reported high patient TSP-1 plasma levels, indicating that the protein can potentially serve as a prognostic marker for pulmonary arterial hypertension.Materials and methodsHere, we aimed to quantify TSP-1 serum levels in hypertensive patients with endothelial dysfunction before and after one year of treatment with Perindopril (an antihypertensive drug with vasoprotective properties).ResultsAfter one year of treatment, TSP-1 levels increased in hypertensive patients compared to baseline (T0: 8061.9 ± 3684.80 vs T1: 15380±5887 ng/mL, p<0.001) and compared to non-hypertensive controls (9221.03 ± 6510.21 ng/mL). In contrast, pentraxin-3 plasma levels were decreased after one year of Perindopril treatment in both hypertensive (T0: 0.91 ± 0.51 vs T1: 0.50 ± 0.24 ng/mL, p<0.001) and control group (1.36 ±1.5 ng/mL) patients, although flow-mediated vasodilation and intima-media thickness assessment parameters were not significantly changed. Systolic and diastolic blood pressure values as well as levels of fibrinogen, high-sensitivity C-reactive protein, triglycerides, and alanine aminotransferase were found to be significantly lower after one year of treatment with Perindopril. High levels of TSP-1 strongly correlated with platelet count (positive), lymphocytes (positive), red cell distribution width-CV (positive), systolic blood pressure (negative), and mean corpuscular hemoglobin (negative) after one year of treatment. Blood urea nitrogen was found to be a protective factor for TSP-1, while glucose and heart rate were found to be risk factors prior to and after treatment.

Purpose The constitutive elements of the metabolic syndrome (MetS) are linked with both non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease. Controlled attenuation parameter (CAP), and vibration controlled transient elastography (VCTE), are able to detect and quantify NAFLD, while conventional and two-dimensional speckle tracking echocardiography (2D-STE) is capable to identify subclinical changes in cardiac function. We wanted to evaluate whether there is any correspondence between left ventricular (LV) diastolic dysfunction and different degrees of liver steatosis and fibrosis in MetS subjects with NAFLD. Patients and Methods A total of 150 adult subjects having MetS and a normal left ventricular (LV) systolic function were recorded in the study, while 150 age- and sex- matched adults without MetS were enrolled as controls. NAFLD was established by VCTE and CAP. The left heart systolic and diastolic function was evaluated by conventional and 2D-ST echocardiography. Left atrial (LA) stiffness was calculated as the ratio between the E/A ratio and the LA reservoir-strain. Results In univariate regression analysis, the variables associated with LV diastolic dysfunction in MetS patients were: liver steatosis grade ≥2, liver fibrosis grade ≥2, the longitudinal LA peak strain during the reservoir phase, the LA strain rate during ventricular contraction and the LA stiffness. In multivariate logistic regression, two variables were selected as independent predictors of LV diastolic dysfunction, namely the liver stiffness (P=0.0003) and the LA stiffness (P<0.0001). LA stiffness predicted subclinical LV diastolic dysfunction in MetS patients with a sensitivity of 45% and a specificity of 96% when using a cut-off value >0.38, and was significantly correlated with liver steatosis stage ≥2 and liver fibrosis stage ≥2. Conclusion The present study confirms the association between liver stiffness, LA stiffness and LV diastolic dysfunction in MetS patients. Our study suggests that liver elastography and 2D-STE should become habitual assessments in MetS patients.