Urosepsis is a very serious condition with a high mortality rate. The immune response is in the center of pathophysiology. The therapeutic management of these patients includes surgical treatment of the source of infection, antibiotic therapy and life support. The management of this pathology is multidisciplinary and requires good collaboration between the urology, intensive care, imaging and laboratory medicine departments. An imbalance of pro and anti-inflammatory cytokines produced during sepsis plays an important role in pathogenesis. The study of cytokines in sepsis has important implications for understanding pathophysiology and for development of other therapeutic solutions. If not treated adequately, urosepsis may lead to serious septic complications and organ sequelae, even to a lethal outcome.

Scleroderma, known also as systemic sclerosis (SSc), is a severe disease associated with high mortality rates, and right ventricular (RV) remodeling and dysfunction, along with pulmonary artery hypertension (PAH), are among the most important internal organ manifestations of this disease. PAH has a higher prevalence in patients with SSc compared to the general population and represents a significant predictor of mortality in SSc. In patients with SSc, the morphological remodeling and alteration of RV function begin even before the setting of PAH and lead to development of a specific adaptive pattern of the RV which is different from the one recorded in patients with IAPH. These alterations cause worse outcomes and increased mortality rates in SSc patients. Early detection of RV dysfunction and remodeling is possible using modern imaging tools currently available and can indicate the initiation of specific therapeutic measures before installation of PAH. The aim of this review is to summarize the current knowledge related to mechanisms involved in the remodeling and functional alteration of the RV in SSc patients.

Background: Little is known on the effect of epicardial fat in pulmonary arterial hypertension (PAH). Therefore, the present study sought to perform a comparative analysis on the influence of epicardial fat thickness (EFT) on the right and left ventricular function, between three different etiological varieties of pulmonary arterial hypertension: caused by congenital heart defects (atrial septum defects with left to right shunt), by systemic sclerosis, and by myocardial ischemia. Materials and Methods: This is a prospective observational study on 50 patients with documented PAH (systolic pulmonary artery pressure -PASP of >35 mmHg). The thickness of the epicardial adipose tissue was evaluated by 2D cardiac ultrasound, on the free wall of the right ventricle, during end-diastole, in the long parasternal axis view. The patients were divided into three study groups: Group 1 -PAH determined by congenital heart defects with left to right shunts (atrial septum defects, n = 25); Group 2 -PAH induced by systemic sclerosis (n = 12); Group 3 -PAH induced by myocardial ischemia (n = 13). Results: The average age was 54.48 ± 10.78 years, 30% (n = 15) of subjects were males, with a mean body mass index of 24.65 ± 4.40 kg/m 2 , EFT was 9.15 ± 2.24 mm, and the PASP was 41.33 ± 5.11 mmHg. Patients in Group 3 were more likely to smoke (p = 0.025) and presented a significantly lower LVEF, compared to the other groups (Group 1: 60% ± 6 vs. Group 2: 60% ± 7 vs. Group 3: 48% ± 7, p <0.0001). The largest EFT was found in Group 3 (11.08 ± 2.39 mm), followed by Group 2 (9.14 ± 2.03 mm), and Group 1 (8.16 ± 1.57 mm) (p = 0.0003). The linear regression analysis found no significant correlations between EFT and other echocardiographic parameters: PASP (r = -0.228, p = 0.118), LVEF (r = -0.265, p = 0.06), TAPSW (r = 0.015, p = 0.912), TEI (r = 0.085, p = 0.552), RVEDD (r = -0.195, p = 0.173), RA area (r = -178, p = 0.214), and LA diameter (r = 0.065, p = 0.650). Conclusions: Epicardial fat thickness was found to be significantly higher in patients with PAH induced by myocardial ischemia, followed by those with systemic sclerosis and congenital heart defects, respectively. EFT did not influence the echocardiographic parameters for left and right ventricular function in patients with pulmonary arterial hypertension of different etiologies.

Background: The impact of pulmonary arterial hypertension (PAH) on left ventricular performance in patients with scleroderma is still unknown. This study aims to perform a comparative echocardiographic analysis of left ventricular function between two different etiological varieties of PAH, namely PAH caused by systemic sclerosis as a representative of systemic inflammatory diseases and PAH caused by myocardial ischemia. Material and method: We conducted a prospective observational study on 82 patients, of which 36 were with documented PAH, with the systolic pressure in the pulmonary artery above 35 mmHg, and 46 were patients with normal pulmonary artery pressure. The study population was divided into two groups, based on the etiology of PAH: group 1 included patients diagnosed with scleroderma (n = 48); group 2 included patients with coronary artery disease (n = 35). Patients from each group were divided into two subgroups based on the diagnosis of PAH: subgroup 1A – subjects with scleroderma and associated PAH (n = 20); subgroup 1B – subjects with scleroderma without PAH (n = 28); subgroup 2A – ischemic patients with associated PAH (n = 16); and subgroup 2B – patients with ischemic disease without PAH (n = 19). Results: A significant difference between LVEF values in patients with PAH versus those without PAH in the ischemic group (p = 0.023) was recorded. Compared to scleroderma subjects, ischemic patients presented significantly lower values of LVEF in both PAH and non-PAH subgroups (p <0.0001 and p <0.0001, respectively). Linear regression analysis between sPAP and LVEF revealed a significant negative correlation only for the ischemia group (r = −0.52, p = 0.001) and the scleroderma 2B subgroup (r = −0.51, p = 0.04). Tissue Doppler analysis of left ventricular function revealed a significant impact of PAH on left ventricular diastolic performance in the ischemic group. Conclusions: Compared to patients with coronary artery disease, those with scleroderma present a less pronounced deterioration of LVEF in response to pulmonary arterial hypertension.

Funding Acknowledgements PlaqueImage Background The relationship between the degree of pulmonary hypertension (PH) and left ventricular performance in patients with systemic sclerosis is still a controversial issue in the literature. We aimed to conduct a comparative analysis of indexes characterizing left ventricular systolic and diastolic function, in two etiological types of pulmonary hypertension involving different pathophysiological mechanisms: PH caused by systemic sclerosis and PH caused by myocardial ischemia. Material and method We performed a prospective study on 83 patients (36 patients with documented PAH with a systolic pulmonary arterial pressure – sPAP of &gt;35 mmHg and 47 subjects with normal sPAP), out of which group 1 – with systemic sclerosis (n = 48); group 2 – significant coronary artery disease - CAD (n = 35). Patients of each group were divided in two subgroups based on the diagnosis of PH: group 1A - subjects with scleroderma and associated PH (n = 20), group 1B - subjects with scleroderma without PH (n = 28), group 2A - ischemic patients with associated PH (n = 16) and subgroup 2B - patients with ischemic disease without PH (n = 19). Results Patients in group 1 presented a significantly higher number of female subjects (p = 0.001) and a higher mean age (p = 0.009) compared to group 2. Patients with associated PH presented a significantly lower left ventricular ejection fraction (LVEF) compared to those without PH within the ischemic group (p = 0.023). There was a significant inverse correlation between the sPAP and LVEF in ischemic patients (r=-0.52, p = 0.001) as well as for scleroderma patients without PH (r=-0.51, p = 0.04). Tissue Doppler analysis of the left ventricular function indicated a significant negative correlation between the septal E’ value versus the sPAP and lateral E’ value versus the sPAP (r=-0.49, p = 0.002; r=-0.43, p = 0,008). Conclusions Intrinsic myocardial damage plays an important role in left ventricular systolic function even in the absence of PAH. Scleroderma patients present a less pronounced deterioration of the LVEF in response to pulmonary hypertension, indicating that in this group, additional compensatory mechanisms could be involved in the complex response of myocardium to elevated pulmonary pressures.