P Pu ur rp po os se e: : Severe pulmonary hypertension (PH) is a major cause of right ventricular (RV) dysfunction. Various iv vasodilator modalities have been used with limited results because of lack of pulmonary selectivity. The aim of the present controlled study was to evaluate the efficacy of inhaled iloprost, a synthetic prostacyclin analogue, in patients with elevated pulmonary vascular resistance (PVR) immediately after separation from cardiopulmonary bypass (CPB).M Me et th ho od ds s: : Twelve patients with persistent PH after discontinuation of CPB were included in the study. In all patients standard hemodynamic monitoring was used. Inhaled iloprost was administered via nebulized aerosol at a cumulative dose of 0.2 µg·kg -1 for a total duration of 20 min. Complete sets of hemodynamic measurements were performed before inhalation (baseline), during and after cessation of the inhalation period. Echocardiographic monitoring of RV function was also used.R Re es su ul lt ts s: : Inhaled iloprost induced a reduction in the transpulmonary gradient at the end of the inhalation period in comparison to baseline (9.33 ± 3.83 mmHg vs 17.09 ± 6.41 mmHg, P < 0.05). The mean pulmonary artery pressure to systemic artery pressure ratio decreased over this period (0.28 ± 0.08 vs 0.45 ± 0.17, P < 0.05). A statistically significant decrease of the PVR to systemic vascular resistance ratio was also observed (0.15 ± 0.05 vs 0.21 ± 0.05, P < 0.05). Improved indices of RV function were observed in echocardiographic monitoring.C Co on nc cl lu us si io on n: : Inhaled iloprost appears to be a selective pulmonary vasodilator and may be effective in the initial treatment of PH and the improvement of RV performance in the perioperative setting. (9,33 ± 3,83 mmHg vs 17,09 ± 6,41 mmHg, P < 0,05). Le ratio de la pression artérielle pulmonaire moyenne sur la pression artérielle systémique a diminué pendant cette période (0,28 ± 0,08 vs 0,45 ± 0,17, P < 0,05). Une baisse statistiquement significative du ratio de la RVP sur la résistance vasculaire générale a été aussi observée (0,15 ± 0,05 vs 0,21 ± 0,05, P < 0,05 Objectif : L'hypertension pulmonaire sévère (HP) est une cause majeure de dysfonction du ventricule droit (VD). Diverses modalités vasodilatatrices iv ont été utilisées et ont donné des résultats limités, étant donné le manque de sélectivité pulmonaire. Notre but était d'é-valuer l'efficacité de l'inhalation d'iloprost, un analogue de la prostacycline synthétique, chez des patients qui présentent une résistance vasculaire pulmonaire (RVP) élevée immédiatement après le sevrage de la circulation extracorporelle (CEC). Méthode : Douze patients présentant une HP persistante après l'interruption de la CEC ont été inclus dans l'étude. Une surveillance standard des paramètres hémodynamiques a été utilisée pour tous les patients. L'administration d'iloprost a été faite à l'aide d'un nébuliseur Résultats : L'iloprost inhalé a provoqué une réduction du gradient transpulmonaire à la fin de l'inhalation, en comparaison avec les m...
Background: Calcific aortic valve stenosis (CAVS) is seen in a large proportion of individuals over 60 years. It is an active process, influenced by lipid accumulation, mechanical stress, inflammation, and abnormal extracellular matrix turnover. Various biomarkers (BMs) are studied, as regards mechanisms, diagnosis and prognosis. Methods: In the calcified valves calcium deposition, elastin fragmentation and disorganization of cellular matrix were assessed, together with expression of OPN, OPG, osteocalcin (OCN) and RL2.We prospectively studied the following serum BMs in 60 patients with CAVS and compared them to 20 healthy controls, free from any cardiac disease: Matrix metalloproteinases (MMP) 2 and 9 and tissue inhibitor of metalloproteinase 1 (TIMP1), which regulate collagen turnover, inflammatory factors, i.e. tumor necrosis factor a (TNFa), interleukin 2 (IL2), transforming growth factor β1 (TGF-β1) which regulates fibrosis, fetuin-A (fet-A), osteopontin (OPN), osteoprotegerin (OPG), sclerostin (SOST), and relaxin-2 (RL2) which positively or negatively regulate calcification. Monocyte chemoattractant protein 1 (MCP-1) which regulates migration and infiltration of monocytes/macrophages was also studied as well as malondialdehyde (MDA) an oxidative marker. Results: Extent of tissue valve calcification (Alizarin Red stain) was negatively correlated with tissue elastin, and RL2, and positively correlated with tissue OCN and serum TIMP1 and MCP-1 and negatively with MMP9.Tissue OCN was positively correlated with OPN and negatively with the elastin. Tissue OPN was negatively correlated with elastin and OPG. Tissue OPN OPG and RL2 were not correlated with serum levels In the serum we found in patients statistically lower TIMP1, fet-A and RL2 levels, while all other BMs were higher compared to the healthy group. Positive correlations between SOST and IL2, OPG and MDA but negative with TNFa and OPN were found; also MMP9 was negatively correlated with TNFa and MCP-1 was negatively correlated with TIMP1. Conclusion: We found that many BMs expressing calcification, collagen breakdown, or formation, and inflammation are increased in the valve tissue and in the serum of patients with CAVS as compared with healthy group. Our findings may give new insights towards diagnosis but also therapy. Thus antisclerostin, and antiflammatory agents could be tried for preventing aortic calcification progression.
During heart transplantation procedures, episodes of pulmonary hypertension can be successfully treated with inhaled iloprost administration, without untoward side-effects or significant systemic impact.
Background: The prognostic utility of B-type natriuretic peptide (BNP) in heart failure is well recognized. Previous studies demonstrated that BNP levels decrease after left ventricular assist device (LVAD) implantation. We sought to investigate the predictive value of baseline and changes in BNP levels in LVAD recipients. Methods: BNP was measured in baseline and follow-up plasma samples from consecutive patients receiving a continuous-flow LVAD from 2010 through 2016. Absolute values and changes from baseline were related to clinical outcomes. Results: Median BNP at baseline was 885 [interquartile range (IQR): 450-1,624] pg/mL, decreasing to 289 (IQR: 154-534) pg/mL at 90 days after LVAD implantation. Cox regression analysis revealed that higher baseline and follow-up BNP levels were not associated with increased risk of death at 180 days (P=0.12 and P=0.32, respectively). In the univariate analysis 90-day BNP, but not baseline BNP, was significantly associated with the combined death/hospitalization outcome 180 days after LVAD implantation [hazard ratio (HR) 1.03, 95% CI: 1.01-1.06; P=0.006]. This significance was not preserved after adjusting for multiple covariates (HR 1.01, 95% CI: 0.98-1.04; P=0.62). At 90 days, there was no BNP lowering in 20.6% of subjects. This was not associated with higher risk for death or the composite of death/hospitalization (P=0.11 and P=0.06 respectively). Conclusions: BNP absolute levels and changes from baseline are not independently associated with clinical outcomes after LVAD-implantation. These findings suggest an impaired prognostic performance of BNP after LVAD implantation.
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