Force-frequency relationship during dobutamine stress echocardiography predicts exercise tolerance and BNP levels in patients with chronic congestive heart failure

Purpose: D obutamine stress echocardiography (DSE) is widely used to evaluate myocardial contractile reserve; it provides prognostic information in patients with chronic congestive heart failure (CHF). The force?frequency relationship (FFR) is a method for evaluate LV contractility during DSE . The aim of our study is to assess the relationship among FFR, BNP levels, and aerobic exercise capacity in CHF patients. Methods and materials: 37 CHF patients (age 67?8 years, 54% with an ischemic etiology), underwent high dose DSE (up to 40 m g/kg/min). FFR was determined as a ratio between systolic cuff pressure and end-systolic volume (biplane using a Simposon rule) assessed at baseline and peak DSE . BNP levels were determined on blood samples withdrawn at baseline. After a few hours, CHF patients underwent cardiopulmonary exercise test with expired gas measurement. Results: Mean ejection fraction was 32?7% and NHYA class 2.5?0.6. FFR was directly related to peak oxygen consumption (Figure Left), LV ejection fraction (r=0.398, p=0.015) and mitral annulus peak systolic velocity (r=0.428, p=0.013). FFR was inversely related to NYHA class (r=-0.43, p=0.013), LV end-diastolic diameter (r=-0.377, p=0.022), LV intraventricular dyssynchrony (r=-0.394, p=0.016), and BNP levels (Figure Right). At multiple regression analysis, FFR (B=0.502, p= 0.004) and E/Ea ratio (B=-0.336, p=0.044) were the best predictors of exercise tolerance. Conclusions: In patients with stable CHF, impaired myocardial contractility during DSE is related to higher BNP levels and poorer exercise tolerance

Metastatic mixed gestational trophoblastic tumour of the uterus: A case report

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Emergency transapical mitral valve-in-valve implantation for bioprosthesis failure: Transapical implantation of an Edwards Sapien-XT in a dysfunctional mitral bioprosthesis in a critical patient

Background: Valve-in-Valve (VIV) Transcatheter Aortic Valve Replacement (TAVR) is now the treatment of choice in high-surgical-risk patients with failing aortic bioprosthesis. Although less performed, VIV-Transcatheter Mitral Valve Replacement (TMVR) is a valid treatment option for selected high-risk patients with degenerated mitral bioprostheses. Several cases of elective ViV- TAVR and -TMVR have been reported but only few were performed in critical hemodynamic conditions. Case presentation: We report the case of a patient underwent balloon-expandable transapical mitral valve-in-valve implantation in an emergency setting due to a severe stenosis of a bioprosthesis in mitral position. The procedure was successfully performed, with no residual mitral regurgitation or paravalvular leaks, and uneventful. Conclusion: Transcatheter transapical mitral valve-in-valve implantation could represent a feasible and effective strategy even in critical setting

Plant Dynamic Metabolic Response to Bacteriophage Treatment After Xanthomonas campestris pv. campestris Infection

Periodic epidemics of black rot disease occur worldwide causing substantial yield losses. Xanthomonas campestris pv. campestris (Xcc) represents one of the most common bacteria able to cause the above disease in cruciferous plants such as broccoli, cabbage, cauliflower, and Arabidopsis thaliana. In agriculture, several strategies are being developed to contain the Xanthomonas infection. The use of bacteriophages could represent a valid and efficient approach to overcome this widespread phenomenon. Several studies have highlighted the potential usefulness of implementing phage therapy to control plant diseases as well as Xcc infection. In the present study, we characterized the effect of a lytic phage on the plant Brassica oleracea var. gongylodes infected with Xcc and, for the first time, the correlated plant metabolic response. The results highlighted the potential benefits of bacteriophages: reduction of bacterium proliferation, alteration of the biofilm structure and/or modulation of the plant metabolism and defense response

An Algebraic Approach for Decoding Spread Codes

In this paper we study spread codes: a family of constant-dimension codes for random linear network coding. In other words, the codewords are full-rank matrices of size (k x n) with entries in a finite field F_q. Spread codes are a family of optimal codes with maximal minimum distance. We give a minimum-distance decoding algorithm which requires O((n-k)k^3) operations over an extension field F_{q^k}. Our algorithm is more efficient than the previous ones in the literature, when the dimension k of the codewords is small with respect to n. The decoding algorithm takes advantage of the algebraic structure of the code, and it uses original results on minors of a matrix and on the factorization of polynomials over finite fields

Inhaled tolafentrine reverses pulmonary vascular remodeling via inhibition of smooth muscle cell migration

BACKGROUND: The aim of the study was to assess the chronic effects of combined phosphodiesterase 3/4 inhibitor tolafentrine, administered by inhalation, during monocrotaline-induced pulmonary arterial hypertension (PAH) in rats. METHODS: CD rats were given a single subcutaneous injection of monocrotaline to induce PAH. Four weeks after, rats were subjected to inhalation of tolafentrine or sham nebulization in an unrestrained, whole body aerosol exposure system. In these animals (i) the acute pulmonary vasodilatory efficacy of inhaled tolafentrine (ii) the anti-remodeling effect of long-term inhalation of tolafentrine (iii) the effects of tolafentrine on the expression profile of 96 genes encoding cell adhesion and extracellular matrix regulation were examined. In addition, the inhibitory effect of tolafentrine on ex vivo isolated pulmonary artery SMC cell migration was also investigated. RESULTS: Monocrotaline injection provoked severe PAH (right ventricular systolic pressure increased from 25.9 ± 4.0 to 68.9 ± 3.2 after 4 weeks and 74.9 ± 5.1 mmHg after 6 weeks), cardiac output depression and right heart hypertrophy. The media thickness of the pulmonary arteries and the proportion of muscularization of small precapillary resistance vessels increased dramatically, and the migratory response of ex-vivo isolated pulmonary artery smooth muscle cells (PASMC) was increased. Micro-arrays and subsequent confirmation with real time PCR demonstrated upregulation of several extracellular matrix regulation and adhesion genes, such as matrixmetalloproteases (MMP) 2, 8, 9, 10, 11, 12, 20, Icam, Itgax, Plat and serpinb2. When chronically nebulized from day 28 to 42 (12 daily aerosol maneuvers), after full establishment of severe pulmonary hypertension, tolafentrine reversed about 60% of all hemodynamic abnormalities, right heart hypertrophy and monocrotaline-induced structural lung vascular changes, including the proportion of pulmonary artery muscularization. The upregulation of extracellular matrix regulation and adhesion genes was reduced by nearly 80% by inhalation of the tolafentrine. When assessed in vitro, tolafentrine blocked the enhanced PASMC migratory response. CONCLUSION: In conclusion, we demonstrate for the first time that inhalation of combined PDE3/4 inhibitor reverses pulmonary hypertension fully developed in response to monocrotaline in rats. This "reverse-remodeling" effect includes structural changes in the lung vascular wall and key molecular pathways of matrix regulation, concomitant with 60% normalization of hemodynamics

Lung vasodilatory response to inhaled iloprost in experimental pulmonary hypertension: amplification by different type phosphodiesterase inhibitors

Inhaled prostanoids and phosphodiesterase (PDE) inhibitors have been suggested for treatment of severe pulmonary hypertension. In catheterized rabbits with acute pulmonary hypertension induced by continuous infusion of the stable thromboxane analogue U46619, we asked whether sildenafil (PDE1/5/6 inhibitor), motapizone (PDE3 inhibitor) or 8-Methoxymethyl-IBMX (PDE1 inhibitor) synergize with inhaled iloprost. Inhalation of iloprost caused a transient pulmonary artery pressure decline, levelling off within <20 min, without significant changes in blood gases or systemic hemodynamics. Infusion of 8-Methoxymethyl-IBMX, motapizone and sildenafil caused each a dose-dependent decrease in pulmonary artery pressure, with sildenafil possessing the highest efficacy and at the same time selectivity for the pulmonary circulation. When combining a per se ineffective dose of each PDE inhibitor (200 μg/kg × min 8-Methoxymethyl-IBMX, 1 μg/kg × min sildenafil, 5 μg/kg × min motapizone) with subsequent iloprost nebulization, marked amplification of the prostanoid induced pulmonary vasodilatory response was noted and the area under the curve of P(PA )reduction was nearly threefold increased with all approaches, as compared to sole iloprost administration. Further amplification was achieved with the combination of inhaled iloprost with sildenafil plus motapizone, but not with sildenafil plus 8MM-IBMX. Systemic hemodynamics and gas exchange were not altered for all combinations. We conclude that co-administration of minute systemic doses of selective PDE inhibitors with inhaled iloprost markedly enhances and prolongs the pulmonary vasodilatory response to inhaled iloprost, with maintenance of pulmonary selectivity and ventilation perfusion matching. The prominent effect of sildenafil may be operative via both PDE1 and PDE5, and is further enhanced by co-application of a PDE3 inhibitor