We evaluated the hypothesis that activation of endogenous angiotensin-converting enzyme (ACE) 2 would improve cardiac dysfunction induced by diabetes. Ten days after diabetes induction (streptozotocin, 50mg/kg, i.v.), male Wistar rats were treated with the ACE2 activator 1-[[2-(dimethylamino)ethyl]amino]-4-(hydroxymethyl)-7-[[(4-methylphenyl)sulfonyl]oxy]-9H-xanthen-9-one (XNT, 1mg/kg/day, gavage) or saline (control) for 30 days. Echocardiography was performed to analyze the cardiac function and kinetic fluorogenic assays were used to determine cardiac ACE and ACE2 activities. Cardiac ACE2, ACE, Mas receptor, AT1 receptor, AT2 receptor and collagen type I and III mRNA and ACE2, ACE, Mas, AT1 receptor, AT2 receptor, ERK1/2, Akt, AMPK-α and AMPK-β1 protein were measured by qRT-PCR and western blotting techniques, respectively. Histological sections of hearts were analyzed to evaluate the presence of hypertrophy and fibrosis. Diabetic animals presented hyperglycemia and diastolic dysfunction along with cardiac hypertrophy and fibrosis. XNT treatment prevented further increase in glycemia and improved the cardiac function, as well as the hypertrophy and fibrosis. These effects were associated with increases in cardiac ACE2/ACE ratios (activity: ~26%; mRNA: ~113%; and protein: ~188%) and with a decrease in AT1 receptor expression. Additionally, XNT inhibited ERK1/2 phosphorylation and prevented changes in AMPK-α and AMPK-β1 expression. XNT treatment did not induce any significant change in AT2 receptor and Akt expression. These results indicate that activation of intrinsic cardiac ACE2 by oral XNT treatment protects the heart against diabetes-induced dysfunction through mechanisms involving ACE, ACE2, ERK1/2, AMPK-α and AMPK-β1 modulation.

The group consisting of pregnant women with GDM or PE showed results for FMD significantly lower than the control group, suggesting possible endothelial injury in these patients.

BackgroundDespite significant advances in understanding the pathophysiology and management of asthma, some of systemic effects of asthma are still not well defined.ObjectivesTo compare heart function, baseline physical activity level, and functional exercise capacity in young patients with mild-to-moderate asthma and healthy controls.MethodsEighteen healthy (12.67 ± 0.39 years) and 20 asthmatics (12.0 ± 0.38 years) patients were enrolled in the study. Echocardiography parameters were evaluated using conventional and tissue Doppler imaging (TDI).ResultsAlthough pulmonary acceleration time (PAT) and pulmonary artery systolic pressure (PASP) were within normal limits, these parameters differed significantly between the control and asthmatic groups. PAT was lower (p < 0.0001) and PASP (p < 0.0002) was higher in the asthma group (114.3 ± 3.70 ms and 25.40 ± 0.54 mmHg) than the control group (135.30 ± 2.28 ms and 22.22 ± 0.40 mmHg). The asthmatic group had significantly lower early diastolic myocardial velocity (E', p = 0.0047) and lower E' to late (E'/A', p = 0.0017) (13.75 ± 0.53 cm/s and 1.70 ± 0.09, respectively) compared with control group (15.71 ± 0.34 cm/s and 2.12 ± 0.08, respectively) at tricuspid valve. In the lateral mitral valve tissue Doppler, the asthmatic group had lower E' compared with control group (p = 0.0466; 13.27 ± 0.43 cm/s and 14.32 ± 0.25 cm/s, respectively), but there was no statistic difference in the E'/A' ratio (p = 0.1161). Right isovolumetric relaxation time was higher (p = 0.0007) in asthmatic (57.15 ± 0.97 ms) than the control group (52.28 ± 0.87 ms), reflecting global myocardial dysfunction. The right and left myocardial performance indexes were significantly higher in the asthmatic (0.43 ± 0.01 and 0.37 ± 0.01, respectively) compared with control group (0.40 ± 0.01 and 0.34 ± 0.01, respectively) (p = 0.0383 and p = 0.0059, respectively). Physical activity level, and distance travelled on the six-minute walk test were similar in both groups.ConclusionChanges in echocardiographic parameters, evaluated by conventional and TDI, were observed in mild-to-moderate asthma patients even with normal functional exercise capacity and baseline physical activity level. Our results suggest that the echocardiogram may be useful for the early detection and evoluation of asthma-induced cardiac changes.

BackgroundInspiratory muscle training (IMT) using a Threshold® device is commonly used to improve the strength and endurance of inspiratory muscles. However, the effect of IMT, alone or with positive end-expiratory pressure (PEEP), on hemodynamic parameters in patients with chronic obstructive pulmonary disease (COPD) remains unknown.ObjectiveTo assess the effects of an overload of inspiratory muscles using IMT fixed at 30% of the maximal inspiratory pressure (MIP), and IMT associated with 5 cmH2O of PEEP (IMT + PEEP), on the echocardiographic parameters in healthy subjects and patients with COPD.MethodsTwenty patients with COPD (forced expiratory volume in 1 second 53.19±24.71 pred%) and 15 age-matched healthy volunteers were evaluated using spirometry, MIP, the COPD assessment test (CAT), and the modified Medical Research Council (mMRC) dyspnea scale. The E- (fast-filling phase) and A- (atrial contraction phase) waves were evaluated at the tricuspid and mitral valves during inspiration and expiration in the following sequence: at basal conditions, using IMT, and using IMT + PEEP.ResultsPatients with COPD had reduced MIPs versus the control group. Ten patients had CAT scores <10 and 12 patients had mMRC scores <2. E-wave values at the mitral valve were significantly decreased with IMT during the inspiratory phase in both groups. These effects were normalized with IMT + PEEP. During the expiratory phase, use of IMT + PEEP normalized the reduction in E-wave values in the COPD group. During inspiration at the tricuspid valve, reduction in E-wave values during IMT was normalized by IMT + PEEP in COPD group. During the expiratory phase, the value of the E-waves was significantly reduced with overload of the inspiratory muscles in both groups, and these effects were normalized with IMT + PEEP. A-waves did not change under any conditions.ConclusionAcute hemodynamic effects induced by overloading of the inspiratory muscles were attenuated and/or reversed by the addition of PEEP in COPD patients.

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A taquicardia fetal ocorre em 0,4-0,6% de todas as gestações. Das taquiarritmias fetais sustentadas, o flutter atrial é a segunda mais comum. Quando não tratada corretamente, causa insuficiência cardíaca fetal e pode ser necessária a interrupção precoce da gestação. O diagnóstico das taquiarritmias é feito, principalmente, pela ecocardiografia intraútero. O tratamento de primeira escolha é a administração oral materna de digoxina. Caso não haja resposta adequada ou o feto evolua com hidropisia, é necessário associar outro antiarrítmico como sotalol ou amiodarona. Neste relato, iniciou-se com digoxina; e, em função da ausência de resposta, foi associada propafenona. Sotalol ou amiodarona não foram usados devido à bradicardia e à hipotensão materna.