function is considered to be precisely measurable only by invasive hemodynamics. We aimed to correlate strain values measured by speckle-tracking echocardiography (STE) with sensitive contractility parameters of pressure-volume (P-V) analysis in a rat model of exercise-induced left ventricular (LV) hypertrophy. LV hypertrophy was induced in rats by swim training and was compared with untrained controls. Echocardiography was performed using a 13-MHz linear transducer to obtain LV long-and short-axis recordings for STE analysis (GE EchoPAC). Global longitudinal (GLS) and circumferential strain (GCS) and longitudinal (LSr) and circumferential systolic strain rate (CSr) were measured. LV P-V analysis was performed using a pressure-conductance microcatheter, and load-independent contractility indices [slope of the end-systolic P-V relationship (ESPVR), preload recruitable stroke work (PRSW), and maximal dP/dt-enddiastolic volume relationship (dP/dtmax-EDV)] were calculated. Trained rats had increased LV mass index (trained vs. control; 2.76 Ϯ 0.07 vs. 2.14 Ϯ 0.05 g/kg, P Ͻ 0.001). P-V loop-derived contractility parameters were significantly improved in the trained group (ESPVR: 3.58 Ϯ 0.22 vs. 2.51 Ϯ 0.11 mmHg/ l; PRSW: 131 Ϯ 4 vs. 104 Ϯ 2 mmHg, P Ͻ 0.01). Strain and strain rate parameters were also supernormal in trained rats (GLS: Ϫ18.8 Ϯ 0.3 vs. Ϫ15.8 Ϯ 0.4%; LSr: Ϫ5.0 Ϯ 0.2 vs. Ϫ4.1 Ϯ 0.1 Hz; GCS: Ϫ18.9 Ϯ 0.8 vs. Ϫ14.9 Ϯ 0.6%; CSr: Ϫ4.9 Ϯ 0.2 vs. Ϫ3.8 Ϯ 0.2 Hz, P Ͻ 0.01). ESPVR correlated with GLS (r ϭ Ϫ0.71) and LSr (r ϭ Ϫ0.53) and robustly with GCS (r ϭ Ϫ0.83) and CSr (r ϭ Ϫ0.75, all P Ͻ 0.05). PRSW was strongly related to GLS (r ϭ Ϫ0.64) and LSr (r ϭ Ϫ0.71, both P Ͻ 0.01). STE can be a feasible and useful method for animal experiments. In our rat model, strain and strain rate parameters closely reflected the improvement in intrinsic contractile function induced by exercise training. speckle-tracking echocardiography; pressure-volume analysis; athlete's heart; contractility; strain LONG-TERM EXERCISE TRAINING induces physiological left ventricular (LV) hypertrophy, a molecular and cellular growth process of the heart in response to altered loading conditions (6). In contrast to pathological hypertrophy, this adaptation leads to maintained or even enhanced cardiac function (2, 14). Hemodynamic changes of exercise-induced hypertrophy were characterized by our research group in a rat model, focusing also on the improved LV inotropic state (23). Contractility is the intrinsic ability of the myocardium to generate force and to shorten independently of changes in preload or afterload with fixed heart rates. In the past few decades, efforts have been made to transfer the physiological concept of contractility to the intact beating heart (4).Pressure-volume (P-V) analysis recently became the gold standard to investigate in vivo hemodynamics in animal models. During preload reduction maneuvers such as gradual occlusion of vena cava inferior, load-independent indices of myocardial contractility could be obtained (20). Th...

The organization of functional brain networks changes across human lifespan. The present study analyzed functional brain networks in healthy full-term infants (N = 139) within 1-6 days from birth by measuring neural synchrony in EEG recordings during quiet sleep. Large-scale phase synchronization was measured in six frequency bands with the Phase Lag Index. Macroscopic network organization characteristics were quantified by constructing unweighted minimum spanning tree graphs. The cortical networks in early infancy were found to be significantly more hierarchical and had a more cost-efficient organization compared with MST of random control networks, more so in the theta and alpha than in other frequency bands. Frontal and parietal sites acted as the main hubs of these networks, the topological characteristics of which were associated with gestation age (GA). This suggests that individual differences in network topology are related to cortical maturation during the prenatal period, when functional networks shift from strictly centralized toward segregated configurations. Hum Brain Mapp 38:4019-4033, 2017. © 2017 Wiley Periodicals, Inc.

AimsHeart failure with preserved ejection fraction (HFpEF) has a great epidemiological burden. The pathophysiological role of cyclic guanosine monophosphate (cGMP) signalling has been intensively investigated in HFpEF. Elevated levels of cGMP have been shown to exert cardioprotective effects in various cardiovascular diseases, including diabetic cardiomyopathy. We investigated the effect of long‐term preventive application of the phosphodiesterase‐5A (PDE5A) inhibitor vardenafil in diabetic cardiomyopathy‐associated HFpEF.Methods and resultsZucker diabetic fatty (ZDF) rats were used as a model of HFpEF and ZDF lean rats served as controls. Animals received vehicle or 10 mg/kg body weight vardenafil per os from weeks 7 to 32 of age. Cardiac function, morphology was assessed by left ventricular (LV) pressure–volume analysis and echocardiography at week 32. Cardiomyocyte force measurements were performed. The key markers of cGMP signalling, nitro‐oxidative stress, apoptosis, myocardial hypertrophy and fibrosis were examined. The ZDF animals showed diastolic dysfunction (increased LV/cardiomyocyte stiffness, prolonged LV relaxation time), preserved systolic performance, decreased myocardial cGMP level coupled with impaired protein kinase G (PKG) activity, increased nitro‐oxidative stress, enhanced cardiomyocyte apoptosis, and hypertrophic and fibrotic remodelling of the myocardium. Vardenafil effectively prevented the development of HFpEF by maintaining diastolic function (decreased LV/cardiomyocyte stiffness and LV relaxation time), by restoring cGMP levels and PKG activation, by lowering apoptosis and by alleviating nitro‐oxidative stress, myocardial hypertrophy and fibrotic remodelling.ConclusionsWe report that vardenafil successfully prevented the development of diabetes mellitus‐associated HFpEF. Thus, PDE5A inhibition as a preventive approach might be a promising option in the management of HFpEF patients with diabetes mellitus.

A real-time method for fetal heart rate (FHR) monitoring based on signal processing of the fetal heart sounds is presented. The acoustic method, which utilizes an adaptive time pattern analysis to select and analyze those heartbeats that can be recorded without artefact, is guided by a number of rules involving an introduced confidence factor on the timing prediction. The algorithm was implemented in a low-power portable electronic instrument to enable long-term fetal surveillance. A large number of clinical tests have shown the very good performance of the phonocardiographic method in comparison with FHR curves simultaneously recorded with ultrasound cardiotocography. Indeed, approximately 90% of the time, the acoustic FHR curve remained inside a +/- 3 beats/min tolerance limit of the reference ultrasound method. The confidence was typically CF > 0.85. The acoustic method exceeded a +/- 5 beats/min limit relative to the ultrasound method approximately 5% of the time. Finally, no relevant FHR data was measured approximately 5% of the time.

Left ventricular (LV) hypertrophy is a physiological or pathological response of LV myocardium to increased cardiac load. We aimed at investigating and comparing hemodynamic alterations in well-established rat models of physiological hypertrophy (PhyH) and pathological hypertrophy (PaH) by using LV pressure-volume (P-V) analysis. PhyH and PaH were induced in rats by swim training and by abdominal aortic banding, respectively. Morphology of the heart was investigated by echocardiography. Characterization of cardiac function was completed by LV P-V analysis. In addition, histological and molecular biological measurements were performed. Echocardiography revealed myocardial hypertrophy of similar degree in both models, which was confirmed by post-mortem heart weight data. In aortic-banded rats we detected subendocardial fibrosis. Reactivation of fetal gene program could be observed only in the PaH model. PhyH was associated with increased stroke volume, whereas unaltered stroke volume was detected in PaH along with markedly elevated end-systolic pressure values. Sensitive indexes of LV contractility were increased in both models, in parallel with the degree of hypertrophy. Active relaxation was ameliorated in athlete's heart, whereas it showed marked impairment in PaH. Mechanical efficiency and ventriculo-arterial coupling were improved in PhyH, whereas they remained unchanged in PaH. Myocardial gene expression of mitochondrial regulators showed marked differences between PaH and PhyH. We provided the first comparative hemodynamic characterization of PhyH and PaH in relevant rodent models. Increased LV contractility could be observed in both types of LV hypertrophy; characteristic distinction was detected in diastolic function (active relaxation) and mechanoenergetics (mechanical efficiency), which might be explained by mitochondrial differences.