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The primary aim is to establish a procedure for short-term spectral estimation of radio frequency (RF) ultrasound images. An approach is described which relies on autoregressive (AR) spectral etimation, constrained through nonquadratic penalty functions.

Arrhythmogenic right ventricular (RV) remodeling has been reported in response to regular training, but it remains unclear how exercise intensity affects the presence and extent of such remodeling. We aimed to assess the relationship between RV remodeling and exercise load in a long-term endurance training model. Wistar rats were conditioned to run at moderate (MOD; 45 min, 30 cm/s) or intense (INT; 60 min, 60 cm/s) workloads for 16 wk; sedentary rats served as controls. Cardiac remodeling was assessed with standard echocardiographic and tissue Doppler techniques, sensor-tip pressure catheters, and pressure-volume loop analyses. After MOD training, both ventricles similarly dilated (~16%); the RV apical segment deformation, but not the basal segment deformation, was increased [apical strain rate (SR): -2.9 ± 0.5 vs. -3.3 ± 0.6 s-1, SED vs. MOD]. INT training prompted marked RV dilatation (~26%) but did not further dilate the left ventricle (LV). A reduction in both RV segments' deformation in INT rats (apical SR: -3.3 ± 0.6 vs. -3.0 ± 0.4 s-1 and basal SR: -3.3 ± 0.7 vs. -2.7 ± 0.6 s-1, MOD vs. INT) led to decreased global contractile function (maximal rate of rise of LV pressure: 2.53 ± 0.15 vs. 2.17 ± 0.116 mmHg/ms, MOD vs. INT). Echocardiography and hemodynamics consistently pointed to impaired RV diastolic function in INT rats. LV systolic and diastolic functions remained unchanged in all groups. In conclusion, we showed a biphasic, unbalanced RV remodeling response with increasing doses of exercise: physiological adaptation after MOD training turns adverse with INT training, involving disproportionate RV dilatation, decreased contractility, and impaired diastolic function. Our findings support the existence of an exercise load threshold beyond which cardiac remodeling becomes maladaptive. NEW & NOTEWORTHY Exercise promotes left ventricular eccentric hypertrophy with no changes in systolic or diastolic function in healthy rats. Conversely, right ventricular adaptation to physical activity follows a biphasic, dose-dependent, and segmentary pattern. Moderate exercise promotes a mild systolic function enhancement at the right ventricular apex and more intense exercise impairs systolic and diastolic function. [ABSTRACT FROM AUTHOR]

Intrauterine growth restriction (IUGR) due to placental insufficiency is associated with blood flow redistribution in order to maintain delivery of oxygenated blood to the brain. Given that, in the fetus the aortic isthmus (AoI) is a key arterial connection between the cerebral and placental circulations, quantifying AoI blood flow has been proposed to assess this brain sparing effect in clinical practice. While numerous clinical studies have studied this parameter, fundamental understanding of its determinant factors and its quantitative relation with other aspects of haemodynamic remodeling has been limited. Computational models of the cardiovascular circulation have been proposed for exactly this purpose since they allow both for studying the contributions from isolated parameters as well as estimating properties that cannot be directly assessed from clinical measurements. Therefore, a computational model of the fetal circulation was developed, including the key elements related to fetal blood redistribution and using measured cardiac outflow profiles to allow personalization. The model was first calibrated using patient-specific Doppler data from a healthy fetus. Next, in order to understand the contributions of the main parameters determining blood redistribution, AoI and middle cerebral artery (MCA) flow changes were studied by variation of cerebral and peripheral-placental resistances. Finally, to study how this affects an individual fetus, the model was fitted to three IUGR cases with different degrees of severity. In conclusion, the proposed computational model provides a good approximation to assess blood flow changes in the fetal circulation. The results support that while MCA flow is mainly determined by a fall in brain resistance, the AoI is influenced by a balance between increased peripheral-placental and decreased cerebral resistances. Personalizing the model allows for quantifying the balance between cerebral and peripheral-placental remodeling, thus providing potentially novel information to aid clinical follow up.

Introduction and Objectives: In hypertrophic cardiomyopathy (HCM), it has been suggested that regional fiber disarray produces segments that exhibit no or severely reduced deformation, and that these segments are distributed nonuniformly within the left ventricle (LV). This contrasts with observations in other types of hypertrophy, such as in athlete's heart or hypertensive left ventricular hypertrophy (HLVH), in which abnormal cardiac deformation may exist but the reduction is not so severe that some segments exhibit no deformation. Our aim was to use the strain distribution to study deformation in HCM., Methods: We used tagged magnetic resonance imaging to reconstruct LV systolic deformation in 12 controls, 10 athletes, 12 patients with HCM, and 10 patients with HLVH. Deformation was quantified using a fast nonrigid registration algorithm and peak radial and circumferential systolic strain values were determined in 16 LV segments., Results: Patients with HCM had significantly lower average strain values than individuals in other groups. However, while the deformation observed in healthy subjects and HLVH patients clustered around the mean, in HCM patients, segments with normal contraction coexisted with segments exhibiting no or significantly reduced deformation, which resulted in a greater heterogeneity of strain values. Moreover, some nondeforming segments were observed even when fibrosis and hypertrophy were absent., Conclusions: The strain distribution characterized specific patterns of myocardial deformation in patients with LVH due to different etiologies. Patients with HCM had significantly lower mean strain values and a greater heterogeneity in strain values than controls, athletes and HLVH patients. In addition, they had nondeforming regions.