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Right ventricular (RV) (dys)function determines outcomes in pulmonary hypertension (PH). We previously found that asymmetric RV myocardial work (MW) corresponds with inefficient RV function in experimental PH models. We therefore aimed to investigate regional distribution of RV MW and its correlation with catheter hemodynamics in children with PH. RV MW was calculated by longitudinal strain and simultaneous catheter pressure measurements in 14 patients with PH. Wasted MW was defined as the ratio of inappropriate myocardial lengthening to favorable shortening work. Segment‐wise and averaged MW and wasted MW were evaluated at baseline and during pulmonary vasodilation therapy with oxygen and nitric oxide, and their relationship to hemodynamic measurements was analyzed. We found that MW was higher for the lateral wall than the septum: 1013 ± 374 mmHg · % versus 532 ± 190 mmHg · % at baseline. Wasted MW ratio did not differ significantly between wall regions. Pulmonary vasodilators slightly reduced mean pulmonary artery pressure and was accompanied by a more symmetrical MW distribution. Averaged MW correlated with the rate of RV pressure development (dP/dt maximum) and decay (dP/dt minimum) at all conditions (p ≤ $\le $ 0.047). The results suggest that MW contribute to, and may be used as a marker of, systolic and diastolic efficiency in the PH RV. [ABSTRACT FROM AUTHOR]

Aims The non-invasive myocardial work index (MWI) has been validated in patients without aortic stenosis (AS). A thorough assessment of methodological limitations is warranted before this index can be applied to patients with AS. Methods and results We simultaneously measured left ventricular pressure (LVP) by using a micromanometer-tipped catheter and obtained echocardiograms in 20 patients with severe AS. We estimated LVP curves and calculated pressure–strain loops using three different models: (i) the model validated in patients without AS; (ii) the same model, but with pressure at the aortic valve opening (AVO) adjusted to diastolic cuff pressure; and (iii) a new model based on the invasive measurements from patients with AS. Valvular events were determined by echocardiography. Peak LVP was estimated as the sum of the mean aortic transvalvular gradient and systolic cuff pressure. In same-beat comparisons between invasive and estimated LVP curves, Model 1 significantly overestimated early systolic pressure by 61 ± 5 mmHg at AVO compared with Models 2 and 3. However, the average correlation coefficients between estimated and invasive LVP traces were excellent for all models, and the overestimation had limited influence on MWI, with excellent correlation (r = 0.98, P < 0.001) and good agreement between the MWI calculated with estimated (all models) and invasive LVP. Conclusion This study confirms the validity of the non-invasive MWI in patients with AS. The accuracy of estimated LVP curves improved when matching AVO to the diastolic pressure in the original model, mirroring that of the AS-specific model. This may sequentially enhance the accuracy of regional MWI assessment. [ABSTRACT FROM AUTHOR]

Left ventricular (LV) circumferential strain and rotation have been introduced as clinical markers of myocardial function. This study investigates how regional LV apical rotation and strain can be used in combination to assess function in the infarcted ventricle. In healthy subjects (n = 15) and patients with myocardial infarction (n = 23), LV apical segmental rotation and strain were measured from apical short-axis recordings by speckle tracking echocardiography (STE) and MRI tagging. Infarct extent was determined by late gadolinium enhancement MRI. To investigate mechanisms of changes in strain and rotation, we used a mathematical finite element simulation model of the LV. Mean apical rotation and strain by STE were lower in patients than in healthy subjects (9.0 [+ or -] 4.9 vs. 12.9 [+ or -] 3.5[degrees] and -13.9 [+ or -]10.7 vs. -23.8 [+ or -] 2.3%, respectively, P < 0.05). In patients, regional strain was reduced in proportion to segmental infarct extent (r = 0.80, P < 0.0001). Regional rotation, however, was similar in the center of the infarct and in remote viable myocardium. Minimum and maximum rotations were found at the infarct borders: minimum rotation at the border zone opposite to the direction of apical rotation, and maximum rotation at the border zone in the direction of rotation. The simulation model reproduced the clinical findings and indicated that the dissociation between rotation and strain was caused by mechanical interactions between infarcted and viable myocardium. Systolic strain reflects regional myocardial function and infarct extent, whereas systolic rotation defines infarct borders in the LV apical region. Regional rotation, however, has limited ability to quantify regional myocardial dysfunction. myocardial infarction; myocardial strain; left ventricular function; left ventricular torsion

A faster three-dimensional (3-D) ultrasound imaging simulation approach is described that can be applied to tasks like simulating 3-D ultrasound images for speckle-tracking. The images simulated using Fusk, fast ultrasound simulation in K-space, are compared with images from Field II simulations.

The present study introduces a new clinical method to define left ventricular (LV) end systole (ES) during tissue Doppler imaging (TDI). Preliminary experiments showed a sharp inflection point in strain traces ([S.sub.IP]) from ischemic borderzones, which coincided with onset of a postsystolic shortening wave ([V.sub.PS]) in the velocity trace. In a single-vessel disease model, we investigated whether [S.sub.IP] and [V.sub.PS] may serve as markers of global ES and their mechanism. In six anesthetized dogs we measured LV pressure and myocardial long-axis function by using TDI and sonomicrometry. Ischemia was induced by left anterior descending coronary artery occlusion. ES was defined by the minimum first derivative of LV pressure. TDI and sonomicrometry demonstrated a sharp [S.sub.IP] and [V.sub.PS] at ES in the ischemic borderzone (defined as moderately ischemic myocardium by pressure-dimension loop analysis). Time differences relative to ES ([+ or -] SD) were -0.1 [+ or -] 2.3 (intraclass correlation coefficient [R.sub.IC] = 0.996) and 6.8 [+ or -] 10.7 ms ([R.sub.IC]= 0.89) for [S.sub.IP] as shown by sonomicrometry and TDI, respectively. There was a strong inverse relationship between postsystolic shortening in the borderzone and simultaneous lengthening of nonischemic myocardium. In 30 patients with acute myocardial infarction, [S.sub.IP], and [V.sub.PS] evaluated by TDI were compared with ES defined by aortic valve closure. Time differences were -4 [+ or -] 14 ([R.sub.IC]= 0.94) and -2 [+ or -] 11 ms ([R.sub.IC]= 0.96), respectively. In the ischemic borderzone, [S.sub.IP] and [V.sub.PS] identified global ES with high accuracy. The force balance or 'tug of war' between borderzone and nonischemic myocardium is a likely underlying mechanism for these markers. The method may be used as an 'all in one heart beat' approach for TDI analysis in acute myocardial ischemia. echocardiography; infarction; reperfusion; ventricular function; tissue Doppler imaging

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We present a method to estimate left ventricular (LV) motion based on three-dimensional (3-D) images that can be derived from any anatomical tomographic or 3-D modality, such as echocardiography, computed tomography, or magnetic resonance imaging. A finite element mesh of the IN was constructed to fit the geometry of the wall. The mesh was deformed by optimizing the nodal parameters to the motion of a sparse number of fiducial markers that were manually tracked in the images through the cardiac cycle. A parameter distribution model (PDM) of LV deformations was obtained from a database of MR tagging studies. This was used to filter the calculated deformation and incorporate a priori information on likely motions. The estimated deformation obtained from 13 normal untagged studies was compared with the deformation obtained from MR tagging. The end systolic (ES) circumferential and longitudinal strain values matched well with a mean difference of 0.1 [+ or -] 3.2% and 0.3 [+ or -] 3.0%, respectively. The calculated apex-base twist angle at ES had a mean difference of 1.0 [+ or -] 2.3[degrees]. We conclude that fiducial marker fitting in conjunction with a PDM provides accurate reconstruction of LV deformation in normal subjects. Index Terms--Free-form deformation, host mesh deformation, left ventricular motion, parameter distribution models.

We have developed a method that decomposes the deformation of the left ventricle (LV) between end diastole (ED) and end systole (ES) into separate deformation modes such as longitudinal shortening, wall thickening, and twisting. The deformation was initially found from the motion of an LV finite-element mesh that was fitted to clinically obtained magnetic resonance (MR) tagged images. A mode coefficient was calculated for each deformation mode to quantify the different modes and, thus allowing for discrimination of normal and abnormal deformation patterns. We applied the method to 13 normal subjects and 13 diabetes patients. By using the ED mesh as reference and adding the extracted deformation modes multiplied by their mode coefficients, an approximate ES mesh was calculated and compared with the 'true' ES mesh found from the MR images. For the 26 subjects the average Euclidean distance was less than 1.7 [+ or -] 0.9 mm between the nodes of the approximated and true ES meshes. The coefficient values for the patient group showed significantly less longitudinal shortening, less wall thickening, more longitudinal twisting and also more bulging of the septum into the LV when compared with the normal subjects. We conclude that the developed method successfully quantifies the deformation into several modes of deformation and is capable of distinguishing the deformation of a group of patients from a group of normal subjects. Index Terms--Finite-element model, left ventricular deformation modes, MRI tagging.