V isual or semiautomated tracking of the endocardial border provide estimates of cardiac volume, which are used to derive ejection fraction, a quantitative indicator of ventricular function. However, the heart is a complex mechanical organ that undergoes cyclic changes in multiple dimensions that ultimately effect a change in chamber volume that results in ejection of blood. Regardless of imaging technique, ejection fraction is unable to provide information on the underlying myocardial mechanical activity. Also, ejection fraction reflects the sum contribution of several regions and does not provide information on regional function. Regional function assessed visually is subjective and prone to error. 1 Quantification of regional myocardial activity (deformation) was feasible only in experimental studies by use of markers attached directly to the myocardium, a technique not practicable in the clinical realm. 2 Myocardial tagging with cardiac magnetic resonance (CMR) introduced the opportunity to noninvasively track regional myocardial mechanics. 3,4 Modifications to the filter settings on pulsed Doppler to image low-velocity, high-intensity myocardial signal rather than the high-velocity, low-intensity signal from blood flow allows similar assessment by ultrasound. This technique is commonly referred to as tissue Doppler imaging (TDI) or Doppler myocardial imaging. 5 Tissue Doppler ImagingThe TDI method depicts myocardial motion (measured as tissue velocity) at specific locations in the heart. Tissue velocity indicates the rate at which a particular point in the myocardium moves toward or away from the transducer.Integration of velocity over time yields displacement or the absolute distance moved by that point (Figure 1A and 1B).Tissue Doppler-derived velocity can be obtained via pulsed Doppler (by placing a sample volume at a particular location), M-mode Doppler, or 2-dimensional color Doppler ( Figure 1C and 1D). 5 Color Doppler acquires tissue velocity information from the entire sector, and thus, multiple sites can be interrogated simultaneously. Individual segments are analyzed ex post facto. Although all of these methods yield the same mechanical information, differences in the peak values exist. Pulsed Doppler measures peak velocity, which is Ϸ20% to 30% higher than the mean velocity measured by color Doppler. This difference should be considered when one estimates left ventricular filling pressure using the E/eЈ ratio. 6 Frame rates are highest with the M mode, lower with pulsed Doppler, and lowest with color Doppler TDI.Tissue Doppler has been validated extensively and examined in a variety of cardiac pathologies. 7,8 Although initial work reported tissue velocity from the septal or posterior wall in the parasternal projections, recent work almost exclusively interrogates tissue velocities in the longitudinal direction (apical projections). In the longitudinal direction, myocardial motion is such that the apex is generally immobile, whereas the base moves toward the apex in systole and away from the apex...

Our results suggest that the N47K and R58Q mutations may act through similar mechanisms, leading to compensatory hypertrophy of the functionally compromised myocardium, but the malignant R58Q phenotype is most likely associated with more severe alterations in cardiac performance manifested as impaired relaxation and global diastolic dysfunction. At the molecular level, we suggest that by reducing the phosphorylation of RLC, the R58Q mutation decreases the kinetics of myosin cross-bridges, leading to an increased myofilament calcium sensitivity and to overall changes in intracellular Ca(2+) homeostasis.

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Myostatin is a negative regulator of muscle growth. Loss of myostatin has been shown to cause increase in skeletal muscle size and improve skeletal muscle function and fibrosis in the dystrophindeficient mdx mouse, an animal model for Duchenne muscular dystrophy. We evaluated whether lack of myostatin has an impact on cardiac muscle growth and fibrosis in vivo. Using genetically modified mice we assessed whether myostatin absence induces similar beneficial effects on cardiac function and fibrosis. Cardiac mass and ejection fraction were measured in wild type, myostatin-null, mdx and double mutant mdx/myostatinnull mice by high resolution echocardiography. Heart mass, myocyte area and extent of cardiac fibrosis were determined post mortem. Myostatin-null mice do not demonstrate ventricular hypertrophy when compared to wild type mice as shown by echocardiography (ventricular mass 0.69± 0.01 g vs.0.69±0.018 g, P = 0.75, respectively) and morphometric analyses including heart/body weight ratio (5.39±0.45mg/g vs. 5.62±0.58mg/g, P = 0.59 respectively) and cardiomyocyte area 113.67±1.5μm 2 , 116.85±1.9μm 2 ; P = 0.2). Moreover, absence of myostatin does not attenuate cardiac fibrosis in the dystrophin deficient mdx mouse model for DMD (12.2% vs. 12% respectively, P = 0.88). The physiological role of myostatin in cardiac muscle appears significantly different than that in skeletal muscle as it does not induce cardiac hypertrophy and does not modulate cardiac fibrosis in mdx mice.