This prospective, longitudinal study examined the effects of participation in team-based exercise training on cardiac structure and function. Competitive endurance athletes (EA, n = 40) and strength athletes (SA, n = 24) were studied with echocardiography at baseline and after 90 days of team training. Left ventricular (LV) mass increased by 11% in EA (116 +/- 18 vs. 130 +/- 19 g/m(2); P < 0.001) and by 12% in SA (115 +/- 14 vs. 132 +/- 11 g/m(2); P < 0.001; P value for the compared Delta = NS). EA experienced LV dilation (end-diastolic volume: 66.6 +/- 10.0 vs. 74.7 +/- 9.8 ml/m(2), Delta = 8.0 +/- 4.2 ml/m(2); P < 0.001), enhanced diastolic function (lateral E': 10.9 +/- 0.8 vs. 12.4 +/- 0.9 cm/s, P < 0.001), and biatrial enlargement, while SA experience LV hypertrophy (posterior wall: 4.5 +/- 0.5 vs. 5.2 +/- 0.5 mm/m(2), P < 0.001) and diminished diastolic function (E' basal lateral LV: 11.6 +/- 1.3 vs. 10.2 +/- 1.4 cm/s, P < 0.001). Further, EA experienced right ventricular (RV) dilation (end-diastolic area: 1,460 +/- 220 vs. 1,650 +/- 200 mm/m(2), P < 0.001) coupled with enhanced systolic and diastolic function (E' basal RV: 10.3 +/- 1.5 vs. 11.4 +/- 1.7 cm/s, P < 0.001), while SA had no change in RV parameters. We conclude that participation in 90 days of competitive athletics produces significant training-specific changes in cardiac structure and function. EA develop biventricular dilation with enhanced diastolic function, while SA develop isolated, concentric left ventricular hypertrophy with diminished diastolic relaxation.

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Background-Functional mitral regurgitation (MR) is caused by systolic traction on the mitral leaflets related to ventricular distortion. Little is known about whether chronic tethering causes the mitral leaflet area to adapt to the geometric needs imposed by tethering, in part because of inability to reconstruct leaflet area in vivo. Our aim was to explore whether adaptive increases in leaflet area occur in patients with functional MR compared with normal subjects and to test the hypothesis that leaflet area influences MR severity. Methods and Results-A new method for 3-dimensional echocardiographic measurement of mitral leaflet area was developed and validated in vivo against 15 sheep heart valves, later excised. This method was then applied in 80 consecutive patients from 3 groups: patients with normal hearts by echocardiography (nϭ20), patients with functional MR caused by isolated inferior wall-motion abnormality or dilated cardiomyopathy (nϭ29), and patients with inferior wall-motion abnormality or dilated cardiomyopathy but no MR (nϭ31). Leaflet area was increased by 35Ϯ20% in patients with LV dysfunction compared with normal subjects. The ratio of leaflet to annular area was 1.95Ϯ0.40 and was not different among groups, which indicates a surplus leaflet area that adapts to left-heart changes. In contrast, the ratio of total leaflet area to the area required to close the orifice in midsystole was decreased in patients with functional MR compared with those with normal hearts (1.29Ϯ0.15 versus 1.78Ϯ0.39, Pϭ0.001) and compared with patients with inferior wall-motion abnormality or dilated cardiomyopathy but no MR (1.81Ϯ0.38, Pϭ0.001). After adjustment for measures of LV remodeling and tethering, a leaflet-to-closure area ratio Ͻ1.7 was associated with significant MR (odds ratio 23.2, 95% confidence interval 2.0 to 49.1, Pϭ0.02). Conclusions-Mitral leaflet area increases in response to chronic tethering in patients with inferior wall-motion abnormality and dilated cardiomyopathy, but the development of significant MR is associated with insufficient leaflet area relative to that demanded by tethering geometry. The varying adequacy of leaflet adaptation may explain in part the heterogeneity of this disease among patients. The results suggest the need to understand the mechanisms that underlie leaflet adaptation and whether leaflet area can potentially be modified as part of the therapeutic approach.

High-frame-rate ultrasonography based on coherent compounding of unfocused beams can potentially transform the assessment of cardiac function. As it requires successive waves to be combined coherently, this approach is sensitive to high-velocity tissue motion. We investigated coherent compounding of tilted diverging waves, emitted from a 2.5 MHz clinical phased array transducer. To cope with high myocardial velocities, a triangle transmit sequence of diverging waves is proposed, combined with tissue Doppler imaging to perform motion compensation (MoCo). The compound sequence with integrated MoCo was adjusted from simulations and was tested in vitro and in vivo. Realistic myocardial velocities were analyzed in an in vitro spinning disk with anechoic cysts. While a 8 dB decrease (no motion versus high motion) was observed without MoCo, the contrast-to-noise ratio of the cysts was preserved with the MoCo approach. With this method, we could provide high-quality in vivo B-mode cardiac images with tissue Doppler at 250 frames per second. Although the septum and the anterior mitral leaflet were poorly apparent without MoCo, they became well perceptible and well contrasted with MoCo. The septal and lateral mitral annulus velocities determined by tissue Doppler were concordant with those measured by pulsed-wave Doppler with a clinical scanner (r(2)=0.7,y=0.9 x+0.5,N=60) . To conclude, high-contrast echo cardiographic B-mode and tissue Doppler images can be obtained with diverging beams when motion compensation is integrated in the coherent compounding process.