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.

Aims Limited data exist concerning fragmented QRS complexes (fQRSs) on the surface electrocardiogram (ECG) of apparently healthy athletes. We aimed to study the prevalence and significance of fQRS in lead V1 (fQRSV1), representing right ventricular (RV) activation, regarding training-induced RV morphological remodelling. Methods and results Between January 2017 and August 2019, 434 consecutive non-sedentary subjects underwent preparticipation cardiovascular screening, including a 12-lead ECG. Three hundred and ninety-three apparently healthy subjects were included, 119 of them were athletes (defined as performing ≥8 h/week for the last 6 months) and 274 were non-athletes. All athletes underwent two-dimensional transthoracic echocardiography. Fragmented QRS complex in lead V1 pattern was defined as a narrow (<120 ms) and quadriphasic QRS complex in lead V1. Fragmented QRS complex in lead V1 was more frequent in athletes compared with non-athletes (22% vs. 5.1%, P < 0.001) and was independently associated with the athlete status [adjusted odds ratio (aOR) = 4.693, 95% confidence interval (95% CI) 2.299—9.583; P < 0.001], the endurance category (aOR = 2.522, 95% CI 1.176—5.408; P = 0.017), and age (aOR = 0.962, 95% CI 0.934–0.989; P = 0.007) in multivariate analysis. In the subgroup of athletes, fQRSV1 was independently associated with mean RV outflow tract diameter (aOR = 1.458, 95% CI 1.105–1.923; P = 0.008) and age (aOR = 0.941, 95% CI 0.894–0.989; P = 0.017) in multivariate analysis. Conclusion Fragmented QRS complex in lead V1 is a newly described, frequent, ECG pattern in young and apparently healthy athletes and is associated with training-induced RV remodelling.

Cyclic AMP phosphodiesterases (PDEs) are important modulators of the cardiac response to βadrenergic receptor (β-AR) stimulation. PDE3 is classically considered as the major cardiac PDE in large mammals and human, while PDE4 is preponderant in rodents. However, it remains unclear whether PDE4 also plays a functional role in large mammals. Our purpose was to understand the role of PDE4 in cAMP hydrolysis and excitation-contraction coupling (ECC) in the pig heart, a relevant pre-clinical model. Methods and Results Real-time cAMP variations were measured in isolated adult pig right ventricular myocytes (APVMs) using a Förster resonance energy transfer (FRET) biosensor. ECC was investigated in APVMs loaded with Fura-2 and paced at 1 Hz allowing simultaneous measurement of intracellular Ca 2+ and sarcomere shortening. The expression of the different PDE4 isoforms was assessed by Western blot in pig right ventricle and APVMs. Similarly to PDE3 inhibition with cilostamide (Cil), PDE4 inhibition with Ro 20-1724 (Ro) increased cAMP levels and inotropy under basal conditions. PDE4 inhibition enhanced the effects of the non-selective β-AR agonist isoprenaline (Iso) and the effects of Cil, and increased spontaneous diastolic Ca 2+ waves (SCWs) in these conditions. PDE3A, PDE4A, PDE4B and PDE4D isoforms are expressed in pig ventricle.. In APVMs isolated from a porcine model of repaired tetralogy of Fallot which leads to right ventricular failure, PDE4 inhibition also exerts inotropic and pro-arrhythmic effects. Conclusions Our results show that PDE4 controls ECC in APVMs and suggest that PDE4 inhibitors exert inotropic and pro-arrhythmic effects upon PDE3 inhibition or β-AR stimulation in our pre-clinical model. Thus, PDE4 inhibitors should be used with caution in clinics as they may lead to arrhythmogenic events upon stress.