Rationale: Tissue Doppler imaging (TDI) is an echocardiographic method that measures the velocity of moving tissue. Objectives: We applied this technique to the diaphragm to assess the velocity of diaphragmatic muscle motion during contraction and relaxation. Methods: In 20 healthy volunteers, diaphragmatic TDI was performed to assess the pattern of diaphragmatic motion velocity, measure its normal values, and determine the intra- and interobserver variability of measurements. In 116 consecutive ICU patients, diaphragmatic excursion, thickening, and TDI parameters of peak contraction velocity, peak relaxation velocity, velocity–time integral, and TDI-derived maximal relaxation rate were assessed during weaning. In a subgroup of 18 patients, transdiaphragmatic pressure (Pdi)-derived parameters (peak Pdi, pressure–time product, and diaphragmatic maximal relaxation rate) were recorded simultaneously with TDI. Measurements and Main Results: In terms of reproducibility, the intercorrelation coefficients were >0.89 for all TDI parameters ( P < 0.001). Healthy volunteers and weaning success patients exhibited lower values for all TDI parameters compared with weaning failure patients, except for velocity–time integral, as follows: peak contraction velocity, 1.35 ± 0.34 versus 1.50 ± 0.59 versus 2.66 ± 2.14 cm/s ( P < 0.001); peak relaxation velocity, 1.19 ± 0.39 versus 1.53 ± 0.73 versus 3.36 ± 2.40 cm/s ( P < 0.001); and TDI-maximal relaxation rate, 3.64 ± 2.02 versus 10.25 ± 5.88 versus 29.47 ± 23.95 cm/s 2 ( P < 0.001), respectively. Peak contraction velocity was strongly correlated with peak transdiaphragmatic pressure and pressure–time product, whereas Pdi-maximal relaxation rate was significantly correlated with TDI-maximal relaxation rate. Conclusions: Diaphragmatic tissue Doppler allows real-time assessment of the diaphragmatic tissue motion velocity. Diaphragmatic TDI-derived parameters differentiate patients who fail a weaning trial from those who succeed and correlate well with Pdi-derived parameters.
Cirrhosis is commonly associated with impaired left ventricular (LV) myocardial contractile reserve to stress and diastolic dysfunction. The aim of this study was to assess LV systolic performance at rest, using both "standard" echocardiographic indices and novel deformation-rotational parameters, in order to elucidate the pathophysiologic basis of cardiac dysfunction in cirrhosis. Seventy-seven men with cirrhosis (mean age 54.4 ± 9.7) of variable Child-Pugh class (A, B, C) and 20 healthy control subjects were prospectively evaluated by standard as well as speckle tracking echocardiography. Left ventricular ejection fraction (LVEF) was significantly higher in patients with cirrhosis compared to controls (64.6 ± 5.7% in controls vs. 71 ± 9.5%, 71.2 ± 7.1%, and 73 ± 7% in Child-Pugh classes A, B, and C, respectively, P = 0.002). Interestingly, LV systolic function augmentation was not associated with changes in LV longitudinal deformation (LV strain -19 ± 1.9% in controls vs. -20.1 ± 5.3% in class A vs. -21.3 ± 2.6% in class B vs. -21 ± 3.4% in class C, P = NS), but a statistically significant increase in LV apical systolic rotation and accordingly in LV twist was observed (LV twist 13.0 ± 3° in controls vs. 14.9 ± 5° in class A vs. 16.5 ± 2.8° in class B vs. 18.2 ± 2.9° in class C, P < 0.0005). Despite the increase in LV rotation, time to both basal and apical peak systolic rotation was significantly delayed in patients compared to healthy controls (P = 0.015 and P = 0.017 accordingly). Increased EF in cirrhosis could be attributed to increased LV torsion. Despite the "improved" rotation values at rest, there is a significant time delay in succeeding peak systolic rotation, hampering also the consequent untwisting-diastolic period.
Aim The investigation of the pathophysiological determinants of cardiac changes following ultra-long duration exercise. Methods Twenty-seven runners who finished a 246 km running race were examined both before and after the finish of the race. Examinations included echocardiography and measurement of body weight and blood biochemical parameters. Results Exercise increased left ventricular end-diastolic interventricular septum thickness (LVIVSd) ( p < 0.001) and posterior wall thickness (LVPWTd) ( p = 0.001) and right ventricular end-diastolic area ( p = 0.005), while reduced tricuspid annular plane systolic excursion (TAPSE) ( p = 0.004). A minor decrease in the peak absolute values of both left ventricular (from −20.9 ± 2.3% to −18.8 ± 2.0%, p = 0.009) and right ventricular (from −22.9 ± 3.6% to −21.2 ± 3.0%, p = 0.040) global longitudinal strains occurred. There was decrease in body weight ( p < 0.001) and increase in both circulating high-sensitivity troponin I ( p = 0.028) and amino-terminal pro-B type natriuretic peptide (NT-proBNP) ( p = 0.018). The change in the sum of LVIVSd and LVPWTd correlated negatively with percentage change of body weight ( r = −0.416, p = 0.049). The only independent determinant of post-exercise NT-proBNP was pulmonary artery systolic pressure ( r = 0.797, p = 0.002). Post-exercise NT-proBNP correlated positively with percentage changes of basal (RVbas) ( r = 0.582, p = 0.037) and mid-cavity (RVmid) ( r = 0.618, p = 0.043) right ventricular diameters and negatively with percentage change of TAPSE ( r = −0.720, p = 0.008). Similar correlations with RVbas, RVmid and TAPSE were found for pulmonary artery systolic pressure. Post-exercise high-sensitivity troponin I correlated negatively with percentage change of body weight ( r = −0.601, p = 0.039), but was not associated with any cardiac parameter. Conclusion The main cardiac effects of ultra-long duration exercise were the decrease in left ventricular end-diastolic dimensions and increase in left ventricular wall thickness, as well as minimal dilatation and alteration in systolic function of right ventricle, possibly due to the altered exercise-related right ventricular afterload.
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