Impact of left ventricular hemodynamic forces in adult patients with treated aortic coarctation and preserved left ventricular systolic function.

BACKGROUND: The LV myocardial strain and hemodynamic forces (HDFs) are innovative markers of LV function. Aortic coarctation is safely repaired in infancy; however, mortality and morbidity remain increased in later life. The study investigated the role of left ventricular myocardial deformation and HDFs in asymptomatic patients who underwent successful aortic coarctation repair. METHODS: Clinical and echocardiographic data were analyzed from 42 repaired CoA, 32 ± 20 years after surgery, 2D echocardiographic global longitudinal strain (GLS), circumferential strain (GCS) and HDFs were determined. CoA patients were compared with 42 patients affected by blood hypertension and 84 healthy controls; all matched for age and gender. RESULTS: All groups had normal LV ejection fraction (LVEF), dimensions, and volumes. CoA patients showed a significantly higher rate of LV mass indexed (p < .001) and left atrial volumes indexed (p < .001). LV myocardial and endocardial global longitudinal and circumferential strain were decreased in CoA patients (p < .001, p < .001; p = .032 and p < .001, respectively). HDF parameters such as LV longitudinal force, LV systolic longitudinal force and LV impulse (LVim) were uniformly reduced (p = .006, p = .001, and p = .001, respectively). LV myocardial strain and HDF parameter values were independently associated with hospitalization for heart failure on univariable Cox regression analysis. CONCLUSION: Despite preserved LVEF, patients with CoA had lower LV myocardial strain and HDF parameters values, independently associated with hospitalization for heart failure.

Prognostic value of echocardiographic evaluation of cardiac mechanics in patients with aortic stenosis and preserved left ventricular ejection fraction.

Left ventricular ejection function (LVEF) is not reliable in identifying subtle systolic dysfunction. Speckle Tracking (ST) plays a promising role and hemodynamic forces (HDFs) are emerging as marker of LV function. The role of LV myocardial deformation and HDFs was investigated in a cohort of patients with aortic stenosis (AS) and normal LVEF. Two hundred fifty three patients (median age 79 years, IQR 73 - 83 years) with mild (n = 87), moderate (n =77) and severe AS (n =89) were retrospectively enrolled. 2D echocardiographic global longitudinal strain (GLS), circumferential strain (GCS) and HDFs were determined. The worsening of AS was associated with raising inappropriate LV mass (p < 0.001) and declined LVEF, despite being in the normal range (p < 0.001). ST and HDFs parameters declined as the AS became severe (p<0.0001, for all). When patients were grouped based on the median of LV endocardial GLS value (> -19,9%) and LV systolic longitudinal force (LVsysLF) value (< 12,49), patients with impaired ST and lower HDFs components had increased incidence of aortic valve replacement (AVR) and worse survival (p <0.024 and p <0.037, respectively). Among ST and HDFs parameters, only LVsysLF was independently associated with AVR and all causes mortality on multivariable Cox regression analysis (HR 0.94; 95% CI 0.89-0.99; p= 0.012). Reduced values of LVsysLF were associated with AVR and reduced survival in AS patients. LVsysLF could provide useful information in the stratification of patients with AS and possibly in the choice of timing for AVR.

Elevated Intrarenal Resistive Index Predicted Faster Renal Function Decline and Long-Term Mortality in Non-Proteinuric Chronic Kidney Disease.

Background. Intrarenal resistive index (RI) ≥ 0.80 predicts renal outcomes in proteinuric chronic kidney disease (CKD). However, this evidence in non-proteinuric patients with CKD of unknown etiology is lacking. In this study, we assessed the effect of intrarenal RI on renal function and all-cause mortality in non-proteinuric patients with CKD of unknown etiology despite an extensive diagnostic work-up. Methods. Non-proteinuric CKD patients were evaluated in a retrospective longitudinal study. Progression of renal disease was investigated by checking serum creatinine levels at 1, 3, and 5 years and defined by a creatinine level increase of at least 0.5 mg/dL. The discrimination performance of intrarenal RI in predicting the 5-year progression of renal disease was assessed by calculating the area under the receiver operating characteristic curve (AUROC). Results. One-hundred-thirty-one patients (76 ± 9 years, 56% males) were included. The median follow-up was 7.5 years (interquartile range 4.3−10.5) with a cumulative mortality of 53%, and 5-year renal disease progression occurred in 25%. Patients with intrarenal RI ≥ 0.80 had a faster increase of serum creatinine levels compared to those with RI < 0.80 (+0.06 mg/dL each year, 95% CI 0.02−0.10, p < 0.010). Each 0.1-unit increment of intrarenal RI was an independent determinant of 5-year renal disease progression (odds ratio 4.13, 95% CI 1.45−12.9, p = 0.010) and predictor of mortality (hazards ratio 1.80, 95% CI 1.05−3.09, p = 0.034). AUROCs of intrarenal RI for predicting 5-year renal disease progression and mortality were 0.66 (95% CI 0.57−0.76) and 0.67 (95% CI 0.58−0.74), respectively. Conclusions. In non-proteinuric patients with CKD of unknown etiology, increased intrarenal RI predicted both a faster decline in renal function and higher long-term mortality, but as a single marker, it showed poor discrimination performance.

The hemodynamic power of the heart differentiates normal from diseased right ventricles.

Cardiac mechanics is primarily described by the pressure-volume relationship. The ventricular pressure-volume loop displays the instantaneous relationship between intraventricular pressure and volume throughout the cardiac cycle; however, it does not consider the shape of the ventricles, their spatiotemporal deformation patterns, and how these balance with the flowing blood. Our study demonstrates that the pressure-volume relationship represents a first level of approximation for the mechanical power of the ventricles, while, at a further level of approximation, the importance of hemodynamic power emerges through the balance between deformation patterns and fluid dynamics. The analysis is preliminarily tested in a healthy subject's right ventricle and two patients. Moreover, patients' geometry was then rescaled to present a normal volumetric profile to verify whether results were affected by volume size or by the spatiotemporal pattern of how that volume profile was achieved. Results show that alterations of hemodynamic power were found in the abnormal ventricles and that they were not directly caused by the ventricular size but by changes in the ability of intraventricular pressure gradient to generate blood flow. Therefore, hemodynamic power represents a physics-based measure that takes into account the dynamics of the space-time shape changes in combination with blood flow. Hemodynamic power is assessed non-invasively using cardiac imaging techniques and can be an early indicator of cardiac dysfunction before changes occur in volumetric measurements. These preliminary results provide a physical ground to evaluate its diagnostic or prognostic significance in future clinical studies.