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Introduction: Right-ventricular-to-pulmonary artery (RV-PA) coupling, measured as the ratio of tricuspid annular plane systolic excursion (TAPSE) to pulmonary artery systolic pressure (PASP), has emerged as a predictor factor in patients undergoing transcatheter aortic valvular replacement (TAVR). Right ventricular longitudinal shortening fraction (RV-LSF) outperformed TAPSE as a prognostic parameter in several diseases. We aimed to compare the prognostic ability of two RV-PA coupling parameters (TAPSE/PASP and the RV-LSF/PASP ratio) in identifying MACE occurrences. Method: A prospective and single-center study involving 197 patients who underwent TAVR was conducted. MACE (heart failure, myocardial infarction, stroke, and death within six months) constituted the primary outcome. ROC curve analysis determined cutoff values for RV-PA ratios. Multivariable Cox regression analysis explored the association between RV-PA ratios and MACE. Results: Forty-six patients (23%) experienced the primary outcome. No significant difference in ROC curve analysis was found (RV-LSF/PASP with AUC = 0.67, 95%CI = [0.58–0.77] vs. TAPSE/PASP with AUC = 0.62, 95%CI = [0.49–0.69]; p = 0.16). RV-LSF/PASP < 0.30%.mmHg−1 was independently associated with the primary outcome. The 6-month cumulative risk of MACE was 59% (95%CI = [38–74]) for patients with RV-LSF/PASP < 0.30%.mmHg−1 and 17% (95%CI = [12–23]) for those with RV-LSF/PASP ≥ 0.30%.mmHg−1; (p < 0.0001). Conclusions: In a contemporary cohort of patients undergoing TAVR, RV-PA uncoupling defined by an RV-LSF/PASP < 0.30%.mmHg−1 was associated with MACE at 6 months.

Introduction: Right ventricular (RV) systolic dysfunction (RVsD) is a common complication of coronavirus infection 2019 disease (COVID-19). The right ventricular free wall longitudinal strain parameter (RV-FWLS) is a powerful predictor of mortality. We explored the performance of RVsD parameters for predicting 30-day mortality and the association between RV-FWLS and 30-day mortality. Methods: COVID-19 patients hospitalized at Amiens University Hospital in the critical care unit with transthoracic echocardiography were included. We measured tricuspid annular plane systolic excursion (TAPSE), the RV S’ wave, RV fractional area change (RV-FAC), and RV-FWLS. The diagnostic performance of RVsD parameters as predictors for 30-day mortality was evaluated by the area under the receiver operating characteristic (ROC) curve (AUC). RVsD was defined by an RV-FWLS < 21% to explore the association between RVsD and 30-day mortality. Results: Of the 116 patients included, 20% (n = 23/116) died and 47 had a RVsD. ROC curve analysis showed that RV-FWLS failed to predict 30-day mortality, as did conventional RV parameters (all p > 0.05). TAPSE (21 (19–26) mm vs. 24 (21–27) mm; p = 0.024) and RV-FAC (40 (35–47)% vs. 47 (41–55)%; p = 0.006) were lowered in the RVsD group. In Cox analysis, RVsD was not associated with 30-day mortality (hazard ratio = 1.12, CI 95% (0.49–2.55), p = 0.78). Conclusion: In severe COVID-19 pneumonia, RV-FWLS was not associated with 30-day mortality.

Introduction: Right ventricular systolic dysfunction (RVsD) increases acute respiratory distress syndrome mortality in COVID-19 infection (CARDS). The RV longitudinal shortening fraction (RV-LSF) is an angle-independent and automatically calculated speckle-tracking parameter. We explored the association between RV-LSF and 30-day mortality in CARDS patients. Methods: Moderate-to-severe CARDS patients hospitalized at Amiens University Hospital with transesophageal echocardiography performed within 48 h of intensive care unit admission were included. RVsD was defined by an RV-LSF of n = 37/86) of the patients showed RVsD and 22% (n = 19/86) of the patients died. RV-LSF was observed in 26 (23.1–29.7)% of the no-RVsD function group and 16.5 (13.7–19.4)% (p < 0.001) of the RVsD group. Cardiogenic shock (n = 7/37 vs. 2/49, p = 0.03) and acute cor pulmonale (n = 18/37 vs. 10/49, p = 0.009) were more frequent in the RVsD group. The 30-day mortality was higher in the RVsD group (15/37 vs. 4/49, p = 0.001). In a multivariable Cox model, RV-LSF was an independent mortality factor (HR 4.45, 95%CI (1.43–13.8), p = 0.01). Conclusion: in a cohort of moderate-to-severe CARDS patients under mechanical ventilation, RVsD defined by the RV-LSF was associated with higher 30-day mortalities.

We aimed to assess variations in the portal vein pulsatility index (PI) during mechanical ventilation following cardiac surgery. Method. After ethical approval, we conducted a prospective monocentric study at Amiens University Hospital. Patients under mechanical ventilation following cardiac surgery were enrolled. Doppler evaluation of the portal vein (PV) was performed by transthoracic echography. The maximum velocity (VMAX) and minimum velocity (VMIN) of the PV were measured in pulsed Doppler mode. The PI was calculated using the following formula (VMAX − VMIN)/(VMax). A positive end-expiratory pressure (PEEP) incremental trial was performed from 0 to 15 cmH2O, with increments of 5 cmH2O. The PI (%) was assessed at baseline and PEEP 5, 10, and 15 cmH2O. Echocardiographic and hemodynamic parameters were recorded. Results. In total, 144 patients were screened from February 2018 to March 2019 and 29 were enrolled. Central venous pressure significantly increased for each PEEP increment. Stroke volumes were significantly lower after PEEP incrementation, with 52 mL (50–55) at PEEP 0 cmH2O and 30 mL (25–45) at PEEP 15 cmH2O, (p < 0.0001). The PI significantly increased with PEEP incrementation, from 9% (5–15) at PEEP 0 cmH2O to 15% (5–22) at PEEP 5 cmH2O, 34% (23–44) at PEEP 10 cmH2O, and 45% (25–49) at PEEP 15 cmH2O (p < 0.001). Conclusion. In the present study, PI appears to be a dynamic marker of the interaction between mechanical ventilation and right heart pressure after cardiac surgery. The PI could be a useful noninvasive tool to monitor venous congestion associated with mechanical ventilation.

(1) Background: Right ventricular (RV) strain parameters derived from the analysis of the tricuspid annular displacement (TAD) are emergent two-dimensional speckle tracking echocardiography (2D-STE) parameter used for the quantitative assessment of RV systolic function. Few data are available regarding 2D-STE parameters and their dependency on RV preload. Our aim was to evaluate the effect of an acute change in RV preload on 2D-STE parameters in healthy volunteers. (2) Methods: Acute modification of RV preload was performed by a fluid challenge (FC): an infusion of 500 mL of 0.9% sodium chloride was given over 5 min in supine position. Preload dependency (responder group) was confirmed by a stroke volume increase of at least 10% measured by echocardiography. (3) Results: Among 32 healthy volunteers, 19 (59%) subjects were classified as non-responders and 13 (41%) as responders. In the responder group, the tricuspid annular plane systolic excursion (TAPSE) significantly increased (20 (20–23.5) mm to 24 (20.5–26.5) mm; p = 0.018), while RV strain parameters significantly decreased after FC: −23.5 ((−22.3)–(−27.3))% to −25 ((−24)–(29.6))%; p = 0.03) for RV free wall longitudinal strain and −22.8 ((−20.4)–(−30.7))% to −23.7 ((−21.2)–(−27))%; p = 0.02) for RV four-chamber longitudinal strain. 2D-STE parameters derived from the TAD analysis were not influenced by the FC (all p > 0.05). (4) Conclusions: In young, healthy volunteers, RV strain parameters and TAPSE are preload dependent, while TAD parameters were not. The loading conditions must be accounted for when evaluating RV systolic function by 2D-STE parameters.

Sarafotoxins (SRTX) are endothelin-like peptides extracted from the venom of snakes belonging to the Atractaspididae family. A recent in vivo study on anesthetized and ventilated animals showed that sarafotoxin-b (SRTX-b), extracted from the venom of Atractaspis engaddensis, decreases cardiac output by inducing left ventricular dysfunction while sarafotoxin-m (SRTX-m), extracted from the venom of Atractaspis microlepidota microlepidota, induces right ventricular dysfunction with increased airway pressure. The aim of the present experimental study was to compare the respiratory effects of SRTX-m and SRTX-b. Male Wistar rats were anesthetized, tracheotomized and mechanically ventilated. They received either a 1 LD50 IV bolus of SRTX-b (n = 5) or 1 LD50 of SRTX-m (n = 5). The low-frequency forced oscillation technique was used to measure respiratory impedance. Airway resistance (Raw), parenchymal damping (G) and elastance (H) were determined from impedance data, before and 5 min after SRTX injection. SRTX-m and SRTX-b injections induced acute hypoxia and metabolic acidosis with an increased anion gap. Both toxins markedly increased Raw, G and H, but with a much greater effect of SRTX-b on H, which may have been due to pulmonary edema in addition to bronchoconstriction. Therefore, despite their structural analogy, these two toxins exert different effects on respiratory function. These results emphasize the role of the C-terminal extension in the in vivo effect of these toxins.