Left Ventricular End-diastolic Area Research Articles

Gestational Age-Specific Markers Associated with Postnatal Intervention in Fetal Suspicion of Coarctation of the Aorta.

Fetal diagnosis of coarctation of the aorta (CoA) is currently associated with a high false-positive rate. Many predictive markers may be gestational age (GA)-specific. We sought to establish GA-specific traditional and speckle-tracking fetal echocardiography (STE) markers predictive of true CoA in neonates with prenatal suspicion. This is a retrospective case-control study. We compared the fetal ventricular and arch dimensions, as well as the deformation parameters by STE, of infants who required a postnatal intervention for their CoA with those who did not. Cohort was stratified based on GA before or after 30 weeks. Data extractors were masked to the outcome. The first fetal echocardiogram available was used. Seventy-five newborns with a fetal echocardiography performed between October 2013 and May 2022 for an antenatal suspicion of CoA were included, of which 59 (79%) had an aortic arch with nonsignificant obstruction upon ductal closure, and 16 (21%) underwent a neonatal intervention for a confirmed CoA. Before 30 weeks' GA, the right ventricular to left ventricular (RV/LV) end-diastolic width and end-diastolic area (EDA) ratios were most associated with postnatal CoA confirmation (area under the curve [AUCs] = 0.96 and 0.92). After 30 weeks' GA, the RV/LV end-diastolic width ratio (AUC = 0.95), the Z-score for the ascending aorta (AUC = 0.93), and the LV end-diastolic width Z-score (AUC = 0.91) performed the best. A decreased RV peak longitudinal strain was observed in those who developed true CoA and performed well by receiver operating characteristic analysis after 30 weeks (AUC = 0.85). In the overall cohort, the RV/LV EDA ratio was the most sensitive predictor of CoA and identified all cases with CoA. Indeed, a cutoff > 1.24 had a specificity of 69.5% and a sensitivity of 100% (receiver operating characteristic curve with an AUC of 0.88). We outlined sensitive and specific fetal markers associated with postnatal CoA based on GA at suspicion. · Fetal ventricular disproportion predicts postnatal coarctation.. · A decreased right ventircular contraction was observed in those with coarctation.. · Fetal markers differ based on gestational age at fetal evaluation..

Right ventricular injury in patients with COVID-19-related ARDS eligible for ECMO support: a multicenter retrospective study

BackgroundCoronavirus disease 2019 (COVID-19)-related acute respiratory distress syndrome (ARDS) is associated with high mortality. Extracorporeal membrane oxygenation (ECMO) has been proposed in this setting, but optimal criteria to select target patients remain unknown. Our hypothesis is that evaluation of right ventricular (RV) function could be helpful. The aims of our study were to report the incidence and outcomes of patients eligible for ECMO according to EOLIA criteria, and to identify a subgroup of patients with RV injury, which could be a target for ECMO.MethodsRetrospective observational study involving 3 French intensive care units (ICUs) of teaching hospitals. Patients with confirmed SARS-CoV-2 infection between March 2020 and March 2021, presenting ARDS and with available echocardiography, were included. Patients were classified in three groups according to whether or not they met the EOLIA criteria and the presence of RV injury (RVI) (“EOLIA −”, “EOLIA + RVI −” and “EOLIA + RVI + ”). RVI was defined by the association of RV to left ventricular end-diastolic area ratio > 0.8 and paradoxical septal motion. Kaplan–Meier survival curves were used to analyze outcome as well as a Cox model for 90 day mortality.Results915 patients were hospitalized for COVID-19, 418 of them with ARDS. A total of 283 patients with available echocardiography were included. Eighteen (6.3%) patients received ECMO. After exclusion of these patients, 107 (40.5%) were classified as EOLIA −, 126 (47.5%) as EOLIA + RVI −, and 32 (12%) as EOLIA + RVI + . Ninety-day mortality was 21% in the EOLIA-group, 44% in the EOLIA + RVI-group, and 66% in the EOLIA + RVI + group (p < 0.001). After adjustment, RVI was statistically associated with 90-day mortality (HR = 1.92 [1.10–3.37]).ConclusionsAmong COVID-19-associated ARDS patients who met the EOLIA criteria, those with significant RV pressure overload had a particularly poor outcome. This subgroup may be a more specific target for ECMO. This represented 12% of our cohort compared to 60% of patients who met the EOLIA criteria only. How the identification of this high-risk subset of patients translates into patient-centered outcomes remains to be evaluated.

Fibroblast-specific SOCS3 deficient mice exhibits decreased myocardial fibrosis and increased cardiomyocyte survival after acute myocardial infarction

Abstract Background Left ventricular (LV) remodeling after acute myocardial infarction (AMI) results in poor cardiac performance leading to heart failure. LV remodeling after AMI is characterized by infarct expansion, LV dilation, and fibrosis of viable myocardium. Suppressor of cytokine signaling-3 (SOCS3) is an endogenous negative-feedback regulator of the STAT3 signaling pathway. We previously reported that myocardial SOCS3 plays a detrimental role in LV remodeling after AMI; however, the role of STAT3 and SOCS3 within fibroblast in LV remodeling after AMI remains elusive. Objective The aim of this study is to clarify the role of STAT3 and SOCS3 within fibroblasts in LV remodeling during AMI in mice. Methods To investigate the role of STAT3 signaling and SOCS3 within fibroblast, we generated tamoxifen-induced fibroblast-specific SOCS3-deficient (fib-SOCS3 KO) mice. AMI was induced by permanent ligation of the left anterior descending artery in mice. After 2 weeks of induction with tamoxifen, histological evaluation by Hematoxylin Eosin staining and Picro-Sirius Red staining, cardiac function evaluation by echocardiography using a Vevo 3100 Echo Imaging System (Visual Sonics), and protein expression using Western blot analysis were performed. Results There was no significant difference in 2-week survival rate between fib-SOCS3 KO group and wild type (WT). Two weeks after AMI, ventricular weight was less in fib-SOCS3 KO mice compared to WT mice (p&amp;lt;0.05). In terms of cardiac function, LV ejection fraction was predominantly increased in fib-SOCS3 KO mice compared with WT mice, as measured by the Area method (p&amp;lt;0.05). There was no difference in LV end-diastolic area, but LV end-systolic area was significantly less in fib-SOCS3 KO mice than in WT mice. Histologically, residual viable myocardium in the infarcted area was greater in fib-SOCS3 KO mice compared with WT mice. The percentage of fibrotic area in the LV short-axis plane was significantly less in fib-SOCS3 KO mice than in WT mice. Western blot analysis revealed that phosphorylated-STAT3 tended to be elevated in fib-SOCS3 KO mice than in WT mice. Conclusions Our data suggest that STAT3 and SOCS3 within fibroblast may play an important role in the prevention of LV remodeling after AMI.

Exploring the predictive value of combined ultrasound parameters for spinal anesthesia-induced hypotension in cesarean section: a prospective observational study

BackgroundProphylactic vasopressor infusion can effectively assist with fluid loading to prevent spinal anesthesia-induced hypotension. However, the ideal dose varies widely among individuals. We hypothesized that hypotension-susceptible patients requiring cesarean section (C-section) could be identified using combined ultrasound parameters to enable differentiated prophylactic medical interventions.MethodsThis prospective observational trial was carried out within a regional center hospital for women and children in Sichuan Province, China. Singleton pregnant women undergoing combined spinal-epidural anesthesia for elective C-sections were eligible. Women with contraindications to spinal anesthesia or medical comorbidities were excluded. Velocity time integral (VTI) and left ventricular end-diastolic area (LVEDA) in the supine and left lateral positions were measured on ultrasound before anesthesia. Stroke volume, cardiac output, and the percentage change (%) in each parameter between two positions were calculated. Vital signs and demographic data were recorded. Spinal anesthesia-induced hypotension was defined as a mean arterial pressure decrease of > 20% from baseline. The area under the receiver operating characteristic curve (AUROC) was used to analyze the associations of ultrasound measurements, vital signs, and demographic characteristics with spinal anesthesia-induced hypotension. This exploratory study did not have a predefined outcome; however, various parameter combinations were compared using the AUROC to determine which combined parameters had better predictive values.ResultsPatients were divided into the normotension (n = 31) and hypotension groups (n = 57). A combination of heart rate (HR), LVEDAs, and VTI% was significantly better at predicting hypotension than was HR (AUROC 0.827 vs. 0.707, P = 0.020) or LVEDAs (AUROC 0.827 vs. 0.711, P = 0.039) alone, but not significantly better than VTI% alone (AUROC 0.827 vs. 0.766, P = 0.098).ConclusionThe combined parameters of HR and LVEDAs with VTI% may predict spinal anesthesia-induced hypotension more precisely than the single parameters. Future research is necessary to determine whether this knowledge improves maternal and neonatal outcomes.Trial registrationChiCTR1900025191.

The haemodynamic effects of phenylephrine after cardiac surgery.

Phenylephrine increases systemic- and pulmonary resistances and therefore may increase blood pressures at the expense of blood flow. Cardio-pulmonary bypass alters vasoreactivity and many patients exhibit chronotropic insufficiency after cardiac surgery. We aimed to describe the haemodynamic effects of phenylephrine infusion after cardiac surgery. Patients in steady state after low-risk cardiac surgery received incremental infusion rates of phenylephrine up to 1.0 μg/kg/min with the aim of increasing systemic mean arterial blood pressure 20 mmHg. Invasive haemodynamic parameters, including pulmonary wedge pressures, were captured along with echocardiographic measures of biventricular function before, during phenylephrine infusion at target systemic blood pressure, and 20 min after phenylephrine discontinuation. Thirty patients were included. Phenylephrine increased mean arterial pressure increased from 78 (±9) mmHg to 98 (±10) mmHg with phenylephrine infusion. Also, pulmonary blood pressure as well as systemic- and pulmonary resistances increased. The ratio between systemic- and pulmonary artery resistances did not change statistically significantly (p = .59). Median cardiac output was 4.35 (interquartile range [IQR] 3.6-5.4) L/min at baseline and increased significantly with phenylephrine infusion (median Δcardiac output was 0.25 [IQR 0.1-0.6] L/min) (p = .012). Pulmonary artery wedge pressure increased from 10.2 (±3.0) mmHg to 11.9 (±3.4) mmHg (p < .001). This was accompanied by significant increases in central venous pressure. Phenylephrine infusion increased left ventricular end-diastolic volume from 105 (±46) mL to 119 (±44) mL (p < .001). All results of phenylephrine infusion were reversed with discontinuation. In haemodynamically stable patients after cardiac surgery, phenylephrine increased PVR and SVR, but did not change the PVR/SVR ratio. Phenylephrine increased biventricular filling pressures and left ventricular end-diastolic area. Consequently, CO increased as ejection fraction was maintained. These findings do not discourage the use of phenylephrine after low-risk cardiac surgery. clinicaltrial.gov (identifier NCT04419662).

Peripheral Intravenous Waveform Analysis Responsiveness to Subclinical Hemorrhage in a Rat Model.

Early detection and quantification of perioperative hemorrhage remains challenging. Peripheral intravenous waveform analysis (PIVA) is a novel method that uses a standard intravenous catheter to detect interval hemorrhage. We hypothesize that subclinical blood loss of 2% of the estimated blood volume (EBV) in a rat model of hemorrhage is associated with significant changes in PIVA. Secondarily, we will compare PIVA association with volume loss to other static, invasive, and dynamic markers. Eleven male Sprague Dawley rats were anesthetized and mechanically ventilated. A total of 20% of the EBV was removed over ten 5 minute-intervals. The peripheral intravenous pressure waveform was continuously transduced via a 22-G angiocatheter in the saphenous vein and analyzed using MATLAB. Mean arterial pressure (MAP) and central venous pressure (CVP) were continuously monitored. Cardiac output (CO), right ventricular diameter (RVd), and left ventricular end-diastolic area (LVEDA) were evaluated via transthoracic echocardiogram using the short axis left ventricular view. Dynamic markers such as pulse pressure variation (PPV) were calculated from the arterial waveform. The primary outcome was change in the first fundamental frequency (F1) of the venous waveform, which was assessed using analysis of variance (ANOVA). Mean F1 at each blood loss interval was compared to the mean at the subsequent interval. Additionally, the strength of the association between blood loss and F1 and each other marker was quantified using the marginal R2 in a linear mixed-effects model. PIVA derived mean F1 decreased significantly after hemorrhage of only 2% of the EBV, from 0.17 to 0.11 mm Hg, P = .001, 95% confidence interval (CI) of difference in means 0.02 to 0.10, and decreased significantly from the prior hemorrhage interval at 4%, 6%, 8%, 10%, and 12%. Log F1 demonstrated a marginal R2 value of 0.57 (95% CI 0.40-0.73), followed by PPV 0.41 (0.28-0.56) and CO 0.39 (0.26-0.58). MAP, LVEDA, and systolic pressure variation displayed R2 values of 0.31, and the remaining predictors had R2 values ≤0.2. The difference in log F1 R2 was not significant when compared to PPV 0.16 (95% CI -0.07 to 0.38), CO 0.18 (-0.06 to 0.04), or MAP 0.25 (-0.01 to 0.49) but was significant for the remaining markers. The mean F1 amplitude of PIVA was significantly associated with subclinical blood loss and most strongly associated with blood volume among the markers considered. This study demonstrates feasibility of a minimally invasive, low-cost method for monitoring perioperative blood loss.

Are There Distinct Cardiovascular Subclasses in Acute Respiratory Distress Syndrome? Maybe.

Are There Distinct Cardiovascular Subclasses in Acute Respiratory Distress Syndrome? Maybe.

Prognostic implication of a novel right ventricular injury score in septic patients.

We aim to investigate the prognostic value of a right ventricular (RV) injury score based on the concept of RV dilation, RV systolic dysfunction, and RV-pulmonary arterial (PA) decoupling in septic patients and to explore whether the RV injury (RVI) score can be used to grade the severity of RV dysfunction in these patients. Septic patients admitted to the ICU were prospectively included. We collected haemodynamic and echocardiographic parameters as well as prognostic information. RV dilation was defined as right and left ventricular end-diastolic area ratio (R/LVEDA)>2/3. RVSD was defined as tricuspid annular plane systolic excursion (TAPSE)<17mm, right ventricular fractional area change (FAC)<35%, or peak velocity of tricuspid annulus via tissue Doppler (S')<10cm/s. RV-PA decoupling was represented by the TAPSE/pulmonary arterial systolic pressure (PASP) ratio. RVI score were determined by the presence of the following findings: RVSD, RV dilation, and RV-PA decoupling, that is, one point for each finding. A total of 327 patients were enrolled in this study, among whom 276 survived and 51 died at 30days after admission. Overall, 18.0% had RV dilation, 35.8% had RVSD, and 21.4% had RV-PA decoupling, with an appreciable overlap present. A multivariate Cox regression analysis showed that RV dilation (HR: 2.19, 95% CI: 1.19-4.01, P=0.011), RVSD (HR: 2.25, 95% CI: 1.23-4.13, P=0.009) and RV-PA decoupling (HR: 2.08, 95% CI: 1.19-3.65, P=0.011) were independently associated with a 30day mortality. Furthermore, RVI score was also an independent predictor, displayed additive effect with respect to 30day mortality (RVI score 1 vs. RVI score 0, HR: 2.94, 95% CI: 1.20-7.20, P=0.018; RVI score 2 vs. RVI score 0, HR: 3.20, 95% CI: 1.28-7.98, P=0.013; RVI score 3 vs. RVI score 0, HR: 7.17, 95% CI: 2.65-19.38, P<0.001), and had the best performance in model goodness of fit, discrimination and variance explained than the other RV indices. The RVI score was independently related to 30day mortality and had the potential to grade the severity of RV dysfunction in septic patients.

Study to Explore the Association of the Renin-Angiotensin System and Right Ventricular Function in Mechanically Ventilated Patients.

Background: Right ventricular (RV) dysfunction is associated with pulmonary vasoconstriction in mechanically ventilated patients. Enhancing the activity of angiotensin-converting enzyme 2 (ACE2), a key enzyme of the renin-angiotensin system (RAS), using recombinant human ACE2 (rhACE2) could alleviate RAS-mediated vasoconstriction and vascular remodeling. Methods: This prospective observational study investigated the association between concentrations of RAS peptides (Ang II or Ang(1–7)) and markers of RV function, as assessed by echocardiography (ratio of RV to left ventricular end-diastolic area, interventricular septal motion, and pulmonary arterial systolic pressure (PASP)). Results: Fifty-seven mechanically ventilated patients were enrolled. Incidence rates of acute cor pulmonale (ACP) and pulmonary circulatory dysfunction (PCD) were consistent with previous studies. In the 45 evaluable participants, no notable or consistent changes in RAS peptides concentration were observed over the observation period, and there was no correlation between Ang II concentration and either PASP or RV size. The model of the predicted posterior distributions for the pre- and post-dose values of Ang II demonstrated no change in the likelihood of PCD after hypothetical dosing with rhACE2, thus meeting the futility criteria. Similar results were observed with the other RAS peptides evaluated. Conclusions: Pre-defined success criteria for an association between PCD and the plasma RAS peptides were not met in the mechanically ventilated unselected patients.

Ultrasound of Fetal Cardiac Function Changes in Pregnancy-Induced Hypertension Syndrome.

Pregnancy-induced hypertension syndrome (PIH) is a common pregnancy syndrome that could cause varying degrees of maternal and fetal organic damage and even endanger their lives. This study aimed to investigate ultrasound of fetal cardiac function changes in PIH. Totally 40 cases of gestational hypertension admitted to Cangzhou Central Hospital between October 2018 and September 2019 were enrolled in the hypertension group, and 40 women with healthy pregnancies during the same period were assigned to the normal group. Ultrasound results showed that PIH was associated with a significantly higher fetal cardiac septal thickness, fetal left ventricular end-diastolic area and end-systolic area, fetal right ventricular end-diastolic area and end-systolic area, fetal left ventricular systolic fraction 1 (VSF1), fetal left ventricular systolic fraction 2 (VSF2), fetal right VSF1, and fetal right VSF2 versus healthy pregnancy. The PIH fetuses had significantly lower neonatal weights versus healthy fetuses. Newborns of hypertensive pregnancies have larger hearts, faster heart rates, increased cardiac contractility, and lower weights versus newborns of healthy pregnancies.

Abstract 12327: Intravenous Waveform Analysis Correlates With Volume Status in Resuscitation in In-Vivo Rat Model

Introduction: Current volume status markers under-perform. Dynamic markers demonstrate improved outcomes in goal directed fluid therapy but maintain validity in a narrow range of clinical parameters. In addition, they assess volume responsiveness over total volume status. Repeated echo assessments may be infeasible. Hypothesis: Intravenous waveform analysis-derived F1 more closely models volume status than current markers in a rat resuscitation model. Methods: Seven Sprague Dawley rats were anesthetized and mechanically ventilated. Pressure transductions occurred via cannulation of the right femoral vein, left femoral artery and right internal jugular vein. Hemorrhage and resuscitation occurred via the left femoral vein. Heparinized rats were bled to 80% of the estimated blood volume (EBV) then resuscitated with their own whole blood in increments of 2% of the EBV until euvolemia was reached. Cardiac output (CO) and left ventricular end diastolic area (LVEDA) were calculated with echocardiography. Fast Fourier transform was performed on venous waveforms to obtain the heart rate linked F1 amplitude. Pearson’s correlation coefficients were compared using Fisher’s Z transformation. Mixed effects modeling goodness-of-fit was assessed with Akaike information criterion (AIC). Significance was set at p=.05. Results: F1 had the strongest correlation with volume status, r= .70, followed by CO, r=.55, LVEDA, r=.55, mean arterial pressure (MAP), r=.50, central venous pressure r= -.02, and pulse pressure variation (PPV), r=.01. When compared, F1 rho was significantly greater than that of all variables except CO and LVEDA, p=.09 and p=.07, respectively. In mixed effects regression, F1 displayed the most significant AIC, -274, followed by CO at -239. Conclusions: The novel marker F1 is strongly correlated with volume status during whole blood resuscitation. F1 may be superior to current markers for directing volume resuscitation therapy.

Abstract 9439: Invasive Evaluation of Left Ventricular Hemodynamics with Veno-Arterial Extracorporeal Membrane Oxygenation

Introduction: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a frequently used hemodynamic support strategy, but considerable debate exists about its hemodynamic effects. We evaluated changes in left ventricular (LV) function, volumes, and work in patients treated with VA-ECMO using invasive LV catheterization and three-dimensional echocardiographic volumes. Methods: In this case series, patients underwent evaluation due to persistent vasoplegia or poor LV function despite treatment with VA-ECMO. Hemodynamic parameters were reported as medians with interquartile ranges. Paired comparisons were done to evaluate hemodynamics at the baseline (highest) and lowest tolerated levels of VA-ECMO support. Results: Six patients aged 53.5 (41.8, 57.8) years were included. Three patients received VA-ECMO for refractory cardiogenic shock and three patients for extracorporeal cardiopulmonary resuscitation. The baseline LV ejection fraction was 22.1% (19.0%, 24.7%). The baseline and lowest VA-ECMO flows were 4.0 (4.0, 4.0) L/min and 1.0 (1.0, 1.5) L/min, respectively. Compared to the lowest flow, full VA-ECMO support reduced LV end-diastolic volume [116 (90, 153) versus 94 (58, 119) mL, p=0.03], LV end-diastolic pressure [16 (12, 24) versus 14 (9,15) mmHg, p=0.03], LV stroke work [2640 (1800, 4275) versus 1953 (759, 2179) mL*mmHg, p=0.03], and pressure-volume area [6864 (4038, 7715) versus 4575 (3142, 5888) mL*mmHg; p=0.046], respectively. The pressure-volume curves at the highest and lowest VA-ECMO flows are represented in blue and red, respectively ( Figure ). Mean arterial pressure and heart rate were similar at the lowest and highest flows (p=0.17 and p=0.60, respectively). All patients were decannulated from VA-ECMO. Four survived the index hospitalization. Conclusion: High flow VA-ECMO support significantly reduced LV end-diastolic volume, end-diastolic pressure, stroke work, and pressure-volume area compared to low flow.

Abstract 9008: Echocardiographic Markers in Early Postnatal Life to Predict Intervention in Coarctation of Aorta

Background: Coarctation of the aorta (CoA) is challenging to diagnose in the early neonatal life due to the patent ductus arteriosus (PDA). We aimed to describe the resource utilization, early post-natal cardiac profile and predictors for need of cardiac surgery. Methods: Retrospective study of infants with an antenatal suspicion of CoA, without major associated cardiac anomalies, born at ≥37 weeks during 2014 to 2020. The analyzed echocardiography (ECHO) was performed within 48 hours after birth. Those not requiring post-natal intervention (normal group) were compared to those that required post-natal cardiac surgery (CoA). Strain was measured using speckle-tracking ECHO (STE). Results: A total of 51 newborns were included, of which 40 (78%) were normal and 11 (22%) underwent intervention. In the normal group, median hospitalization was 4 [2-6] days, 6 (15%) were exposed to prostaglandin E (PGE) infusion, 38 (95%) were on intravenous fluids, 9 (23%) required gavage and age at full feeds was 3 days (IQR: 2-5). Ductus was patent in all newborns and aortic arch measurements were significantly smaller in the CoA (ascending [p=0.01], proximal, distal, isthmus [ p &lt;0.001]). Right ventricular (RV) predominance was higher in the CoA group, as demonstrated by the left ventricular (LV) end-systolic eccentricity index (EI) (1.60 [0.28] vs 2.16 [0.45]; p &lt;0.001) and by a larger end-diastolic area (EDA) of the RV in apical 4 chamber (A4C) relative to the LV-EDA - with a ratio of 1.02 [0.2] vs 1.56 [0.23]; p &lt;0.001. Isthmus and EI were predictive for intervention (OR 26, 95%CI (-42 to -9); p =0.002, OR 4.5, 95%CI (1.5-7.5); p =0.003). A RV to LV EDA ratio in A4C greater than 1.3 demonstrated a high probability for intervention (AUC = 0.97). CoA newborns had a lower RV deformation by STE (peak systolic strain rate (SR); -0.98 [0.17] vs -0.83 [0.2]; p =0.02, early diastolic SR; 1.05 [0.2] vs 0.85 [0.26]; p =0.01). Conclusions: Most infants with antenatal suspicion of CoA did not require intervention but were high consumers of resources. Despite PDA patency, isthmus and RV predominance on first post-natal ECHO were predictors for surgery. The novel markers of strain by STE and ventricular EDA ratio in A4C may help predicting those with true CoA requiring intervention.

Right ventricular improvement is associated with left ventricular diastolic function and size enhancement in PAH patients: an echocardiographic study

Abstract Background While pulmonary vasodilation therapy improves right ventricular (RV) function in pulmonary arterial hypertension (PAH), data regarding left ventricular (LV) function remain sparse. Purpose We aimed to investigate whether PAH therapy improve LV function in PAH patients. Methods Between 2002 and 2020, all incident PAH patients from one PH referral centers were included, treated and followed-up according to current ESC/ERS guidelines. All patients had comprehensive echocardiography both investigating right and left ventricular function before and after 1-year of vasodilation therapy. In addition to RV echocardiographic evaluation, we focused on LV ejection fraction from Modified Simpson method, LV diameters by M-mode, transmitral pulsed-wave E/A ratio, Flow to tissue Doppler imaging E/e' ratio, and left atrial size. Results 126 patients were included (63% female, 57±17 yo), mainly from connectivite tissue associated and idiopathic PAH (24% and 28% respectively) causes. Compared to baseline, 1-year NYHA functional class (p&amp;lt;0.01), NTproBNP plasma level (p&amp;lt;0.001), invasive mean pulmonary arterial pressure (p&amp;lt;0.01) and cardiac index (p&amp;lt;0.01) significantly improved. While LV ejection fraction (p=0.68), LV end-diastolic diameter (p=0.11) as well as LA area and volume (p=0.09) were not significantly enhanced under vasodilation therapy, LV diastolic function, assessed by mitral E wave (p&amp;lt;0.01), tissue doppler imaging mitral e' wave (p=0.04), and E/A ratio (p=0.045) were significantly improved at 1-year. There was a significant correlation between LV end-diastolic diameter (p&amp;lt;0.001) and RV end-diastolic area (p&amp;lt;0.001) owing to the normalization of right- to left ventricular interdependence, as well as between mitral E wave and TAPSE (p=0.045). Conclusion By improving RV function, PAH vasodilation therapy enhances LV size and diastolic function and normalizes the biventricular interdependence. Funding Acknowledgement Type of funding sources: None.

Echocardiographic assessment of dilated cardiomyopathy in dogs

Dilated cardiomyopathy (DCM) is a frequent cause of cardiac disability, congestive heart failure (CHF), and arrhythmic death in dogs. The etiology of DCM is usually idiopathic/genetic, but some causes of a DCM phenotype are reversible. The disease is classified into preclinical (occult) and clinical (overt) stages; the latter stems from heart failure with reduced ejection fraction. DCM is further characterized by clinical, electrocardiographic, circulating biomarker, and imaging abnormalities. The diagnosis of clinical DCM with CHF is straightforward; however, identification of the preclinical stage can be challenging. Echocardiography is central to the diagnosis of both stages and characterized by left ventricular (LV) systolic dysfunction with progressive chamber dilation and variable enlargements of the left atrium and right-sided chambers. Left ventricular dilation is defined by increased LV end-diastolic volumes, areas, and internal dimensions normalized to body size or indexed to the aorta. Systolic dysfunction is characterized by decreased LV ejection fraction, increased end-systolic volume, and reduced shortening across minor and longitudinal LV axes. Dyssynchrony can confound the interpretation of linear indices of systolic function. A comprehensive echocardiogram in DCM includes two-dimensional and M-mode studies, spectral and tissue Doppler imaging, and potentially three-dimensional echocardiography and myocardial strain imaging. Echocardiographic findings should be interpreted within the context of identifiable risks and comorbidities, physical diagnosis, complementary diagnostic testing, and limitations of current reference intervals. Ambiguous examinations should be repeated. Specific echocardiographic criteria for the diagnosis of DCM are proposed to encourage discussion and additional outcome and breed-specific echocardiographic studies of canine DCM.

The impact of fluid status and decremental PEEP strategy on cardiac function and lung and kidney damage in mild-moderate experimental acute respiratory distress syndrome

BackgroundWe evaluated the effects of abrupt versus gradual PEEP decrease, combined with standard versus high-volume fluid administration, on cardiac function, as well as lung and kidney damage in an established model of mild-moderate acute respiratory distress syndrome (ARDS).MethodsWistar rats received endotoxin intratracheally. After 24 h, they were treated with Ringer’s lactate at standard (10 mL/kg/h) or high (30 mL/kg/h) dose. For 30 min, all animals were mechanically ventilated with tidal volume = 6 mL/kg and PEEP = 9 cmH2O (to keep alveoli open), then randomized to undergo abrupt or gradual (0.2 cmH2O/min for 30 min) PEEP decrease from 9 to 3 cmH2O. Animals were then further ventilated for 10 min at PEEP = 3 cmH2O, euthanized, and their lungs and kidneys removed for molecular biology analysis.ResultsAt the end of the experiment, left and right ventricular end-diastolic areas were greater in animals treated with high compared to standard fluid administration, regardless of PEEP decrease rate. However, pulmonary arterial pressure, indicated by the pulmonary acceleration time (PAT)/pulmonary ejection time (PET) ratio, was higher in abrupt compared to gradual PEEP decrease, independent of fluid status. Animals treated with high fluids and abrupt PEEP decrease exhibited greater diffuse alveolar damage and higher expression of interleukin-6 (a pro-inflammatory marker) and vascular endothelial growth factor (a marker of endothelial cell damage) compared to the other groups. The combination of standard fluid administration and gradual PEEP decrease increased zonula occludens-1 expression, suggesting epithelial cell preservation. Expression of club cell-16 protein, an alveolar epithelial cell damage marker, was higher in abrupt compared to gradual PEEP decrease groups, regardless of fluid status. Acute kidney injury score and gene expression of kidney injury molecule-1 were higher in the high versus standard fluid administration groups, regardless of PEEP decrease rate.ConclusionIn the ARDS model used herein, decreasing PEEP abruptly increased pulmonary arterial hypertension, independent of fluid status. The combination of abrupt PEEP decrease and high fluid administration led to greater lung and kidney damage. This information adds to the growing body of evidence that supports gradual transitioning of ventilatory patterns and warrants directing additional investigative effort into vascular and deflation issues that impact lung protection.

Prevalence and prognostic value of various types of right ventricular dysfunction in mechanically ventilated septic patients

IntroductionRight ventricle (RV) dilation in combination with elevated central venous pressure (CVP), which is a state of RV congestion, is seen as a sign of RV failure (RVF). On the other hand, RV systolic function is usually assessed by tricuspid annular plane systolic excursion (TAPSE) and fractional area change (FAC). This study aimed to investigate the prevalence and prognostic value of RVF and RV systolic dysfunction (RVSD) in septic patients.MethodsMechanically ventilated sepsis and septic shock patients were included. We collected haemodynamic and echocardiographic parameters as well as prognostic information including mechanical ventilation duration, length of ICU stay and 30-day mortality. RVF was defined as a right and left ventricular end-diastolic area ratio ≥ 0.6 in combination with CVP ≥ 8 mmHg. RVSD was defined as TAPSE < 16 mm or FAC < 35%.ResultsA total of 215 patients were enrolled in this study, and the patients were divided into 4 groups: patients with normal RV function (normal, n = 101), patients with RVF but without RVSD (RVF only, n = 38), patients with RVSD but without RVF (RVSD only, n = 44), and patients with combined RVF–RVSD (RVF/RVSD, n = 32). The RVF/RVSD group and RVSD only group had a lower cardiac index than the RVF only group and normal groups (p < 0.05). At 30 days after ICU admission, 50.0% of patients had died in the RVF/RVSD group, which was much higher than the mortality in the RVF only group (13.2%) and normal group (13.9%) (p < 0.05). In a Cox regression analysis, the presence of RVF/RVSD was independently associated with 30-day mortality (HR 3.004, 95% CI:1.370–6.587, p = 0.006). In contrast, neither the presence of RVF only nor the presence of RVSD only was associated with 30-day mortality (HR 0.951, 95% CI:0.305–2.960, p = 0.931; HR 1.912, 95% CI:0.853–4.287, p = 0.116, respectively).ConclusionThe presence of combined RVF–RVSD was associated with 30-day mortality in mechanically ventilated septic patients. Additional studies are needed to confirm and expand this finding.

Right Ventricular Dysfunction and Its Association With Mortality in Coronavirus Disease 2019 Acute Respiratory Distress Syndrome.

To assess whether right ventricular dilation or systolic impairment is associated with mortality and/or disease severity in invasively ventilated patients with coronavirus disease 2019 acute respiratory distress syndrome. Retrospective cohort study. Single-center U.K. ICU. Patients with coronavirus disease 2019 acute respiratory distress syndrome undergoing invasive mechanical ventilation that received a transthoracic echocardiogram between March and December 2020. None. Right ventricular dilation was defined as right ventricular:left ventricular end-diastolic area greater than 0.6, right ventricular systolic impairment as fractional area change less than 35%, or tricuspid annular plane systolic excursion less than 17 mm. One hundred seventy-two patients were included, 59 years old (interquartile range, 49-67), with mostly moderate acute respiratory distress syndrome (n = 101; 59%). Ninety-day mortality was 41% (n = 70): 49% in patients with right ventricular dilation, 53% in right ventricular systolic impairment, and 72% in right ventricular dilation with systolic impairment. The right ventricular dilation with systolic impairment phenotype was independently associated with mortality (odds ratio, 3.11 [95% CI, 1.15-7.60]), but either disease state alone was not. Right ventricular fractional area change correlated with Pao2:Fio2 ratio, Paco2, chest radiograph opacification, and dynamic compliance, whereas right ventricular:left ventricle end-diastolic area correlated negatively with urine output. Right ventricular systolic impairment correlated with pulmonary pathophysiology, whereas right ventricular dilation correlated with renal dysfunction. Right ventricular dilation with systolic impairment was the only right ventricular phenotype that was independently associated with mortality.

Combination of Static Echocardiographic Indices for the Prediction of Fluid Responsiveness in Patients Undergoing Coronary Surgery: A Pilot Study.

We investigated the role of echocardiographic indices consisting of left ventricular end-diastolic area (LVEDA) in combination with Doppler-derived surrogates of diastolic compliance and filling (E/E′, E′/S′, E′/A′; early transmitral flow velocity (E), tissue Doppler-derived early (E′) diastolic, late (A′) diastolic, or peak systolic (S′) velocity of the mitral annulus) in predicting fluid responsiveness in off-pump coronary surgery. Hemodynamic and echocardiographic variables were prospectively assessed under general anesthesia before and after a fluid challenge of 6 mL/kg during apnea at atmospheric pressure in 64 patients with LV ejection fraction ≥40%. Forty patients (63%) were fluid responders (≥15% increase in stroke volume index). E/E′ and E′/S′ could predict fluid responsiveness with area under the receiver operating characteristic curve (AUROC) of 0.71 (95% confidence interval [CI], 0.56–0.85; p = 0.006) and 0.68 (95% CI, 0.54–0.82; p = 0.017), respectively. The combination of LVEDA and E/E′ showed incremental predictive ability for fluid responsiveness compared with LVEDA (AUROC, 0.60; p = 0.170) or pulse pressure variation (AUROC, 0.70; p = 0.002), yielding the highest AUROC of 0.78 (95% CI, 0.66–0.90; p < 0.001). The combined index of echocardiographic variables reflecting LV dimension (LVEDA) and diastolic compliance and filling (E/E′) is a potentially useful predictor of fluid responsiveness.

Intravascular volume assessment using internal jugular vein ultrasonography in pediatric renal transplant surgery: a prospective observational study

Purpose Assessment of the intravascular volume status during surgery is challenging, especially in pediatric patients. Ultrasound has become a versatile noninvasive modality for assessing volume status. This study aimed to evaluate the reliability of ultrasonographic internal jugular vein (IJV) dimensions as a new tool to assess the intravascular volume status in pediatric patients undergoing living donor renal transplant surgery. Patients and methods This prospective observational study included pediatric renal transplant recipients, aged 3–12 years, weighing more than 10 kg, and having an end-stage renal disease. Hemodynamic data (heart rate, systolic, diastolic, and mean blood pressures), central venous pressure (CVP), sonographic measurement of IJV (diameter and cross-sectional area), and left ventricular end-diastolic area (LVEDA) were measured 1 min after induction, before clamping of renal vessels, and after declamping of renal vessels. The correlations between the ultrasonographic IJV dimensions and both LVEDA (primary outcome) and CVP were evaluated. Results Overall, 18 pediatric patients (12 females, six males) with end-stage renal disease were eligible for this study. The mean age was 9.33±2.57 years, and the mean weight was 21.67±5.99 kg. There was a poor correlation between IJV dimensions (diameter and cross-sectional area) and both LVEDA and CVP at the three-time points of assessments. Conclusion Ultrasonographic IJV dimensions (diameter and cross-sectional area) were not reliable for assessing intravascular volume status in living donor renal transplant surgery in pediatric patients.