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Introduction and Objectives: The role of N-terminal pro-B-type natriuretic peptide (NT-proBNP) in the risk prediction of patients with systemic right ventricles (sRV) is not well defined. The aim of this study was to analyze the prognostic value of NT-proBNP in patients with an sRV., Methods: The prognostic value of NT-proBNP was assessed in 98 patients from the SERVE trial. We used an adjusted Cox proportional hazards model, survival analysis, and c-statistics. The composite primary outcome was the occurrence of clinically relevant arrhythmia, heart failure, or death. Correlations between baseline NT-proBNP values and biventricular volumes and function were assessed by adjusted linear regression models., Results: The median age [interquartile range] at baseline was 39 [32-48] years and 32% were women. The median NT-proBNP was 238 [137-429] ng/L. Baseline NT-proBNP concentrations were significantly higher among the 20 (20%) patients developing the combined primary outcome compared with those who did not (816 [194-1094] vs 205 [122-357]; P=.003). In patients with NT-proBNP concentrations> 75th percentile (> 429 ng/L), we found an exponential increase in the sex- and age-adjusted hazard ratio for the primary outcome. The prognostic value of NT-proBNP was comparable to right ventricular ejection fraction and peak oxygen uptake on exercise testing (c-statistic: 0.71, 0.72, and 0.71, respectively)., Conclusions: In patients with sRVs, NT-proBNP concentrations correlate with sRV volumes and function and may serve as a simple tool for predicting adverse outcomes., (Copyright © 2024 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.)

Background: Pulmonary arterial hypertension (PAH) is a disease of progressive right ventricular (RV) failure with high morbidity and mortality. Our goal is to investigate proteomic features and pathways associated with RV-focused outcomes including mortality, RV dilation, and NT-proBNP (N-terminal pro-B-type natriuretic peptide) in PAH., Methods: Participants in a single-institution cohort with 3 years of follow-up underwent proteomic profiling of their plasma using 7288 aptamers (targeting 6467 unique human proteins). Partial least squares discriminant analysis was performed to assess global protein variation associated with mortality, RV dilation, and NT-proBNP levels. Differentially abundant proteins and enriched pathways associated with outcomes were identified following baseline adjustments. RV vulnerability models estimated associations for individuals with similar afterload following adjustment for pulmonary vascular resistance., Results: A total of 117 participants with PAH were included. Partial least squares discriminant analysis of the proteome showed clear separation between survivors and nonsurvivors, participants with dilated versus nondilated RVs, and across NT-proBNP levels. Proteins and pathways involving the ECM (extracellular matrix) were upregulated in participants who died during follow-up, those with severe RV dilation, and those with higher levels of NT-proBNP. Pulmonary vascular resistance adjustment reinforced the importance of ECM proteins in the association with RV vulnerability, independent of afterload. These findings were confirmed in independent PAH cohorts with available plasma proteomics and RV tissue gene and protein expression., Conclusions: Distinct plasma proteomic profiles are associated with mortality, RV dilation, and NT-proBNP in PAH. Proteins and pathways governing tissue remodeling are strongly associated with poor outcomes, may mediate RV vulnerability to right heart failure, and represent promising candidates as biomarkers and potential therapeutic targets., Competing Interests: Drs Pi, Suresh, Hemnes, Bravo, Rayner, Shojaie, Leary, and Gharib have received research funding from the National Institutes of Health. Dr Hemnes has done consulting work for GossamerBio, United Therapeutics, Janssen, Merck, and Tenax Therapeutics. She is a stockholder (negligible value) in Tenax Therapeutics. Dr Rayner received research funding from Bayer Pharmaceuticals and United Therapeutics. Dr Leary has received grants and research support from the CHEST Foundation, the American Heart Association, Bayer, Janssen, and Acceleron/Merck. He has been a grant review consultant for Bayer and has adjudicated clinical end points for Sumitomo Pharma. He is on the scientific leadership council for the Pulmonary Hypertension Association and the medical advisory board for Team PHenomenal Hope. The other authors report no conflicts.

Background: In pulmonary hypertension (PH), the identification of easily obtainable prognostic markers associated with right ventricular (RV) dysfunction and survival is needed., Objective: To evaluate the association of red cell distribution width (RDW) with clinical, echocardiographic parameters and survival in patients with pre-capillary PH, with the development of a mortality prediction model., Methods: Observational, longitudinal, and prospective study conducted from May 2019 to December 2022. Thirty-four patients with pre-capillary PH underwent two-dimensional echocardiography and complete blood count. A cutoff point of 14.5% was considered to define RDW as altered (≥14.5%) or normal (<14.5%). P values <0.05 were considered significant., Results: The median RDW was 14.4%. There was a significant difference in peripheral arterial oxygen saturation (SpO2) (p=0.028), RV strain (p=0.047), and pericardial effusion (p=0.002) between the normal and elevated RDW groups. During a median follow-up of 15 months, 20.6% died. Patients with increased RDW had a shorter overall survival (44.7%, log-rank p=0.019), which was a predictor of mortality in univariate Cox regression (HR 8.55, p=0.048). The addition of RV strain <16% and SpO2 ≤93% to the model including RDW alone showed incremental value in predicting mortality (χ2=8.2, p=0.049; χ2=12.4, p=0.041), with increased area under the receiver operating characteristic curve (0.729 vs. 0.837 vs. 0.909) and decreased probability of survival (44.7% vs. 35.6% vs. 25%, log-rank p=0.019)., Conclusions: RDW provides information on the severity of pre-capillary PH by correlating with echocardiographic parameters of RV dysfunction and mortality, which is best predicted by a model including RDW, RV strain and SpO2.

Background: Adults with a systemic right ventricle (sRV) are at a high risk for heart failure (HF) hospitalization and mortality. Bioactive adrenomedullin (bio-ADM) has been proposed as a marker of congestion and prognosis in patients with cardiovascular disease. We aimed to evaluate the association between bio-ADM and mortality and HF events in sRV patients., Methods: Plasma bio-ADM was measured by a novel immunoassay in plasma of 85 sRV patients. A composite endpoint of all-cause mortality and HF events was used as outcome. HF events were defined as onset or progression of HF signs or symptoms requiring hospitalization, initiation or intensification of therapy. Multivariable Cox regression analyses were performed to evaluate the association between bio-ADM and outcome., Results: The mean age of the patients was 37 ± 9 years and 65% were male. Patients with higher plasma bio-ADM concentrations were more often treated with diuretics (p = 0.007), possibly because of signs and/or symptoms of congestion. During a median follow-up of 10.2 years, 33.7% of the patients reached the endpoint. After adjustment for age and N-terminal pro B-type natriuretic peptide (NT-pro BNP), higher bio-ADM levels were associated with a higher risk of the composite endpoint (hazard ratio: 2.09 [95%-confidence interval: 1.15-3.78]). Bio-ADM improved risk prediction when added to NT-proBNP and age (C-statistic improved from 0.748 to 0.776 [p = 0.03])., Conclusions: Bio-ADM can be considered as a marker of congestion and independent predictor of death and HF events in adult patients with a sRV. Moreover, in terms of risk prediction, it has added value to NT-proBNP., Competing Interests: Declaration of competing interest The authors report no relationships that could be construed as a conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Objectives: Electrocardiogram (ECG) and measurement of plasma brain natriuretic peptides (BNP) are established markers of right ventricular dysfunction (RVD) in the setting of acute pulmonary embolism (PE) but their value at long-term follow-up is largely unknown. The purpose of this prospective study was to determine the prevalence of ECG abnormalities, describe levels of N-terminal proBNP (NT-proBNP), and establish their association with dyspnea at long-term follow-up after PE., Design: All Swedish patients diagnosed with acute PE in 2005 ( n  = 5793) were identified through the Swedish National Patient Registry. Surviving patients in 2007 ( n  = 3510) were invited to participate. Of these, 2105 subjects responded to a questionnaire about dyspnea and comorbidities. Subjects with dyspnea or risk factors for development of chronic thromboembolic pulmonary hypertension were included in the study in a secondary step, which involved collection of blood samples and ECG registration., Results: Altogether 49.3% had a completely normal ECG. The remaining participants had a variety of abnormalities, 7.2% had atrial fibrillation/flutter (AF). ECG with any sign of RVD was found in 7.2% of subjects. Right bundle branch block was the most common RVD sign with a prevalence of 6.4%. An abnormal ECG was associated with dyspnea. AF was associated with dyspnea, whereas ECG signs of RVD were not. 61.2% of subjects had NT-proBNP levels above clinical cut-off (>125 ng/L). The degree of dyspnea did not associate independently with NT-proBNP levels., Conclusions: We conclude that the value of ECG and NT-proBNP in long term follow-up after PE lies mostly in differential diagnostics.

Background: Right ventricle (RV) dysfunction increases the risk of death from pulmonary embolism (PE). C-reactive protein (CRP) might identify RV inflammation and dysfunction in patients with PE., Methods: This cohort study enrolled consecutive stable patients with acute PE between 2017 and 2023. We stratified patients by quartiles of CRP. We evaluated the association between CRP quartiles and the presence of RV dysfunction, and used multivariable models to assess for an association between CRP and the outcomes of all-cause and PE-specific mortality during the 30 days of follow-up after PE diagnosis., Results: The study included 633 stable patients with PE. Patients without RV dysfunction had significantly lower median (IQR) CRP levels compared with patients with RV dysfunction (n=509, 31.7 [10.0-76.4]mg/L vs n=124, 45.4 [16.0-111.4]mg/L; P=0.018). CRP showed a statistically significant positive association with the presence of RV dysfunction (P<0.01). On multivariable analysis, CRP level was not significantly associated with 30-day all-cause mortality (adjusted odds ratio [OR] per mg/L increment, 1.00; 95% CI, 1.00-1.01; P=0.095), but higher CRP was associated with significantly higher PE-related mortality (adjusted OR, 1.01; 95% CI, 1.00-1.01; P=0.026). Compared with patients in CRP quartile 1, patients in quartiles 2, 3, and 4 had a stepwise increase in the adjusted odds of 30-day all-cause death of 2.41 (P=0.148), 3.04 (P=0.062), and 3.15 (P=0.052), respectively., Conclusions: As an indicator of RV dysfunction, CRP may improve risk stratification algorithms for hemodynamically stable patients with acute symptomatic PE., (Copyright © 2024 SEPAR. Published by Elsevier España, S.L.U. All rights reserved.)

Aims: Regulation of the renin-angiotensin system (RAS) in heart failure (HF) with reduced ejection fraction (HFrEF) still raises questions, as a large proportion of patients show normal renin levels despite manifest disease. Experimental venous congestion results in reduced renal perfusion pressure and stimulates renin secretion. We hypothesized that excess renin levels are mainly a result of right ventricular failure as a sequalae of left ventricular dysfunction. The study aimed to link right ventricular function (RVF) with renin levels and to investigate further contributors to excess RAS activation., Methods and Results: Three hundred thirty-two chronic HFrEF patients undergoing routine ambulatory care were consecutively enrolled in a prospective, registry-based, observational study. Laboratory parameters, including cardiac-specific markers renin, aldosterone, and N-terminal pro-brain natriuretic peptide (NT-proBNP), echocardiographic examination (n = 247), and right heart catheterization (n = 85), were documented. The relationship between renin and its respective parameters was analysed. Renin concentration was not associated with the New York Heart Association class or NT-proBNP. Systolic blood pressure, systemic vascular resistance, serum sodium, aldosterone, and lactate dehydrogenase were associated with increased renin levels (P < 0.035 for all). Renin levels similarly increased with worsening of RVF parameters such as fractional area change, tricuspid annular plane systolic excursion, tissue Doppler imaging, and inferior vena cava diameter (P < 0.011 for all), but not with pulmonary pressure. Excess renin levels were observed when worsening RVF was combined with reduced renal perfusion {625 μIU/mL [interquartile range (IQR): 182-1761] vs. 67 μIU/mL [IQR: 16-231], P < 0.001}, which was associated with worse survival., Conclusions: While unrelated to classical indices of HF severity, circulating renin levels increase with the worsening of RVF, especially in the combined presence of forward and backward failure. This might explain normal renin levels in HFrEF patients but also excess renin levels in poor haemodynamic conditions., (© 2024 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Background: The determinants and prognostic value of high-sensitivity cardiac troponin T (hs-cTnT) among patients with a systemic right ventricle are largely unknown., Methods and Results: Ninety-eight patients from the randomized controlled SERVE (Effect of Phosphodiesterase-5 Inhibition With Tadalafil on Systemic Right Ventricular Size and Function) trial were included. The correlation between baseline hs-cTnT concentrations and biventricular volumes and function quantified by cardiac magnetic resonance or cardiac multirow detector computed tomography was assessed by adjusted linear regression models. The prognostic value of hs-cTnT was assessed by adjusted Cox proportional hazards models, survival analysis, and concordance statistics. The primary outcome was time to the composite of clinically relevant arrhythmia, hospitalization for heart failure, or all-cause death. Median age was 39 (interquartile range, 32-48) years, and 32% were women. Median hs-cTnT concentration was 7 (interquartile range, 4-11) ng/L. Coefficients of determination for the relationship between hs-cTnT concentrations and right ventricular end-systolic volume index and right ventricular ejection fraction (RVEF) were +0.368 ( P =0.046) and -0.381 ( P =0.018), respectively. The sex- and age-adjusted hazard ratio for the primary outcome of hs-cTnT at 2 and 4 times the reference level (5 ng/L) were 2.89 (95% CI, 1.14-7.29) and 4.42 (95% CI, 1.21-16.15), respectively. The prognostic performance quantified by the concordance statistics for age- and sex-adjusted models based on hs-cTnT, right ventricular ejection fraction, and peak oxygen uptake predicted were comparable: 0.71% (95% CI, 0.61-0.82), 0.72% (95% CI, 0.59-0.84), and 0.71% (95% CI, 0.59-0.83), respectively., Conclusions: Hs-cTnT concentration was significantly correlated with right ventricular ejection fraction and right ventricular end-systolic volume index in patients with a systemic right ventricle. The prognostic accuracy of hs-cTnT was comparable to that of right ventricular ejection fraction and peak oxygen uptake predicted., Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03049540.

Aim: This study assessed the utility of osteopontin (OPN) and galectin-3 (Gal-3) as biomarkers of maladaptive right ventricular remodeling in pulmonary hypertension (PH). Materials & methods: We examined plasma levels of OPN and Gal-3 in patients with PH (n = 62), dilated cardiomyopathy (n = 34), left ventricular hypertrophy (LVH; n = 47), and controls without right ventricle (RV) or LV abnormalities (n = 38). Results: OPN and Gal-3 levels were higher in PH, dilated cardiomyopathy and LVH than in the controls. OPN concentrations in PH patients with maladaptive RV were significantly higher than in those with adaptive RV. Gal-3 did not differentiate between adaptive and maladaptive RV remodeling in PH. OPN and Gal-3 levels did not correlate with parameters of LV remodeling. Conclusion: OPN is a potential biomarker of RV maladaptation.

COVID-19 has rapidly spread around the world and threatened global health. Although this disease mainly affects the respiratory system, there is increasing evidence that SARS-CoV-2 also has effects on the cardiovascular system. Echocardiography is a valuable tool in the assessment of cardiovascular disease. It is cost-effective, widely available and provides information that can influence management. Given the risk of personnel infection and equipment contamination during echocardiography, leading world societies have recommended performing echocardiography only when a clinical benefit is likely, favouring focussed evaluations and using smaller portable equipment. In the past months, multiple reports have described a wide pattern of echocardiographic abnormalities in patients with COVID-19. This review summarises these findings and discusses the possible mechanisms involved., (Copyright © 2021 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Background: Right ventricular dysfunction after CABG is associated with poor peri- and postoperative outcomes. We aimed to identify clinical and experimental predictors for preoperative inapparent right ventricular dysfunction and therefore hypothesized that reduced myofilament force development as well as altered levels of biomarkers might predict inapparent right ventricular dysfunction., Methods: From 08/2016 to 02/2018, 218 patients scheduled for CABG were divided into two groups (TAPSE ≥ 20 mm, n = 178; TAPSE < 20 mm, n = 40). Baseline serum samples for biomarkers (Galectin, TGFß1, N Acyl-SDMA, Arginine, ADMA and Pentraxin-3), clinical laboratory and transthoracic echocardiographic parameters were evaluated. To examine the myocardial apparatus of the right ventricle intraoperative right auricular tissue was harvested for stepwise skinned fiber force measurements., Results: Patients with TAPSE < 20 mm had a higher incidence of DM (55 vs. 34%, p = 0.018), preoperative AFib (43 vs. 16%, p < 0.001), reduced GFR (67 ± 18 vs. 77 ± 24 ml/min/1.73 m 2 , p = 0.013), larger LA area (22 ± 6 vs. 20 ± 5 cm 2 , p = 0.005) and reduced LVEF (50 vs. 55%, p = 0.008). Furthermore, higher serum ADMA (0.70 ± 0.13 vs. 0.65 ± 0.15 µmol/l, p = 0.046) and higher serum Pentraxin-3 levels (3371 ± 1068 vs. 2681 ± 1353 pg/dl, p = 0.004) were observed in these patients. Skinned fiber force measurements showed significant lower values at almost every step of calcium concentration (pCa 4.52 to pCa 5.5, p < 0.01 and pCa 5.75-6.0, p < 0.05). Multivariable analysis revealed DM (OR 2.53, CI 1.12-5.73, Euro Score II (OR 1.34, CI 1.02-1.78), preoperative AF (OR 4.86, CI 2.06-11.47), GFR (OR 7.72, CI 1.87-31.96), albumin (OR 1.56, CI 0.52-2.60), Pentraxin-3 (OR 19.68, CI 14.13-25.24), depressed LVEF (OR 8.61, CI 6.37-10.86), lower force values: (pCa 5.4; OR 2.34, CI 0.40-4.29 and pCa 5.2; OR 2.00, CI 0.39-3.60) as predictors for clinical inapparent right heart dysfunction., Conclusions: These preliminary data showed that inapparent right heart dysfunction in CAD is already associated with reduced force development of the contractile apparatus.

The relationship between inflammation and venous thrombosis is not well understood. An inflammatory response may be both the cause and consequence of venous thromboembolism (VTE). In fact, several risk factors of VTE modulate thrombosis through inflammatory markers. Acute pulmonary embolism (PE) is burdened by a remarkable mortality rate, up to 34% in severely ill patients presenting with hemodynamic instability. Initial mortality risk stratification is based on hemodynamic instability. Patients with a situation of hemodynamic stability require immediate further risk assessment based on clinical, imaging, and circulating biomarkers, as well as the presence of comorbidities. Some inflammatory biomarkers have shown potential usefulness in the risk stratification of patients with VTE, especially acute PE. C-reactive protein on admission is associated with 30-day mortality and bleeding in VTE patients. P-selectin is associated with right ventricle dysfunction in PE patients and might be associated with VTE recurrences and the extension of thrombosis. Tissue factor microparticles are associated with VTE recurrence in cancer-associated thrombosis. Other inflammatory biomarkers present scarce evidence (inflammatory cytokines, erythrocyte sedimentation rate, fibrinogen, leukocyte count). In this manuscript, we will review the prognostic role of different inflammatory biomarkers available both for clinical practice and research in VTE patients.

Sickle cell disease (SCD) is an inherited hemolytic disorder, defined by a point mutation in the β-globin gene. Stress conditions such as infection, inflammation, dehydration, and hypoxia trigger erythrocyte sickling. Sickled red blood cells (RBCs) hemolyze more rapidly, show impaired deformability, and increased adhesive properties to the endothelium. In a proinflammatory, pro-coagulative environment with preexisting endothelial dysfunction, sickled RBCs promote vascular occlusion. Hepatobiliary involvement related to the sickling process, such as an acute sickle hepatic crisis, is observed in about 10% of acute sickle cell crisis incidents. In mice, ligation of CD40 with an agonistic antibody leads to a macrophage activation in the liver, triggering a sequence of systemic inflammation, endothelial cell activation, thrombosis, and focal ischemia. We found that anti-CD40 antibody injection in sickle cell mice induces a systemic inflammatory and hemodynamic response with accelerated hemolysis, extensive vaso-occlusion, and large ischemic infarctions in the liver mimicking an acute hepatic crisis. Administration of the tumor necrosis factor-α (TNF-α) blocker, etanercept, and the heme scavenger protein, hemopexin attenuated end-organ damage. These data collectively suggest that anti-CD40 administration offers a novel acute liver crisis model in humanized sickle mice, allowing for evaluation of therapeutic proof-of-concept., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Yalamanoglu, Dubach, Schulthess, Ingoglia, Swindle, Humar, Schaer, Buehler, Irwin and Vallelian.)

After congenital heart disease repair, right heart dysfunction facilitates venous stasis and elevated central venous pressure; however, methods to evaluate right heart dysfunction are limited. We aimed to evaluate right heart function using liver biomarkers. We investigated 62 patients more than 5 years after congenital heart surgery. The patients underwent cardiac catheterization in our hospital between January 2015 and December 2019. To evaluate liver status, type IV collagen 7s, procollagen type III peptide, and hyaluronic acid levels were measured. The mean age of the 62 patients was 14.0 ± 7.2 years. The mean central venous pressure was 6.8 ± 3.5 mmHg and mean right ventricular end-diastolic pressure was 7.9 ± 3.5 mmHg. The mean levels of serum type IV collagen 7s, procollagen type III peptide, and hyaluronic acid were 5.9 ± 1.6 ng/mL, 24.3 ± 15.5 ng/mL, and 18.5 ± 13.6 ng/mL, respectively. There was a good correlation between central venous pressure, right ventricular end-diastolic pressure and type IV collagen 7s (r = 0.67 and r = 0.64). There was no correlation between central venous pressure and the procollagen type III peptide (r = 0.003), and slight correlation between central venous pressure and hyaluronic acid (r = 0.31). There was no correlation between right ventricular end-diastolic pressure and the procollagen type III peptide (r = 0.003), and slight correlation between right ventricular end-diastolic pressure and hyaluronic acid (r = 0.31). We found that changes in the hemodynamics of the right heart system can be evaluated using liver fibrosis markers. Type IV collagen 7s reflects central venous pressure and right ventricular end-diastolic pressure in postoperative patients with congenital heart disease.

Right heart failure and right ventricular (RV) remodeling were the main reason for mortality of pulmonary hypertension (PH) patients. Apolipoprotein AV (ApoA5) is a key regulator of plasma triglyceride and have multifunction in several target organs. We detected decreased ApoA5 in serum of patients with PH and both in serum and RV of monocrotaline-induced PH model. Exogenously, overexpression ApoA5 by adenovirus showed protective effects on RV failure and RV fibrosis secondary to PH. In addition, in vitro experiments showed ApoA5 attenuated the activation of fibroblast induced by transforming growth factor β1 and synthesis and secretion of extracellular matrix by inhibiting focal adhesion kinase-c-Jun N-terminal kinase-Smad3 pathway. Finally, we suggest that ApoA5 may potentially be a pivotal target for RV failure and fibrosis secondary of PH., (© 2020 Wiley Periodicals LLC.)

Background: Rapid and accurate identification of right ventricular (RV) dysfunction is essential for decreasing mortality associated with acute pulmonary embolism (PE), particularly for non-high-risk patients without hypotension on admission. This study aimed to develop a rapid and accurate tool for predicting the risk of RV dysfunction in non-high-risk patients with acute PE., Methods: The medical records of non-high-risk patients with acute PE admitted to Shengjing Hospital of China Medical University between January 2011 and May 2020 were retrospectively analysed. The primary outcome of this study was RV dysfunction within 24 h after admission. The enrolled patients were randomized into training or validation sets as a ratio of 2:1. In the training set, a nomogram was developed, and the consistency was corroborated in the validation set. The areas under the receiver operating characteristic curves (AUCs) and 95% confidence intervals (CIs) were calculated., Results: A total of 845 patients were enrolled, including 420 men and 425 women with an average age of 60.05 ± 15.43 years. Right ventricular dysfunction was identified in 240 patients (28.40%). The nomogram for RV dysfunction included N-terminal pro-brain natriuretic peptide, cardiac troponin I, and ventricular diameter ratios, which provided AUC values of 0.881 in the training dataset (95% confidence interval (CI): 0.868-0.898, p < 0.001) and 0.839 in the validation set (95% CI: 0.780-0.897, p < 0.001). The predictive tool was published as a web-based calculato ( https://gaoyzcmu.shinyapps.io/APERVD/ )., Conclusions: The combination of CT and laboratory parameters forms a predictive tool that may facilitate the identification of RV dysfunction in non-high-risk patients with acute PE.

Galectin-3 is a biomarker of fibrosis, inflammation and oxidative stress, and its role in heart remodelling and exercise intolerance has not been conclusively proven in heart failure (HF) patients with reduced ejection fraction (rEF). We prospectively assessed 67 consecutive patients with symptomatic HF and left ventricular (LV) EF ≤ 35% during optimal medical therapy, with a mean serum galectin-3 concentration of 15.3 ± 6.4 and a median of 13.5 ng/mL. The group with galectin-3 concentrations greater than or equal to the median had significantly worse right ventricular (RV) systolic function parameters (s', TAPSE), higher pulmonary artery systolic pressure, more advanced tricuspid regurgitation and lower RV-to-pulmonary circulation coupling index, while no significant differences were found in LV parameters. Moreover, this group achieved significantly lower parameters in cardiopulmonary exercise testing. Significant negative correlations were found between galectin-3 concentration and RV parameters and exercise capacity parameters and have persisted after adjustment for glomerular filtration rate, but not all of them have persisted after adjustment for NT-proBNP. Multivariate regression analysis revealed that TAPSE (β coefficient: - 0.605; p < 0.001) and heart rate at peak exercise (β coefficient: - 0.98; p = 0.009) were independently related to galectin-3 concentration. Elevated galectin-3 concentration in patients with HFrEF might indicate concomitant RV dysfunction and exercise intolerance.

Coronavirus 2019 disease (COVID-19), caused by SARS-CoV-2, can lead to cardiac impairment with various types of clinical manifestations, including heart failure and cardiogenic shock. A possible expression of cardiac impairment is non-ischemic ventricular dysfunction, which can be related to different pathological conditions, such as myocarditis, stress and cytokine-related ventricular dysfunction. The diagnosis of these pathological conditions can be challenging during COVID-19; furthermore, their prevalence and prognostic significance have not been elucidated yet. The purpose of this review is to take stock of the various aspects of non-ischemic ventricular dysfunction that may occur during COVID-19 and of the diagnostic implications related to the use of cardiac imaging techniques.

Objective: The number of patients with congenitally corrected transposition of the great arteries (ccTGA) surviving to old age is increasing. This study therefore sought to characterize 'geriatric' systemic right ventricle (sRV) in terms of clinical profile, cardiac biomarkers, and echocardiography-derived function when compared with findings in younger patients., Methods: A single-center cross-sectional study of adults with ccTGA was performed. Patients underwent clinical assessment; transthoracic echocardiography; and venous blood sampling including N-terminal pro-B-type natriuretic peptide (NTproBNP), galectin-3, and soluble suppression of tumorgenicity 2 (sST2) measurements. In the echocardiographic study, the sRV function was assessed using fractional area change (FAC), tricuspid annular plane systolic excursion (TAPSE), systolic pulsed-wave Doppler velocity (s'), and longitudinal strain (LS)., Results: Ten patients with ccTGA aged 60 years or older and 53 patients younger than 60 years of age were included. There were significantly more individuals with hypertension (40% vs. 5.7%), dyslipidaemia (50% vs. 5.7%), and atrial fibrillation (70% vs. 20.7%) in the older group; similarly, we found higher NTproBNP (2706 pg/mL vs. 784.7 pg/mL; p<0.001), and galectin-3 (10.15 ng/mL vs. 7.24 ng/mL; p=0.007) concentrations in elderly ccTGA individuals, while sST2 content did not vary significantly according to age. Upon echocardiographic assessment, lower sRV FAC (28.6% vs. 36.1%; p=0.028) and LS (-12% vs. -15.5%; p=0.017) values were observed in patients aged 60 years or older. TAPSE and s' did not differ between the age groups., Conclusion: Careful screening for acquired comorbidities, particularly atrial fibrillation, in elderly ccTGA patients is warranted. Examining selected cardiac biomarkers and echocardiography-derived parameters are useful in the assessment of the aging sRV.

Background: Adiponectin is a biomarker closely related to heart failure. However, its role in pulmonary hypertension remains unclear. In this study, we investigated the association between adiponectin and hemodynamic abnormalities, right ventricular function in patients with congenital heart disease associated pulmonary hypertension (CHD-PH)., Methods: Patients with CHD-PH were enrolled in this cross-sectional study. Linear regression analysis was performed to assess the association between adiponectin, N-terminal pro-Brain Natriuretic Peptide (NT-proBNP) and different clinical parameters. Results were depicted as beta-estimates(ß) with 95%-confidence intervals (95% CI). In addition, mediation and receiver operating characteristic curve analyses were used to analyze the relationships among adiponectin, NT-proBNP and right ventricular function., Results: A total of 86 CHD-PH patients were included. The overall mean adiponectin concentration was 7.9 ± 5.8 μg/ml. Log adiponectin was positively correlated with pulmonary circulation index (ß = 2.2, 95% CI 0.5, 4.0), log NT-proBNP (ß = 0.22, 95% CI 0.04, 0.41) and inversely with the tricuspid annular plane systolic excursion (TAPSE, ß = -4.7, 95% CI -8.6, - 0.8). The mediation analysis revealed the association between NT-proBNP and TAPSE was fully mediated by adiponectin (total effect c = - 5.4, 95% CI -9.4, - 1.5, p = 0.013; direct effect c' = - 3.7, 95% CI -7.5, 0.1, p = 0.067). Additionally, the efficiency of adiponectin for detecting right ventricular dysfunction was not inferior to NT-proBNP (AUC = 0.84, 95% CI 0.67-1.00 vs AUC = 0.74, 95% CI 0.51-0.97, p = 0.23)., Conclusions: Adiponectin is closely correlated with pulmonary blood flow and right ventricular function and may be a valuable biomarker for disease assessment in patients with pulmonary hypertension.

The aim of the study is to discuss the risk factor of right heart failure (RHF) especially the association of iron deficiency with RHF in Tibetan children who live in high altitude area. In this retrospective study, we collected the data of Tibetan children from January 2011 to December 2018 in our hospital. The patients included in the study had the following data: age, gender, ferritin, echocardiography, hemoglobin, C-reaction protein, and altitude of residence. According to whether RHF was diagnosed, the patients were divided into RHF group and non-RHF group. Totally 133 patients were included with 59 in RHF group and 74 in non-RHF group. In single factor analysis, age (P = .008), altitude of residence (P < .001), ferritin (P < .001), and pulmonary arterial systolic pressure (P < .001) showed significant difference between the 2 groups. Binary logistic regression was performed to further identify the association of the clinical factors with RHF. Higher pulmonary arterial systolic pressure (odds ratio: 29.303, 95% confidence interval: 5.249-163.589, P < .001) and lower ferritin level (odds ratio: 5.849, 95% confidence interval: 1.585-21.593, P = .008) were independent risk factors associated with RHF. In receiver-operating characteristic curve, the optimal cutoff value of ferritin level was 14.6 μg/L with the sensitivity of 81.4% and specificity of 89.2%. As continuous variable, the correlation between ferritin and RHF was not certain (P = .281). Due to the possibility that iron deficiency be a risk factor of RHF in Tibetan children, prevention and treatment of iron deficiency might be a potential way in reducing the incidence of RHF in this high altitude area.

Aim: This study assessed the utility of SPARC-like protein 1 (SPARCL1) as a biomarker of maladaptive right ventricular (RV) function in patients with pulmonary hypertension (PH). Methods: In this prospective study, we examined SPARCL1 levels in 105 patients with adaptive ( n  = 34) and maladaptive RV ( n  = 32) pressure overload caused by PH, dilated cardiomyopathy (DCM, n  = 18) with LVEF < 35% and preserved RV function and controls without LV or RV abnormalities ( n  = 21). Results: The median SPARCL1 concentration in patients with maladaptive RV function was higher than in those with adaptive RV function ( p  < 0.01), DCM ( p  < 0.001) or controls ( p  < 0.001). Patients with adaptive RV function had higher SPARCL1 concentrations than controls ( p  < 0.05), whereas there was no difference between adaptive RV and DCM. SPARCL1 showed good predictive power for maladaptive RV (AUC 0.77, p  < 0.001) with an optimal cut-off value of 9.66 ng/ml. The TAPSE/PASP ratio was the only independent predictor of SPARCL1 ≥ 9.66 ng/ml in multivariable logistic regression analysis. Conclusion: SPARCL1 shows potential as novel biomarker of RV pathological remodelling and is associated with RV maladaptation and ventriculoarterial uncoupling in PH.

Several risk stratification tools are available to predict short-term mortality in patients with acute pulmonary embolism (PE). The presence of right ventricular (RV) dysfunction is an independent predictor of mortality and may be a more efficient way to stratify risk for patients assessed by a Pulmonary Embolism Response Team (PERT). We evaluated 571 patients presenting with acute PE, then stratified them by the pulmonary embolism severity index (PESI), by the BOVA score, or categorically as low risk (no RV dysfunction by imaging), intermediate risk/submassive (RV dysfunction by imaging), or high risk/massive PE (RV dysfunction with sustained hypotension). Using imaging data to firstly define the presence of RV strain, and plasma cardiac biomarkers as additional evidence for myocardial dysfunction, we evaluated whether PESI, BOVA, or RV strain by imaging were more appropriate for determining patient risk by a PERT where rapid decision making is important. Cardiac biomarkers poorly distinguished between PESI classes and BOVA stages in patients with acute PE. Cardiac TnT and NT-proBNP easily distinguished low risk from submassive PE with an area under the curve (AUC) of 0.84 (95% CI 0.73-0.95, p < 0.0001), and 0.88 (95% CI 0.79-0.97, p < 0.0001), respectively. Cardiac TnT and NT-proBNP easily distinguished low risk from massive PE with an area under the curve (AUC) of 0.89 (95% CI 0.78-1.00, p < 0.0001), and 0.89 (95% CI 0.82-0.95, p < 0.0001), respectively. In patients with RV dysfunction, the predicted short-term mortality by PESI score or BOVA stage was lower than the observed mortality by a two-fold order of magnitude. The presence of RV dysfunction alone in the context of acute PE is sufficient for the purposes of risk stratification. More complicated risk stratification tools which require the consideration of multiple clinical variables may under-estimate short-term mortality risk.

Right ventricular failure is common in critically ill patients, as it frequently results from pulmonary embolism or pulmonary hypertension, and can complicate sepsis and the acute respiratory distress syndrome. Right ventricular dysfunction can be challenging to manage and is associated with poor outcomes in this wide array of disease. Laboratory biomarkers are rapid, noninvasive, accurate, and widely available and thus are useful in the diagnosis and management of right ventricular dysfunction in the critically ill patient. This article discusses the pathophysiology of right ventricular failure and reviews the applications of commonly used biomarkers in right ventricular dysfunction in critical care., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Assessing right ventricular (RV) functional reserve is important for determining clinical status and prognosis in patients with pulmonary hypertension (PH). In this study, we aimed to establish RV oxygen (O 2 ) delivery as a determinant for RV functional reserve during exercise in swine with chronic PH. Chronic PH was induced by pulmonary vein banding (PVB), with sham operation serving as control. RV function and RV O 2 delivery were measured over time in chronically instrumented swine, up to 12 wk after PVB at rest and during exercise. At rest, RV afterload (pulmonary artery pressure and arterial elastance) and contractility ( E es and dP/d t max ) were higher in PH compared with control with preserved cardiac index and RV O 2 delivery. However, RV functional reserve, as measured by the exercise-induced relative change (Δ) in cardiac index, dP/d t max , and end-systolic elastance ( E es ), was decreased in PH, and RV pulmonary arterial coupling was lower both at rest and during exercise in PH. Furthermore, the increase in RV O 2 delivery was attenuated in PH during exercise principally due to a lower systolic coronary blood flow in combination with an attenuated increase in aorta pressure while arterial O 2 content was not significantly altered in PH. Moreover, RV O 2 delivery reserve correlated with RV functional reserve, Δcardiac index ( r 2  = 0.85), ΔdP/d t max ( r 2  = 0.49), and Δ E es ( r 2  = 0.70), all P < 0.05. The inability to sufficiently increase RV O 2 supply to meet the increased O 2 demand during exercise is principally due to the reduced RV perfusion relative to healthy control values and likely contributes to impaired RV contractile function and thereby to the limited exercise capacity that is commonly observed in patients with PH. NEW & NOTEWORTHY Impaired right ventricular (RV) O 2 delivery reserve is associated with reduced RV functional reserve during exercise in a swine model of pulmonary hypertension (PH) induced by pulmonary vein banding. Our data suggest that RV function and exercise capacity might be improved by improving RV O 2 delivery.

Purpose: To investigate whether acute and transient pressure overload in patients with pregnancy-induced hypertension affects cardiac function in fetuses., Methods: We enrolled 104 singleton pregnant women with gestational ages ranging 30 to 33 weeks, visiting for prenatal care. Among them, 34 had gestational hypertension (GH), 32 had preeclampsia (PE), and 38 were healthy and formed the control group. Conventional echocardiographic and velocity vector imaging (VVI) variables were prospectively collected. Blood levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured from cord blood drawn at birth., Results: The fetuses of mothers with preeclampsia had significantly lower left (LV) and right ventricle (RV) diastolic strain rate (SRd) and RV strain (S) and systolic strain rate (SRs) than controls. LV and RV S, SRd, and SRS were not different in fetuses of mothers with GH and controls. The NT-proBNP levels were higher in fetuses of patients with PE than in GH and controls., Conclusions: In the third trimester of pregnancy, fetal biventricular function and NT-proBNP levels are not significantly influenced by GH. Fetuses of mothers with PE present signs of LV and RV diastolic dysfunction, right ventricular systolic dysfunction, and elevated NT-pro-BNP levels. VVI echocardiography appears more sensitive than conventional echocardiography to evaluate fetal cardiac function., (© 2019 Wiley Periodicals, Inc.)

Purpose: Emerging data demonstrate that type 2 diabetes mellitus (T2DM) is associated with right ventricular (RV) dysfunction. A cutoff point of 155 mg/dL for the 1-hour (h) post-load plasma glucose, during oral glucose tolerance test (OGTT), identifies patients with normal glucose tolerance (NGT) at high risk to develop T2DM and cardiovascular (CV) disease. We investigated if 1-h post-load glucose may affect RV geometry and function in a group of never-treated hypertensive individuals., Methods: We enrolled 446 Caucasian newly diagnosed hypertensive outpatients. All patients underwent an OGTT and a standard echocardiography. The tricuspid annular plane systolic excursion (TAPSE) and the RV fractional area change (RVFAC) were measured together with systolic pulmonary arterial pressure (s-PAP) and pulmonary vascular resistances (PVR). Insulin sensitivity was evaluated using the Matsuda index., Results: Among all partecipants, 296 had NGT, 100 impaired glucose tolerance (IGT), and 50 T2DM. Considering the cutoff point of 155 mg/dl for 1-h glucose, NGT subjects were stratified into two groups: NGT < 155 (n = 207), NGT ≥ 155 (n = 89). Subjects NGT ≥ 155 presented a worse metabolic and inflammatory profile than NGT < 155. RV functional parameters (TAPSE, RVFAC, TAPSE/s-PAP, and TAPSE/PVR) were significantly reduced in NGT ≥ 155 subjects compared with NGT < 155 patients. On the contrary, s-PAP and PVR were significantly higher. At multiple regression analysis, 1-h glucose was the strongest predictor of TAPSE in NGT ≥ 155, IGT, and T2DM., Conclusions: The presence of RV impairment in hypertensive NGT ≥ 155 subjects further complicates their CV burden and it may, at least in part, justify the worse clinical outcome in this setting of patients.

The fetal myocardium is known to be sensitive to hemodynamic load, responding to systolic overload with cellular hypertrophy, proliferation, and accelerated maturation. However, the fetal cardiac growth response to primary volume overload is unknown. We hypothesized that increased venous return would stimulate fetal cardiomyocyte proliferation and terminal differentiation, particularly in the right ventricle (RV). Vascular catheters and pulmonary artery flow probes were implanted in 16 late-gestation fetal sheep: a right carotid artery-jugular vein (AV) fistula was surgically created in nine fetuses, and sham operations were performed on seven fetuses. Instrumented fetuses were studied for 1 wk before hearts were dissected for component analysis or cardiomyocyte dispersion for cellular measurements. Within 1 day of AV fistula creation, RV output was 20% higher in experimental than sham fetuses ( P < 0.0001). Circulating atrial natriuretic peptide levels were elevated fivefold in fetuses with an AV fistula ( P < 0.002). On the terminal day, RV-to-body weight ratios were 35% higher in the AV fistula group ( P < 0.05). Both left ventricular and RV cardiomyocytes grew longer in fetuses with an AV fistula ( P < 0.02). Cell cycle activity was depressed by >50% [significant in left ventricle ( P < 0.02), but not RV ( P < 0.054)]. Rates of terminal differentiation were unchanged. Based on these studies, we speculate that atrial natriuretic peptide suppressed fetal cardiomyocyte cell cycle activity. Unlike systolic overload, fetal diastolic load appears to drive myocyte enlargement, but not cardiomyocyte proliferation or maturation. These changes could predispose to RV dysfunction later in life. NEW & NOTEWORTHY Adaptation of the fetal heart to changes in cardiac load allows the fetus to maintain adequate blood flow to its systemic and placental circulations, which is necessary for the well-being of the fetus. Addition of arterial-venous fistula flow to existing venous return increased right ventricular stroke volume and output. The fetal heart compensated by cardiomyocyte elongation without accelerated cellular maturation, while cardiomyocyte proliferation decreased. Even transient volume overload in utero alters myocardial structure and cardiomyocyte endowment.

Background: Systemic inflammation during implant of a durable left ventricular assist device (LVAD) may contribute to adverse outcomes. We investigated the association of the preoperative inflammatory markers with subsequent right ventricular failure (RVF)., Materials and Methods: Prospective data was collected on 489 patients from 2003 through 2017 who underwent implantation of a durable LVAD. Uni- and multivariable correlation with leukocytosis was determined using linear and binary logistic regression. The population was also separated into low (< 10.5 K/ul, n = 362) and high (> 10.5 K/ul, n = 127) white blood cell count (WBC) groups. Mantel-Cox statistics was used to analyze survival data., Results: Postop RVF was associated with a higher preop WBC (11.3 + 5.7 vs 8.7 + 3.1) and C-reactive protein (CRP, 5.6 + 4.4 vs 3.3 + 4.7) levels. Multivariable analysis identified an independent association between increased WBC preoperatively with increased lactate dehydrogenase (LDH, P < 0.001), heart rate (P < 0.001), CRP (P = 0.006), creatinine (P = 0.048), and INR (P = 0.049). The high WBC group was more likely to be on preoperative temporary circulatory support (17.3% vs 6.4%, P < 0.001) with a trend towards greater use of an intra-aortic balloon pump (55.9% vs 47.2%, P = 0.093). The high WBC group had poorer mid-term survival (P = 0.042)., Conclusions: Postop RVF is associated with a preoperative pro-inflammatory environment. This may be secondary to the increased systemic stress of decompensated heart failure. Systemic inflammation in the decompensated heart failure may contribute to RVF after LVAD implant.

Background: Trappin-2/pre-elafin is an endogenous inhibitor of human neutrophil elastase involved in inflammation, innate immunity and vascular remodelling, which consist of the complex pathological process of systemic sclerosis (SSc)., Objectives: To clarify the potential role of trappin-2 in SSc., Methods: Serum trappin-2 levels were determined by enzyme-linked immunosorbent assay in 51 SSc and 18 healthy subjects. Trappin-2 expression was evaluated in SSc lesional skin and cultured endothelial cells treated with FLI1 siRNA by immunohistochemistry, reverse transcription-real-time PCR and/or immunoblotting. Friend leukaemia virus integration 1 (Fli1) binding to the PI3 promoter was assessed by chromatin immunoprecipitation., Results: Since serum trappin-2 levels inversely correlated with estimated glomerular filtration rate in SSc patients with renal dysfunction, SSc patients with normal renal function were analysed. Although serum trappin-2 levels were comparable between diffuse cutaneous SSc, limited cutaneous SSc and control subjects, the prevalence of digital ulcers or elevated right ventricular systolic pressure (RVSP) was significantly higher in SSc patients with elevated serum trappin-2 levels than in those with normal levels. Furthermore, serum trappin-2 levels were significantly increased in SSc patients with digital ulcers or elevated RVSP compared to those without. Moreover, serum trappin-2 levels positively correlated with RVSP values in SSc patients. Importantly, trappin-2 expression was enhanced in small vessels of SSc lesional skin. In cultured endothelial cells, trappin-2 expression was elevated by gene silencing of FLI1 at mRNA and protein levels and Fli1 occupied the PI3 promoter., Conclusions: Endothelial trappin-2 up-regulation partially due to Fli1 deficiency can be associated with the development of SSc vasculopathy., (© 2018 European Academy of Dermatology and Venereology.)

Aims: Patients with acute pulmonary embolism (PE) classified as low risk by the Pulmonary Embolism Severity Index (PESI), its simplified version (sPESI), or the Hestia criteria may be considered for early discharge. We investigated whether the presence of right ventricular (RV) dysfunction may aggravate the early prognosis of these patients., Methods and Results: We did a systematic review and meta-analysis of studies including low-risk patients with acute PE to investigate the prognostic value of RV dysfunction. Diagnosis of RV dysfunction was based on echocardiography or computed tomography pulmonary angiography. In addition, we investigated the prognostic value of elevated troponin or natriuretic peptide levels. The primary outcome was all-cause mortality at 30 days or during hospitalization. We included 22 studies (N = 3295 low-risk patients) in the systematic review: 21 were selected for quantitative analysis. Early all-cause mortality rates in patients with vs. without RV dysfunction on imaging were 1.8% [95% confidence interval (CI) 0.9-3.5%] vs. 0.2% (95% CI 0.03-1.7%), respectively, [odds ratio (OR) 4.19, 95% CI 1.39-12.58]. For troponins, rates were 3.8% (95% CI 2.1-6.8%) vs. 0.5% (95% CI 0.2-1.3%), (OR 6.25, 95% CI 1.95-20.05). For natriuretic peptides, only data on early PE-related mortality were available: rates were 1.7% (95% CI 0.4-6.9%) vs. 0.4% (95% CI 0.1-1.1%), (OR 3.71, 95% CI 0.81-17.02)., Conclusions: In low-risk patients with acute PE, the presence of RV dysfunction on admission was associated with early mortality. Our results may have implications for the management of patients who appear at low risk based on clinical criteria alone, but present with RV dysfunction as indicated by imaging findings or laboratory markers., (© The Author(s) 2018. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Pulmonary arterial hypertension (PAH) is more prevalent in females. Paradoxically, female patients have better right ventricular (RV) function and higher survival rates than males. However, the effects of 17β-estradiol (E2) on RV function in PAH has not been studied. Twenty-four male rats were exposed to monocrotaline (MCT) to induce experimental PAH, while treated with E2 or vehicle respectively. Together with eight control rats, thirty-two rats were examined by echocardiography 4 weeks after drug administration. Echocardiographic measurement of RV function included: tricuspid annular plane systolic excursion (TAPSE), RV index of myocardial performance (RIMP), RV fractional area change (RVFAC) and tricuspid annular systolic velocity (s'). RV free wall longitudinal strain (RVLS FW ) and RV longitudinal shortening fraction (RVLSF) were also used to quantify RV function. RV morphology was determined by echocardiographic and histological analysis. TAPSE, RVFAC and s' were reduced, and RIMP was elevated in the MCT-treated group and vehicle-treated group, when compared with control group (P < 0.01). TAPSE, RVFAC and s' in the E2 group were higher, while RIMP was lower than those in the MCT-treated group and vehicle-treated group (P < 0.01). Myocardial functional parameters (RVLS FW and RVLSF) were also higher in the E2 group. Enhanced serum E2 levels were closely correlated with the improvement in RV functional parameters and enhancement of serum BNP levels (P < 0.01 for all groups). RV function decreased significantly in male rats with MCT-induced PAH, while E2 exhibited a protective effect on RV function, suggesting that E2 is a critical modulator of sex differences in PAH.

B-type natriuretic peptide (BNP) is a cardiac neurohormone known to correlate with left ventricular (LV) dilation, decreased contractility, and increased stiffness. Consequently, BNP has been used as a prognostic tool to assess the degree of LV unloading for patients supported by continuous-flow LV assist devices (LVADs). We assessed the prognostic value of changes in BNP in the 2 weeks after LVAD implantation. This retrospective study analyzed laboratory findings and outcomes of 189 LVAD patients. Patients were separated into two groups based on whether serum BNP levels had improved from preoperative levels by postoperative day 14. Group 1 had improvement in BNP levels, whereas group 2 had no improvement or worsening in BNP. There were no significant differences between the groups in age, gender, race, body mass index, or comorbidities. Group 1 had preoperative BNP 1,125 ± 1,078.3 pg/dl and postoperative BNP 440.2 ± 267.7 pg/dl (preoperative minus postoperative [ΔBNP] = -693.09 ± 942.4 pg/dl), whereas group 2 had preoperative BNP 346.0 ± 309.1 pg/dl and postoperative BNP 631.57 ± 483.4 pg/dl (ΔBNP = 289.32 ± 329.7 pg/dl). Postoperative survival in group 2 was significantly worse than in group 1. Rates of right ventricular failure (RVF) were significantly higher in group 2 (group 1: 39%, group 2: 52.7%; p = 0.01). In most patients implanted with a LVAD, BNP improves significantly in the postoperative period as the LV is unloaded. Our results indicate that lack of improvement in postoperative BNP is associated with longer length of stay, increased rates of RVF, and is an independent risk factor for reduced postoperative survival.

In this study, the association between the right ventricular dysfunction (RVD) and CHA2DS2-VASc (C: congestive heart failure or left ventricular systolic dysfunction, H: hypertension, A: age of ≥ 75 years, D: diabetes mellitus, S: previous stroke, V: vascular disease, A: age between 65 and 74 years, Sc: female gender) scores was investigated in patients with acute pulmonary thromboembolism (PTE). The patients have been assigned to 3 subgroups as massive, submassive, and nonmassive PTE. The CHA2DS2-VASc scores were calculated for all of the patients, and the scores have been classified into 3 groups as the scores between 0 and 1, the scores of 2, and the scores of 3 and over. The independent predictors of the RVD were investigated by the univariate and multivariate regression analyses. The independent predictors of the RVD were determined to be the CHA2DS2-VASc scores ( P = .034), the systolic pulmonary artery pressure ( P < .001), the presence of acute deep vein thrombosis ( P = .007), high simplified Pulmonary Embolism Severity Index ( P < .001), D-dimer ( P < .006), and the mean platelet volume ( P < .001). The CHA2DS2-VASc scores predicted the RVD with 70% sensitivity and 50% specificity as determined by the receiver operating characteristic analysis. The CHA2DS2-VASc score is an independent predictor of the RVD in patients with acute PTE.

Aim: The effect of intratracheal lipopolysaccharide (LPS) instillation on right ventricular dysfunction in rats was studied with the aim of exploring underlying mechanisms., Main Methods: A single dose of LPS (10 mg/kg) or an equal volume of saline was instilled intratracheally and lung injury evaluated using histopathologic scoring and wet/dry (W/D) weight ratio at 6 or 12 h post-administration. Besides, serum atrial natriuretic peptide (ANP) was detected using an enzyme-linked immunosorbent assay (ELISA) and right ventricle β-myosin heavy chain (β-MHC) presence was examined using reverse transcription polymerase chain reaction (RT-PCR). Echocardiography examined pulmonary artery acceleration time (PAAT), right ventricular free wall thickness (RVFWT), tricuspid annular plane systolic excursion (TAPSE), and right ventricular end-diastolic diameter (RVEDD). In addition, right ventricular TUNEL staining and Western blots of Bax and Bcl-2 were performed. Right ventricle and left ventricle caspases-3, -8, and -9 activity were examined using fluorometric assay. Finally, right ventricle myeloperoxidase (MPO) neutrophil staining, and right ventricle and plasma cytokines TNF-α, IL-1β, IL-6 detection was performed., Key Findings: Histopathologic lung injury and increased W/D weight ratio was seen at 6 h after LPS intratracheal instillation, along with increased ANP, but not β-MHC. Pulmonary hypertension was indicated by decreased PAAT at 6 h post-exposure. Right ventricular systolic dysfunction and dilation were observed at 12 h post-exposure, as indicated by a significant decrease of TAPSE and increase of RVEDD. Of note, the procedure led to an increased right ventricle TUNEL positive cardiomyocytes, an increased Bax/Bcl-2 ratio, and increased right and left ventricle caspases-3, -8, and -9 activity as early as 6 h post-exposure, which was paralleled by increased right ventricle MPO staining and increased expression of right ventricle and serum cytokines TNF-α, IL-1β, and IL-6., Significance: As well as acute lung injury, a single dose of LPS intratracheally instilled can induce pulmonary hypertension at 6 h post-exposure, with obvious right ventricular systolic dysfunction and right ventricular dilation present at 12 h post-exposure, possibly via cardiomyocytes apoptosis and inflammation., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Objective: To investigate the diagnostic value of N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin Ⅰ (TnI) for detecting right ventricular dysfunction (RVD) in patients with non-high-risk acute pulmonary thromboembolism (APE). Methods: A retrospective analysis was performed in 96 adult patients [44 males, 52 females, aged (61±14) years] with non-high-risk APE from January 2015 to June 2016. All patients were divided into RVD group and non-RVD group according to whether there was right ventricular enlargement on echocardiography. The baseline data, serumTnI and NT-proBNP levels were compared between the 2 groups and the diagnostic value of the 2 cardiac markers for RVD was analyzed. Results: There were no significant differences in age, gender, body mass index between the 2 groups ( P> 0.05). The creatinine clearance rate of the RVD group was lower than that of the non-RVD group [96.4 (77.5,99.6) vs 101.7 (95.1,106.5), P= 0.021]. NT-proBNP [2 300 (1 056,3 396) vs 188 (61,535), P< 0.01] and TnI [0.13 (0.09,0.25) vs 0.00 (0.00,0.02), P< 0.01] were significant higher in the RVD group than in the non-RVD group. The univariate logistic regression analyses showed that NT-proBNP (per 100 ng/L, OR 1.199, 95% CI 1.117-1.287), TnI (per 0.01 μg/L, OR 1.164, 95% CI 1.079-1.256) and creatinine clearance rate ( OR 0.968, 95% CI 0.938-0.998) were significantly associated with RVD. Multivariate regression analysis showed that NT-proBNP (per 100 ng/L, OR 1.155, 95% CI 1.074-1.241) and TnI (per 0.01 μg/L, OR 1.079, 95% CI 1.011-1.151) were independently associated with RVD. The areas under the ROC curve (AUC) of NT-proBNP, TnI, and the combination of them were 0.908 (95% CI 0.841-0.976), 0.896 (95% CI 0.826-0.966) and 0.925 (95% CI 0.862-0.988), respectively. The cut-off value of NT-proBNP was 503.5 ng/L, with a sensitivity of 85.7%, specificity of 75.4%, positive predictive value (PPV) of 66.7% and negative predictive value (NPV) of 90.2%.The cut-off value of TnI was 0.05 μg/L, and the sensitivity, specificity, PPV and NPV was 80.0%, 86.9%, 77.8% and 88.3%, respectively. The optimal probability derived from the logistic regression model in which the 2 biomarkers were the independent variables was 0.779, with a sensitivity, specificity, PPV and NPV of 65.7%, 96.7%, 92.0%, 83.1%, respectively. Conclusion: Both NT-proBNP and TnI had preferably good diagnostic value for RVD in patients with non-high-risk APE, but their clinical application needed comprehensive evaluation combined with the overall manifestations of the patients and experimental methods. The diagnostic value was higher when the 2 biomarkers were evaluated together.

Background: Bronchial asthma may lead to pulmonary hypertension, right ventricular (RV) dysfunction, and cor pulmonale due to elevated afterload on the RV later in life. The aim of this study was to determine whether serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) might serve as a biomarker for detecting subclinical RV dysfunction using echocardiography during the early stages of bronchial asthma., Methods: Sixty-eight pediatric patients with asthma (asthma group) and 69 age- and sex-matched healthy children (control group) were enrolled. The study was conducted in a tertiary woman and child diseases education and research hospital from January 2013 to December 2013. RV function (2-D and tissue-Doppler echocardiography), pulmonary function (spirometry) and serum NT-proBNP concentration were evaluated., Results: Mean age was 10.5 ± 2.8 years in the asthma group and 10.2 ± 2.7 years in the control group (P = 0.522). RV diastolic function was significantly decreased in the asthma group (ratio of tricuspid lateral annular early diastolic peak velocity to tricuspid lateral annular late diastolic peak velocity [E'/A'], 1.29 ± 0.68 vs 1.74 ± 0.89, P = 0.001). RV myocardial performance index was significantly higher in the asthma group than in the control group (0.28 ± 0.06 vs 0.24 ± 0.07, respectively; P = 0.003). Finally, serum NT-proBNP concentration was significantly higher in the asthma group than in the control group (292.3 ± 142.2 pg/mL vs 208.2 ± 70.1 pg/mL, respectively; P = 0.003)., Conclusion: Increased serum NT-proBNP is associated with subclinical RV dysfunction in asthmatic children. RV function is significantly affected in children with bronchial asthma., (© 2018 Japan Pediatric Society.)

Background: Thrombus burden in pulmonary embolism (PE) is associated with higher D-Dimer-levels and poorer prognosis. We aimed to investigate i) the influence of right ventricular dysfunction (RVD), deep venous thrombosis (DVT), and high-risk PE-status on D-Dimer-levels and ii) effectiveness of D-Dimer to predict RVD in normotensive PE patients., Methods: Overall, 161 PE patients were analyzed retrospectively, classified in 5 subgroups of thrombus burden according to clinical indications and compared regarding D-Dimer-levels. Linear regression models were computed to investigate the association between D-Dimer and the groups. In hemodynamically stable PE patients, a ROC curve was calculated to assess the effectiveness of D-Dimer for predicting RVD., Results: Overall, 161 patients (60.9% females, 54.0% aged >70 years) were included in this analysis. The D-Dimer-level was associated with group-category in a univariate linear regression model (β 0.050 (95%CI 0.002-0.099), P = .043). After adjustment for age, sex, cancer, and pneumonia in a multivariate model we observed an association between D-Dimer and group-category with borderline significance (β 0.047 (95%CI 0.002-0.096), P = .058). The Kruskal-Wallis test demonstrated that D-Dimer increased significantly with higher group-category. In 129 normotensive patients, patients with RVD had significantly higher D-Dimer values compared to those without (1.73 (1.11/3.48) vs 1.17 (0.65/2.90) mg/l, P = .049). A ROC curve showed an AUC of 0.61, gender non-specific, with calculated optimal cut-off of 1.18 mg/l. Multi-variate logistic regression model confirmed an association between D-Dimer >1.18 mg/l and RVD (OR2.721 (95%CI 1.196-6.190), P = .017)., Conclusions: Thrombus burden in PE is related to elevated D-Dimer levels, and D-Dimer values >1.18 mg/l were predictive for RVD in normotensive patients. D-Dimer levels were influenced by DVT, but not by cancer, pneumonia, age, or renal impairment., (Copyright © 2018 Elsevier Inc. All rights reserved.)

During the perioperative period of cardiac disease, as many risk factors exist, such as primary cardiac diseases, the use of vasopressors, ischemia-reperfusion injury during cardiopulmonary bypass (CPB), and surgical stress, the gut suffered from ischemia, anoxia and oxidative stress, which would lead to the enterocyte injury. The aim of this study was to explore whether serum intestinal fatty acid-binding protein (IFABP), which is excreted specifically from damaged intestinal enterocytes, as a predictor of prognosis in postoperative cardiac surgery patients.From January 2017 to December 2017, 40 postoperative cardiac surgery patients were enrolled in this observational study. Serum IFABP levels and prognostic biomarkers were recorded at intensive care unit (ICU) admission.The serum IFABP levels were significantly higher in postoperative cardiac surgery patients who complicated with multiple organ dysfunction syndrome (MODS) (median, 883.20 pg/mL vs 426.10 pg/mL; P < .001), infective complications (median, 917.70 pg/mL vs 409.40 pg/mL; P < .001), or who stayed in ICU beyond 4 days (median, 807.65 pg/mL vs 426.10 pg/mL; P < .001). Moreover, in patients who suffered from right ventricular dysfunction, the serum IFABP levels were significantly higher (median, 737.85 pg/mL vs 445.55 pg/mL; P = .016). The serum IFABP levels also showed great precision for the prediction of MODS (the area under curve, AUC 0.923), infective complications (AUC 0.961) and ICU stay beyond 4 days (AUC 0.853). And it correlated significantly with the acute physiology and chronic health evaluation (APACHE) II score (P < .05), sequential organ failure assessment (SOFA) score (P < .05), and acute gastrointestinal injury (AGI) grade (P < .001).The serum IFABP level at ICU admission is a valuable, convenient, and objective early predictor of prognosis in postoperative cardiac surgery patients.

Introduction: Patients with acute pulmonary embolism(APE)who present with right ventricular dysfunction (RVD) have a worse prognosis. This study aimed to evaluate the value of routine biochemical parameters in predicting RVD and 30-day mortality in patients with APE., Methods: We retrospectively collected the clinical data for 154 enrolled patients, including the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), D-dimer, cardiac troponin I (cTnI), and N-terminal pro-brain natriuretic peptide (NT-proBNP). We analyzed the correlation between RVD and the parameters and conducted a receiver operating characteristic (ROC) curve to confirm the cut-off values for predicting RVD and 30-day mortality. Formulas were built with relevant parameters to predict RVD and 30-day mortality., Results: Age, NLR, PLR, D-dimer, the ratio of cTnI (+), and NT-proBNP (+) were significantly higher in RVD (+) patients. The ratio of cTnI (+) and NT-proBNP (+) in 30-day mortality (+) patients was significantly higher than that in 30-day mortality (-) patients. According to the logistic regression analysis, NLR, cTnI (+), and NT-proBNP (+) correlated with RVD. The formula for the RVD risk score is 0.072 × NLR+1.460 × NT-proBNP (+)+2.113 × cTnI (+), and the area under the curve (AUC) = 0.890 (95% CI: 0.839-0.941, P = .001). The formula for the 30-day mortality risk score is 0.115 × NLR + 2.046 × NT-proBNP (+) + 1.946 × cTnI (+) -0.016 × PLR, and the AUC = 0.903 (95% CI: 0.829-0.976, P = .001)., Conclusions: The rapid on-site evaluation of routine biochemical parameters, including NLR, cTnI, and NT-proBNP levels, and the formula developed using these parameters are valuable for predicting RVD and 30-day mortality in patients with APE., (© 2017 Wiley Periodicals, Inc.)

Background: Heart failure is a serious event in patients with transposition of the great arteries (D-TGA) after atrial redirection surgery. We aimed to determine the association between myocardial fibrosis and systolic and diastolic systemic right ventricle (sRV) dysfunction., Methods: Diastolic and systolic function of sRV was prospectively assessed using echocardiography and cardiac magnetic resonance imaging (CMR) in 48 patients with atrially switched D-TGA and 26 healthy subjects. Diastolic function of the subaortic ventricle was assessed by echocardiography Doppler and DTI. In CMR, ejection fraction of sRV and wall stress defined as the product of the systolic blood pressure and volume/mass ratio were assessed. Fibrosis extent within sRV myocardium was evaluated using gadolinium-enhanced magnetic resonance and serum collagen turnover biomarkers., Results: Late gadolinium enhancement (LGE) was found in 35% of D-TGA patients, and the collagen degradation biomarker pro-MMP1:TIMP1 ratio was significantly increased in D-TGA patients compared to healthy subjects (1.0 × 10 -2 vs. 2.5 × 10 -2 , p = 0.04). Increase in sRV wall stress was significantly associated with LGE (p = 0.01) and pro-MMP1:TIMP1 ratio (r = 0.77, p < 0.01). After adjustment for age, sex, BMI, blood pressure and cardiac treatment, pro-MMP1:TIMP1 ratio was the strongest determinant of sRVEF (R 2  = 0.85, p < 0.01). Pro-MMP1:TIMP1 ratio was also significantly correlated with the early diastolic filling parameter E/E' (r = 0.53, p = 0.02), but this was not anymore the case after adjustment., Conclusions: Diastolic and systolic sRV dysfunction is related to myocardial collagen degradation and fibrosis. Research in medical therapies that reduce systemic sRV afterload and limit collagen degradation is warranted in this setting., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background: An elevated serum level of interleukin-6 (IL-6) in pulmonary arterial hypertension (PAH) patients results in a greater symptom burden and increased mortality; however, the mechanisms underlying these observations remain unclear. Because both pre-clinical and clinical data associate elevated IL-6 levels with impaired cardiac function, we hypothesized that the adverse effects of IL-6 in PAH result, in part, from right ventricular (RV) dysfunction., Methods: We analyzed the relationship between IL-6 and RV function in 40 patients with PAH identified in our institutional PAH registry. Serum IL-6 levels was quantified by enzyme-linked immunoassay., Results: PAH patients had higher IL-6 levels than age- and gender-matched controls. Circulating IL-6 levels correlated inversely with echocardiography-based measures of RV function and RV-pulmonary artery (RV-PA) coupling. When dividing PAH patients by median IL-6 level, patients with higher IL-6 had significantly worse RV function (fractional area change [FAC] 23 ± 12% vs 38 ± 11%, tricuspid annular plane systolic excursion [TAPSE] 1.3 ± 0.3 cm vs 2.1 ± 0.5 cm), impaired RV-PA coupling (0.6 ± 0.5%/mm Hg vs 0.9 ± 0.5%/mm Hg), higher right atrial pressure (13 ± 7 mm Hg vs 9 ± 5 mm Hg), reduced cardiac index (2.0 ± 0.5 liters/min/m 2 vs 2.8 ± 1.0 liters/min/m 2 ) and lower stroke volume (48 ± 20 ml vs 70 ± 28 ml). In contrast, the relationships between IL-6 and mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR) and pulmonary arterial compliance (PAC) were not significant. Finally, IL-6 was independently associated with RV function and RV-PA coupling after adjusting for static (PVR) and pulsatile (PAC) after-load on the RV., Conclusions: Serum IL-6 levels are independently associated with RV function and RV-PA coupling in PAH. Patients with higher IL-6 levels have more severe RV dysfunction and diminished RV-PA coupling despite a comparable severity of pulmonary vascular disease., (Copyright © 2018 International Society for the Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.)

Objective: Right ventricular (RV) functions are clinically important in acute pulmonary embolism (APE). Measurement of systolic function of the right ventricular outflow tract (RVOT) with echocardiography is a simple method to evaluate RV function. The aim of this study was to determine the relationship between RVOT systolic function and the Pulmonary Embolism Severity Index (PESI)., Methods: A total of 151 patients diagnosed with APE by pulmonary computed tomography angiography or ventilation/perfusion scintigraphy were included. Patients were assigned to 2 groups based on the simplified PESI (sPESI): sPESI <1 (n=85) and sPESI ≥1 (n=66). RV conventional parameters, RVOT dimensions, and fractional shortening (RVOT-FS) were also measured., Results: Mean age was similar between sPESI <1 and >1 patients (58.7±12.9 years vs. 61.1±12.7 years, respectively). Frequency of male gender was significantly higher in PESI <1 group (61.2% vs. 40.2%, p=0.013). No significant differences were found between the groups in fasting glucose, serum creatinine, hemoglobin, C-reactive protein, erythrocyte sedimentation rate, troponin, and D-dimer levels, and left ventricular ejection fraction. RVOT-FS was higher in patients with sPESI <1 than in patients with sPESI ≥1 (34.41±3.56 vs. 22.98±4.22), and this difference was significant (p<0.001). Tricuspid annular plane systolic excursion values were lower and pulmonary artery systolic pressure values were higher in the sPESI ≥1 group, which was also statistically significant (p<0.05). Mortality occurred in 7 patients with sPESI <1 and in 16 patients with sPESI ≥1. The mortality rate was higher in patients with lower RVOT-FS, and a RVOT-FS <0.22 predicted mortality with a sensitivity of 54.5% (AUC: 0.674, 95% CI 0.552-0.796; p=0.009)., Conclusion: The RVOT-FS is a noninvasive measurement of RV systolic function, is well-correlated with the sPESI score, and associated with mortality in patients with APE. This easily applied measurement may be used to predict short-term mortality in patients with APE.

Background: Our aim was to develop a model of acute right heart failure (ARHF) in the setting of pulmonary hypertension and to characterize acute right ventricular lesions that develop early after hemodynamic restoration., Methods and Results: We used a described piglet model of chronic pulmonary hypertension (cPH) induced by pulmonary artery occlusions. We induced ARHF in animals with cPH (ARHF-cPH group, n = 9) by volume loading and iterative acute pulmonary embolism until hemodynamic compromise followed by dobutamine infusion for hemodynamic restoration before sacrifice for right ventricular tissue evaluation. The median duration of ARHF before sacrifice was 162 (135-189) minutes. Although ventriculoarterial coupling (measured with multibeat pressure-volume loops) and stroke volume decreased after iterative pulmonary embolism and improved with dobutamine, relative pulmonary to systemic pressure increased by 2-fold and remained similarly increased with dobutamine. Circulating high-sensitivity troponin I increased after hemodynamic restoration. We found an increase in right ventricular subendocardial and subepicardial focal ischemic lesions and in expression of autophagy-related protein LC3-II (Western blot) in the ARHF-cPH group compared with the cPH (n = 5) and control (n = 5) groups., Conclusions: We developed and phenotyped a novel large animal model of ARHF on cPH in which right ventricular ischemic lesions were observed early after hemodynamic restoration., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Pulmonary vascular remodeling is a pathophysiological feature that common to all classes of pulmonary hypertension (PH) and right ventricular dysfunction, which is the major prognosis-limiting factor. Vascular, as well as cardiac tissue remodeling are associated with a re-expression of fetal variants of cellular adhesion proteins, including tenascin-C (Tn-C). We analyzed circulating levels of the fetal Tn-C splicing variants B⁺ and C⁺ Tn-C in serum of PH patients to evaluate their potential as novel biomarkers reflecting vascular remodeling and right ventricular dysfunction. Serum concentrations of B⁺ and C⁺ Tn-C were determined in 80 PH patients and were compared to 40 healthy controls by enzyme-linked immunosorbent assay. Clinical, laboratory, echocardiographic, and functional data were correlated with Tn-C levels. Serum concentrations of both Tn-C variants were significantly elevated in patients with PH ( p < 0.05). Significant correlations could be observed between Tn-C and echocardiographic parameters, including systolic pulmonary artery pressure (B⁺ Tn-C: r = 0.31, p < 0.001, C⁺ Tn-C: r = 0.26, p = 0.006) and right atrial area (B⁺ Tn-C: r = 0.46, p < 0.001, C⁺ Tn-C: r = 0.49, p < 0.001), and laboratory values like BNP (B⁺ Tn-C: r = 0.45, p < 0.001, C⁺ Tn-C: r = 0.42, p < 0.001). An inverse correlation was observed between Tn-C variants and 6-minute walk distance as a functional parameter (B⁺ Tn-C: r = -0.54, p < 0.001, C⁺ Tn-C: r = -0.43, p < 0.001). In a multivariate analysis, B⁺ Tn-C, but not C⁺ Tn-C, was found to be an independent predictor of pulmonary hypertension. Both fetal Tn-C variants may represent novel biomarkers that are capable of estimating both pulmonary vascular remodeling and right ventricular load. The potential beneficial impact of Tn-C variants for risk stratification in patients with PH needs further investigation., Competing Interests: The authors declare no conflict of interest

BackgroundTo test the hypothesis that infants born to obese women with pre-gestational type 2 diabetes mellitus (IBDMs) have ventricular dysfunction at 1 month that is associated with markers of maternal lipid and glucose metabolism.MethodsIn a prospective observational study of IBDMs (OB+DM, n=25), echocardiographic measures of septal, left (LV) and right ventricular (RV) function, and structure were compared at 1 month of age with those in infants born to OB mothers without DM (OB, n=24) and to infants born to non-OB mothers without DM (Lean, n=23). Basal maternal lipid and glucose kinetics and maternal plasma and infant (cord) plasma were collected for hormone and cytokine analyses.ResultsRV, LV, and septal strain measures were lower in the OB+DM infants compared with those in other groups, without evidence of septal hypertrophy. Maternal hepatic insulin sensitivity, maternal plasma free-fatty-acid concentration, and cord plasma insulin and leptin most strongly predicted decreased septal strain in OB+DM infants.ConclusionIBDMs have reduced septal function at 1 month in the absence of septal hypertrophy, which is associated with altered maternal and infant lipid and glucose metabolism. These findings suggest that maternal obesity and DM may have a prolonged impact on the cardiovascular health of their offspring, despite the resolution of cardiac hypertrophy.

The right ventricular longitudinal strain (RVLS) of pulmonary hypertension (PH) patients and its relationship with RV function parameters measured by echocardiography and hemodynamic parameters measured by right heart catheterization was investigated. According to the WHO functional class (FC), 66 PH patients were divided into FC I/II (group 1) and III/IV (group 2). RV function parameters were measured by echocardiographic examinations. Hemodynamic parameters were obtained by right heart catheterization. Patients in group 2 had higher systolic pulmonary artery pressure (sPAP; P < 0.05) than patients in group (1) significant between-group differences were observed in global RVLS (RVLS global ), free wall RVLS (RVLS FW ; P < 0.01), and RV conventional function parameters (all P < 0.05). Moreover, mPAP and PVR increased remarkably and CI decreased significantly in group (2) RVLS global had a positive correlation with 6-min walking distance (6MWD; r = 0.492, P < 0.001) and N-terminal pro-brain natriuretic peptide (NT-proBNP; r = 0.632, P < 0.001), while RVLS FW had a positive correlation with 6MWD (r = 0.483, P < 0.001) and NT-proBNP (r = 0.627, P < 0.001). Hemodynamics analysis revealed that RVLS global had a positive correlation with mPAP (r = 0.594, P < 0.001), PVR (r = 0.573, P < 0.001) and CI (r = 0.366, P = 0.003), while RVLS FW had a positive correlation with mPAP (r = 0.597, P < 0.001), PVR (r = 0.577, P < 0.001) and CI (r = 0.369, P = 0.002). According to receiver operating characteristic curves, the optimal cut-off values of RVLS global (-15.0%) and RVLS FW (-15.3%) for prognosis detection with good sensitivity and specificity. Evidence has shown that RVLS measurement can provide the much-needed and reliable information on RV function and hemodynamics. Therefore, this qualifies as a patient-friendly approach for the clinical management of PH patients.

Background: This study aimed to assess the prevalence of right ventricular diastolic dysfunction (RVDD) and its potential predictors in peripartum cardiomyopathy (PPCM) patients., Methods: This was a cross-sectional study carried out in Nigeria. RVDD was defined and graded using Doppler filling and myocardial tissue Doppler velocities obtained at tricuspid annular level., Results: Forty-three subjects with PPCM and mean age of 26.6 ± 7.0 years were recruited over 6 months. RVDD was found in 30 (69.8 %) subjects, of whom 16 (53.3 %) had grade I, 12 (40.0 %) had grade II and 2 (6.7 %) had grade III severity. RV systolic dysfunction (RVSD), defined as RV fractional area change <35 %, was found in 88.4 %, while combined RVSD and RVDD was found in 58.1 % of patients. Subjects with RVDD had significantly higher tricuspid E/e' ratio (5.1 ± 2.8 versus 3.5 ± 1.0, p = 0.012) and prevalence of pulmonary hypertension (76.7 versus 46.2 %; p < 0.05), and lower serum selenium concentration (55.6 ± 12.1 versus 72.5 ± 12.0 µg/L, p = 0.001) than those with preserved RV diastolic function. Regression analyses showed serum selenium [odds ratio (OR) = 1.14; 95 % confidence interval (CI) = 1.0-1.3; p = 0.049] and combined RVSD and pulmonary hypertension (OR = 79.2; CI = 3.9-1593.7; p = 0.004) as the only predictors of RVDD, and serum selenium <70 µg/L increased the odds of RVDD by 6.67-fold (CI = 1.18-37.78; p = 0.032)., Conclusions: Both RVDD and RVSD were common in PPCM patients. Selenium deficiency and combined RVSD and pulmonary hypertension seemed to be the only determinants of RVDD in this small cohort, a finding that needs verification in a larger sample of patients.

Purpose: ST2 receptor, which is a member of the Toll-like/interleukin-1 (IL-1) receptor family, has been found to be increased in the serum of patients 1 day after myocardial infarction. Several other studies have shown that soluble ST2 levels correlate with severity of heart failure (HF), left ventricular ejection fraction, creatinine clearance, B-type natriuretic peptide and C-reactive protein, and are predictors of mortality in HF. Most of these studies were not only limited to ischemic heart disease but also concentrated on left-sided HF. We therefore decided to study the relationship between soluble ST2 and some markers of right ventricular (RV) function in a cohort of hypertensive HF subjects., Patients and Methods: This is a prospective cohort study of hypertensive HF patients presenting to the University of Abuja Teaching Hospital, Abuja, over a 12-month period. ST2 was measured in plasma sample by the enzyme-linked immunosorbent assay (ELISA) method. Right ventricular diameters in diastole (RVDD) and right atrial area (RAA) were obtained on echocardiography, while right ventricular systolic pressure (RVSP) was estimated from echocardiography by the addition of the pressure gradient between the right ventricle and right atrium (RA) to the pressure in the RA., Results: There was a significant correlation between RVSP and soluble ST2 ( t =0.75, p <0.0001), RVDD ( t =0.28, p =0.004) and RAA ( t =0.46, p =0.002)., Conclusion: In a cohort of hypertensive HF subjects, soluble ST2 correlates significantly with RVSP, RVDD and RAA., Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Background: The mechanisms and relevance of impaired glucose homeostasis in advanced heart failure (HF) are poorly understood. The study goals were to examine glucose regulation, pancreatic endocrine function, and metabolic factors related to prognosis in patients with nondiabetic advanced HF., Methods and Results: In total, 140 advanced HF patients without known diabetes mellitus and 21 sex-, age-, and body mass index-matched controls underwent body composition assessment, oral glucose tolerance testing, and measurement of glucose-regulating hormones to model pancreatic β-cell secretory response. Compared with controls, HF patients had similar fasting glucose and insulin levels but higher levels after oral glucose tolerance testing. Insulin secretion was not impaired, but with increasing HF severity, there was a reduction in glucose, insulin, and insulin/glucagon ratio-a signature of starvation. The insulin/C-peptide ratio was decreased in HF, indicating enhanced insulin clearance, and this was correlated with lower cardiac output, hepatic insufficiency, right ventricular dysfunction, and body wasting. After a median of 449 days, 41% of patients experienced an adverse event (death, urgent transplant, or assist device). Increased glucagon and, paradoxically, low fasting plasma glucose displayed the strongest relations to outcome ( P =0.01). Patients in the lowest quartile of fasting plasma glucose (3.8-5.1 mmol·L -1 , 68-101 mg·dL -1 ) had 3-times higher event risk than in the top quartile (6.0-7.9 mmol·L -1 , 108-142 mg·dL -1 ; relative risk: 3.05 [95% confidence interval, 1.46-6.77]; P =0.002)., Conclusions: Low fasting plasma glucose and increased glucagon are robust metabolic predictors of adverse events in advanced HF. Pancreatic insulin secretion is preserved in advanced HF, but levels decrease with increasing HF severity due to enhanced insulin clearance that is coupled with right heart failure and cardiac cachexia., (© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.)