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BackgroundCOVID-19 infection may cause severe respiratory distress and is associated with increased morbidity and mortality. Impaired cardiac function and/or pre-existing cardiovascular disease may be associated with poor prognosis. In the present study, we report a comprehensive cardiovascular characterization in the first consecutive collective of patients that was admitted and treated at the University Hospital of Tübingen, Germany.Methods123 consecutive patients with COVID-19 were included. Routine blood sampling, transthoracic echocardiography and electrocardiography were performed at hospital admission.ResultsWe found that impaired left-ventricular and right-ventricular function as well as tricuspid regurgitation > grade 1 were significantly associated with higher mortality. Furthermore, elevated levels of myocardial distress markers (troponin-I and NT pro-BNP) were associated with poor prognosis in this patient collective.ConclusionImpaired cardiac function is associated with poor prognosis in COVID-19 positive patients. Consequently, treatment of these patients should include careful guideline-conform cardiovascular evaluation and treatment. Thus, formation of a competent Cardio-COVID-19 team may represent a major clinical measure to optimize therapy of cardiovascular patients during this pandemic.

Patients with pulmonary hypertension due to left heart disease (PH-LHD) and a diastolic pulmonary vascular pressure gradient ≥ 7 mm Hg, representing PH out of proportion to pulmonary arterial wedge pressure, have pulmonary vascular disease and increased mortality. Little information exists on this condition, recently labeled as \"combined pre- and post-capillary PH\" (Cpc-PH). To investigate epidemiology, risk factors, right ventricular function, and outcomes in patients with chronic heart failure and Cpc-PH. The study population was identified from a retrospective chart review of a clinical database of 3,107 stable patients who underwent first diagnostic right heart catheterization and from a prospective cohort of 800 consecutive patients at a national university-affiliated tertiary center. The retrospective cohort had 664 patients with systolic heart failure (SHF) and 399 patients with diastolic heart failure (DHF), 12% of whom were classified as Cpc-PH. The prospective cohort had 172 patients with SHF (14% Cpc-PH) and 219 patients with DHF (12% Cpc-PH). Chronic obstructive pulmonary disease (P = 0.034) and the tricuspid annular plane systolic excursion to systolic pulmonary artery pressure ratio (P = 0.015) predicted Cpc-PH in SHF. Younger age (P = 0.004), valvular heart disease (P = 0.046), and the tricuspid annular plane systolic excursion to systolic pulmonary artery pressure ratio predicted Cpc-PH in DHF (P = 0.016). Right ventricular-pulmonary vascular coupling was worse in Cpc-PH patients (end-systolic elastance to effective arterial elastance [Ees/Ea]: SHF: 1.05 ± 0.25; P = 0.002; DHF: 1.17 ± 0.27; P = 0.027) than in those with isolated post-capillary PH (Ees/Ea: SHF: 1.52 ± 0.51; DHF: 1.45 ± 0.29). Cpc-PH is rare in chronic heart failure. Right ventricular-pulmonary vascular coupling is poor in Cpc-PH and could be one explanation for dismal outcomes.

Aim To investigate the prevalence and prognostic impact of right heart failure and right ventricular-arterial uncoupling in Corona Virus Infectious Disease 2019 (COVID-19) complicated by an Acute Respiratory Distress Syndrome (ARDS). Methods Ninety-four consecutive patients (mean age 64 years) admitted for acute respiratory failure on COVID-19 were enrolled. Coupling of right ventricular function to the pulmonary circulation was evaluated by a comprehensive trans-thoracic echocardiography with focus on the tricuspid annular plane systolic excursion (TAPSE) to systolic pulmonary artery pressure (PASP) ratio Results The majority of patients needed ventilatory support, which was noninvasive in 22 and invasive in 37. There were 25 deaths, all in the invasively ventilated patients. Survivors were younger (62 ± 13 vs. 68 ± 12 years, p  = 0.033), less often overweight or usual smokers, had lower NT-proBNP and interleukin-6, and higher arterial partial pressure of oxygen (PaO 2 )/fraction of inspired O 2 (FIO 2 ) ratio (270 ± 104 vs. 117 ± 57 mmHg, p  < 0.001). In the non-survivors, PASP was increased (42 ± 12 vs. 30 ± 7 mmHg, p  < 0.001), while TAPSE was decreased (19 ± 4 vs. 25 ± 4 mm, p  < 0.001). Accordingly, the TAPSE/PASP ratio was lower than in the survivors (0.51 ± 0.22 vs. 0.89 ± 0.29 mm/mmHg, p  < 0.001). At univariate/multivariable analysis, the TAPSE/PASP (HR: 0.026; 95%CI 0.01–0.579; p : 0.019) and PaO 2 /FIO 2 (HR: 0.988; 95%CI 0.988–0.998; p : 0.018) ratios were the only independent predictors of mortality, with ROC-determined cutoff values of 159 mmHg and 0.635 mm/mmHg, respectively. Conclusions COVID-19 ARDS is associated with clinically relevant uncoupling of right ventricular function from the pulmonary circulation; bedside echocardiography of TAPSE/PASP adds to the prognostic relevance of PaO 2 /FIO 2 in ARDS on COVID-19.

Right ventricular (RV) adaptation to acute and chronic pulmonary hypertensive syndromes is a significant determinant of short- and long-term outcomes. Although remarkable progress has been made in the understanding of RV function and failure since the meeting of the NIH Working Group on Cellular and Molecular Mechanisms of Right Heart Failure in 2005, significant gaps remain at many levels in the understanding of cellular and molecular mechanisms of RV responses to pressure and volume overload, in the validation of diagnostic modalities, and in the development of evidence-based therapies. A multidisciplinary working group of 20 international experts from the American Thoracic Society Assemblies on Pulmonary Circulation and Critical Care, as well as external content experts, reviewed the literature, identified important knowledge gaps, and provided recommendations. This document reviews the knowledge in the field of RV failure, identifies and prioritizes the most pertinent research gaps, and provides a prioritized pathway for addressing these preclinical and clinical questions. The group identified knowledge gaps and research opportunities in three major topic areas: 1) optimizing the methodology to assess RV function in acute and chronic conditions in preclinical models, human studies, and clinical trials; 2) analyzing advanced RV hemodynamic parameters at rest and in response to exercise; and 3) deciphering the underlying molecular and pathogenic mechanisms of RV function and failure in diverse pulmonary hypertension syndromes. This statement provides a roadmap to further advance the state of knowledge, with the ultimate goal of developing RV-targeted therapies for patients with RV failure of any etiology.

A new infectious outbreak sustained by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is now spreading all around the world. The aim of this study was to evaluate the prognostic value of left ventricular global longitudinal strain (LV-GLS) and right ventricular longitudinal strain (RV-LS) in patients with coronavirus disease 2019 (COVID-19). In this prospective, single-center study, data were gathered from patients treated for COVID-19 between April 15 and April 30, 2020. Two-dimensional echocardiography (2-DE) and speckle tracking echocardiography (STE) images were obtained for all patients. Patients were divided into three groups: those with severe COVID-19 infection, those with non-severe COVID-19 infection, and those without COVID-19 infection (the control group). Data regarding clinical characteristics and laboratory findings were obtained from electronic medical records. The primary endpoint was in-hospital mortality. A total of 100 patients hospitalized for COVID-19 were included in this study. The mean age of the severe group (n = 44) was 59.1 ± 12.9, 40% of whom were male. The mean age of the non-severe group (n = 56) was 53.7 ± 15.1, 58% of whom were male. Of these patients, 22 died in the hospital. In patients in the severe group, LV-GLS and RV-LS were decreased compared to patients in the non-severe and control groups (LV-GLS: − 14.5 ± 1.8 vs. − 16.7 ± 1.3 vs. − 19.4 ± 1.6, respectively [p < 0.001]; RV-LS: − 17.2 ± 2.3 vs. − 20.5 ± 3.2 vs. − 27.3 ± 3.1, respectively [p < 0.001]). The presence of cardiac injury, D-dimer, arterial oxygen saturation (SaO2), LV-GLS (OR 1.63, 95% confidence interval [CI] 1.08–2.47; p = 0.010) and RV-LS (OR 1.55, 95% CI 1.07–2.25; p = 0.019) were identified as independent predictors of mortality via multivariate analysis. LV-GLS and RV-LS are independent predictors of in-hospital mortality in patients with COVID-19.

Right ventricular (RV) function has proven to be a prognostic factor in heart failure with reduced and preserved ejection fraction and in pulmonary hypertension. RV function is also a cornerstone in the management of novel clinical issues, such as mechanical circulatory support devices or grown-up congenital heart disease patients. Despite the notable amount of circumferentially oriented myofibers in the subepicardial layer of the RV myocardium, the non-longitudinal motion directions are often neglected in the everyday assessment of RV function by echocardiography. However, the complex RV contraction pattern incorporates different motion components along three anatomically relevant axes: longitudinal shortening with traction of the tricuspid annulus towards the apex, radial motion of free wall often referred as the “bellows effect”, and anteroposterior shortening of the chamber by stretching the free wall over the septum. Advanced echocardiographic techniques, such as speckle-tracking and 3D echocardiography allow an in-depth characterization of RV mechanical pattern, providing better understanding of RV systolic and diastolic function. In our current review, we summarize the existing knowledge regarding RV mechanical adaptation to pressure- and/or volume-overloaded states and also other physiologic or pathologic conditions.

•Impaired strain can identify both right and left ventricular involvement in ARVC.•Biventricular strain assessment is crucial as patients can present LV involvement only.•Patients can be grouped into normal, discordant (LV or RV) or impaired (both) strain.•Involvement of one or both ventricles is associated with mortality and arrhythmias.•Biventricular strain impairment has prognostic value across ARVC diagnosis spectrum. The upper panel shows the RV and LV strain measurements (RV free wall strain and LV global longitudinal strain) performed to define the strain groups based on the relative ventricular function and with the cut-off value of 18%: impaired strain, discordant and normal strain. Lower panel depicts the difference in outcome between the strain groups based on Kaplan-Meier analysis (left) and the incremental value of using strain groups in assessing prognosis in addition to age, sex and ARVC diagnosis, as compared to solely using LV or RV strain (right). ARVC, Arrhythmogenic Right Ventricular Cardiomyopathy; FWLS, right ventricular free wall longitudinal strain; LV, left ventricle; LV GLS, left ventricular global longitudinal strain; RV, Right ventricle. [Display omitted] Despite arrhythmogenic right ventricular cardiomyopathy (ARVC) being predominantly a right ventricular (RV) disease, concomitant left ventricular (LV) involvement has been recognized. ARVC is diagnosed by the RV-centric 2010 Task Force Criteria(TFC) using routine echocardiography, but previous studies have suggested that strain imaging may be more sensitive to detect RV and LV dysfunction. No data however are available regarding the additional value of combining biventricular strain for risk stratification. This study aims to assess the prognostic value of both LV global longitudinal strain (GLS) and RV free wall strain (FWLS) in patients with ARVC. To accomplish this, 204 patients who met the TFC for the ARVC spectrum were included. Patients (age 41 ± 17 years,55% men) were divided into impaired(n = 33), discordant (RV or LV impaired, n = 70), and normal (n = 101) strain groups based on a value of ≥18% for both ventricles. During a follow-up of 87 [24–136] months, 57 (28%) experienced the composite outcome of all-cause mortality, arrhythmic events, implantable cardioverter defibrillator therapy and heart failure events, and a significant difference in event-free survival was observed (p <0.001) between the 3 groups. In the multivariable analysis, the strain groups remained associated with outcomes (p = 0.014) after adjusting for age, sex, history of syncope and definite ARVC diagnosis. A subanalysis including only definite and borderline diagnosed ARVC confirmed that the strain groups were independently predictive of the endpoint (p = 0.023). In conclusion, biventricular involvement by strain analysis may help risk stratification in ARVC patients, with the worst outcomes of patients with both RV and LV impaired strain.

Despite progressive improvements over the decades, the rich temporally resolved data in an echocardiogram remain underutilized. Human assessments reduce the complex patterns of cardiac wall motion, to a small list of measurements of heart function. All modern echocardiography artificial intelligence (AI) systems are similarly limited by design – automating measurements of the same reductionist metrics rather than utilizing the embedded wealth of data. This underutilization is most evident where clinical decision making is guided by subjective assessments of disease acuity. Predicting the likelihood of developing post-operative right ventricular failure (RV failure) in the setting of mechanical circulatory support is one such example. Here we describe a video AI system trained to predict post-operative RV failure using the full spatiotemporal density of information in pre-operative echocardiography. We achieve an AUC of 0.729, and show that this ML system significantly outperforms a team of human experts at the same task on independent evaluation. The echocardiogram allows for a comprehensive assessment of the cardiac musculature and valves, but its rich temporally resolved data remain underutilized. Here, the authors develop a video AI system trained to predict post-operative right ventricular failure.

Background Two‐dimensional speckle‐tracking echocardiography (2D‐STE) has emerged as a valuable tool for assessing cardiac function in patients with type 1 (T1DM) and type 2 diabetes mellitus (T2DM). Hypothesis This review synthesizes recent studies utilizing 2D‐STE in diabetic patients, highlighting its clinical applications and findings. Methods In this review, relevant studies were identified through comprehensive searches of major scientific databases, including PubMed, Scopus, Google Scholar, ScienceDirect, and other reputable sources. Results The results of this study indicate that 2D‐STE is capable of detecting subclinical cardiac dysfunction in patients with both T1DM and T2DM, even in instances where conventional echocardiographic parameters appear to be within normal limits. Assessment of right ventricular (RV) function through 2D‐STE has demonstrated impaired right ventricular free wall longitudinal strain (RVFWLS) and global longitudinal strain (RVGLS) in individuals with T2DM, which correlates with suboptimal glycemic control. Furthermore, evaluation of left ventricular (LV) function has revealed decreased global longitudinal strain (GLS) and impaired LV twist mechanics in T2DM patients, particularly under conditions of physiological stress. In T1DM patients, 2D‐STE has identified early changes in myocardial deformation, with studies reporting reduced LV and RV strain values compared to healthy controls. The technique has also been effective in assessing the impact of disease duration and glycemic control on cardiac function in both T1DM and T2DM. Conclusions These findings underscore the potential of 2D‐STE as a sensitive and comprehensive tool for early detection of cardiac dysfunction in both T1DM and T2DM, potentially guiding management strategies and improving outcomes in these high‐risk populations. This figure illustrates the application of 2D speckle‐tracking echocardiography (2D‐STE) in assessing cardiac function in diabetes patients. At the center, a detailed anatomical representation of the heart is shown, highlighting the areas that can be evaluated using this advanced imaging technique. The left side of the image explains that 2D‐STE can detect subclinical cardiac dysfunction before overt clinical manifestations appear in type 2 diabetes mellitus (T2DM) patients. The figure also demonstrates that 2D‐STE shows impaired left atrial function in poorly controlled T2DM patients with coronary artery disease, as well as in those with nonalcoholic fatty liver disease (NAFLD). On the right side, the image includes a human figure representing a T2DM patient, with an illustration suggesting cellular‐level changes. The bottom right corner shows the 2D‐STE equipment used for these cardiac assessments, indicating its role in evaluating both left ventricular (LV) and right ventricular (RV) function comprehensively in diabetes patients.

The right ventricle (RV) differs developmentally, anatomically and functionally from the left ventricle (LV). Therefore, characteristics of LV adaptation to chronic pressure overload cannot easily be extrapolated to the RV. Mitochondrial abnormalities are considered a crucial contributor in heart failure (HF), but have never been compared directly between RV and LV tissues and cardiomyocytes. To identify ventricle-specific mitochondrial molecular and functional signatures, we established rat models with two slowly developing disease stages (compensated and decompensated) in response to pulmonary artery banding (PAB) or ascending aortic banding (AOB). Genome-wide transcriptomic and proteomic analyses were used to identify differentially expressed mitochondrial genes and proteins and were accompanied by a detailed characterization of mitochondrial function and morphology. Two clearly distinguishable disease stages, which culminated in a comparable systolic impairment of the respective ventricle, were observed. Mitochondrial respiration was similarly impaired at the decompensated stage, while respiratory chain activity or mitochondrial biogenesis were more severely deteriorated in the failing LV. Bioinformatics analyses of the RNA-seq. and proteomic data sets identified specifically deregulated mitochondrial components and pathways. Although the top regulated mitochondrial genes and proteins differed between the RV and LV, the overall changes in tissue and cardiomyocyte gene expression were highly similar. In conclusion, mitochondrial dysfuntion contributes to disease progression in right and left heart failure. Ventricle-specific differences in mitochondrial gene and protein expression are mostly related to the extent of observed changes, suggesting that despite developmental, anatomical and functional differences mitochondrial adaptations to chronic pressure overload are comparable in both ventricles.