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Introduction Arrhythmia‐induced cardiomyopathy (AIC) is an underrecognized condition resulting in left ventricular systolic dysfunction (LVSD) that is primarily caused by atrial fibrillation (AFib). The relationship between AIC, right ventricular (RV) function, and quality of life (QoL) has not been well studied. Methods We performed a post‐hoc analysis of our AIC trial in which we prospectively screened for patients with tachyarrhythmia and newly diagnosed, otherwise unexplained LVSD. Following rhythm restoration, patients were followed up at 2, 4, and 6 months. Only patients with persistent sinus rhythm were analyzed. RV function was assessed via echocardiography (tricuspid annular plane systolic excursion [TASPE] and fractional area change [FAC]) and QoL by the Minnesota Living with Heart Failure Questionnaire. Results Of a total of 50 patients recovering from LVSD, 41 were diagnosed with AIC and 9 with non‐AIC. Initially, RV function was reduced in the AIC group and recovered after rhythm restoration, whereas no relevant changes were noted in the non‐AIC group. QoL was reduced in both groups and also improved after rhythm restoration. Regression analysis identified low TAPSE as a predictive parameter for AIC diagnosis and worse QoL in AIC patients. Conclusion We demonstrated that RV function and QoL are impaired in patients with AIC. Six months after rhythm restoration, TAPSE may serve as an early indicator of AIC while also correlating with QoL. This underscores the importance of detailed echocardiographic evaluation with a focus on RV function in patients with concomitant tachyarrhythmia and LVSD. Initial tricuspid annular plane systolic excursion (TAPSE), quality of life (QoL) as measured by the Minnesota Living with Heart Failure Questionnaire and left ventricular ejection fraction (LVEF) during atrial fibrillation (AFib) or atrial flutter (AFlut) were reduced in patients with arrhythmia‐induced cardiomyopathy (AIC) compared with values at the end of 6 months of follow‐up in sinus rhythm. In this paper we show that low TAPSE (optimal cut‐off 18.5 mm) has good predictive power for the diagnosis of AIC and that a low quality of life is associated with low TAPSE. Values in red indicate the relative percent the baseline values were reduced compared with the post‐recovery measurement at the end of follow‐up.

BackgroundHypoxic pulmonary vasoconstriction leads to an increase in pulmonary artery pressure (PAP) and potentially right heart failure in healthy individuals and patients with respiratory diseases. Previous studies in patients with chronic obstructive pulmonary disease (COPD) exposed to hypobaric hypoxia have shown an increase in PAP, while traditional echocardiographic parameters revealed only minimal changes at high altitude. Speckle-tracking-derived analysis is potentially more sensitive to assess right ventricular (RV) function and we used this method to investigate the impact on RV function of patients with COPD ascending to high altitude and compared the results with the traditional echocardiographic parameters.MethodsThis post hoc analysis evaluates echocardiographic RV free wall strain (RVFWS) in patients with COPD GOLD grade 1–3 travelling from 760 m to 3100 m for a 2-day stay. An RVFWS over −20% was considered as an indicator of RV dysfunction.ResultsA total of 54 patients (57% men, mean±SD age 58±9 years, forced expiratory volume in 1 s (FEV1 % predicted 77.3±22.5)) with echocardiographs of sufficient quality were included. The mean RVFWS worsened significantly from −26.0±4.9% at 760 m to −23.9±5.4% at 3100 m (p=0.02). The number of patients with relevant RV dysfunction based on RVFWS increased from 7.4% at 760 m to 25.9% at 3100 m (p=0.02), whereas the prevalence of RV dysfunction assessed by traditional indices remained unchanged.ConclusionExposure to hypoxia led to RVFWS impairment in more than one quarter of patients with COPD. Strain analysis is a promising, non-invasive method for evaluating RV dysfunction, even in subclinical cases and might be prognostically relevant in patients with lung diseases.Trial registration numbersNCT02450968 and NCT03173508.

Purpose To evaluate the effects of acute hypercapnia induced by positive end-expiratory pressure (PEEP) variations at constant plateau pressure ( P plat ) in patients with severe acute respiratory distress syndrome (ARDS) on right ventricular (RV) function. Methods Prospective observational study in two academic intensive care units enrolling 11 adults with severe ARDS (PaO 2 /FiO 2 <150 mmHg at PEEP >5 cmH 2 O). We compared three ventilatory strategies, each used for 1 h, with P plat at 22 (20–25) cmH 2 O: low PEEP (5.4 cmH 2 O) or high PEEP (11.0 cmH 2 O) with compensation of the tidal volume reduction by either a high respiratory rate (high PEEP/high rate) or instrumental dead space decrease (high PEEP/low rate). We assessed RV function (transesophageal echocardiography), alveolar dead space (expired CO 2 ), and alveolar recruitment (pressure–volume curves). Results Compared to low PEEP, PaO 2 /FiO 2 ratio and alveolar recruitment were increased with high PEEP. Alveolar dead space remained unchanged. Both high-PEEP strategies induced higher PaCO 2 levels [71 (60–94) and 75 (53–84), vs. 52 (43–68) mmHg] and lower pH values [7.17 (7.12–7.23) and 7.20 (7.16–7.25) vs. 7.30 (7.24–7.35)], as well as RV dilatation, LV deformation and a significant decrease in cardiac index. The decrease in stroke index tended to be negatively correlated to the increase in alveolar recruitment with high PEEP. Conclusions Acidosis and hypercapnia induced by tidal volume reduction and increase in PEEP at constant P plat were associated with impaired RV function and hemodynamics despite positive effects on oxygenation and alveolar recruitment ( ClinicalTrials.gov #NCT00236262).

Objective To analyse the incidence and the impact on outcome of right ventricular failure (RVF) in patients with acute respiratory distress syndrome (ARDS). Patients and methods A total of 145 ARDS patients included in the previously published French Pulmonary Artery Catheter (PAC) study were randomly assigned to receive a PAC. All patients were ventilated according to a strategy aimed at limiting plateau pressure. The RVF was defined by the concomitant presence of: (1) a mean pulmonary artery pressure (MPAP) > 25 mmHg, (2) a central venous pressure (CVP) higher than pulmonary artery occlusion pressure (PAOP) and (3) a stroke volume index < 30 mL m −2 . Results Right ventricular failure was present in 9.6% of patients. Mortality was 68% at day-90 with no difference between patients with RVF (RVF+) and without RVF (71 vs. 67%, respectively). SAPS II, PaO 2 /FiO 2 and PaCO 2 were similar in both groups. Tidal volume and I/E ratio were significantly higher in RVF+ (9.7 ± 2.8 vs. 8.6 ± 1.8 ml m −2 and 0.7 ± 0.5 vs. 0.5 ± 0.2). Plateau pressure tended to be higher in RVF+ (28 ± 6 vs. 25 ± 6 cmH 2 O, NS). In multivariate analysis, PaO 2 /FiO 2 , mean arterial pressure, arterial pH, SvO 2 , MPAP and presence of CVP > PAOP, but not RVF, were independently associated with day-90 mortality. Conclusion In this group of patients investigated early in the course of ARDS and ventilated according to a strategy aimed at limiting plateau pressure, the presence of RVF was about 10%. Unlike MPAP and the presence of CVP > PAOP, RVF at this early stage did not appear as an independent factor of mortality.

Renin-angiotensin-aldosterone system (RAAS) inhibition with angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors is beneficial in patients with acquired left ventricular dysfunction. Adult patients with tetralogy of Fallot (TOF) with right ventricular (RV) dysfunction are at high risk for heart failure, arrhythmias, and sudden cardiac death. However, the efficacy of RAAS inhibition has not been established in these patients. The REDEFINE is an investigator-initiated, multicenter, prospective, randomized, double-blind, placebo-controlled trial to study the effects of the angiotensin II receptor blocker losartan (target dosage of 150 mg once daily) in adult patients with TOF. Patients with RV dysfunction in the absence of severe valvular dysfunction are eligible for inclusion. The primary end point is the change in RV ejection fraction after 18 to 24 months, as measured by cardiovascular magnetic resonance imaging. In addition, laboratory measurements, echocardiography, and cardiopulmonary exercise testing are performed. The REDEFINE trial will study the effects of RAAS inhibition with losartan in TOF patients with RV dysfunction.

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.

Without effective treatment, pulmonary arterial hypertension results in high morbidity and mortality. This review discusses the pathogenesis of the disorder, the thorough clinical evaluation required to establish the diagnosis, available therapies, and future directions.

Abstract Background 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. Methods 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. Results 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. Conclusions 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.

The cardiovascular system plays a key role in sepsis, and septic myocardial depression is a common finding associated with increased morbidity and mortality. Myocardial depression during sepsis is not clearly defined, but it can perhaps be best described as a global (systolic and diastolic) dysfunction of both the left and right sides of the heart. The pathogenesis of septic myocardial depression involves a complex mix of systemic (hemodynamic) factors and genetic, molecular, metabolic, and structural alterations. Pulmonary artery catheterization and modern echo-Doppler techniques are important diagnostic tools in this setting. There are no specific therapies for septic myocardial depression, and the cornerstone of management is control of the underlying infectious process (adequate antibiotic therapy, removal of the source) and hemodynamic stabilization (fluids, vasopressor and inotropic agents). In this review, we will summarize the pathogenesis, diagnosis, and treatment of myocardial depression in sepsis. Additional studies are needed in order to improve diagnosis and identify therapeutic targets in septic myocardial dysfunction.

ObjectiveTo assess the prevalence, characteristics and prognostic value of pulmonary hypertension (PH) and right ventricular dysfunction (RVD) in hospitalised, non-intensive care unit (ICU) patients with coronavirus disease 2019 (COVID-19).MethodsThis single-centre, observational, cross-sectional study included 211 patients with COVID-19 admitted to non-ICU departments who underwent a single transthoracic echocardiography (TTE). Patients with poor acoustic window (n=11) were excluded. Clinical, imaging, laboratory and TTE findings were compared in patients with versus without PH (estimated systolic pulmonary artery pressure >35 mm Hg) and with versus without RVD (tricuspid annular plane systolic excursion <17 mm or S wave <9.5 cm/s). The primary endpoint was in-hospital death or ICU admission.ResultsA total of 200 patients were included in the final analysis (median age 62 (IQR 52–74) years, 65.5% men). The prevalence of PH and RVD was 12.0% (24/200) and 14.5% (29/200), respectively. Patients with PH were older and had a higher burden of pre-existing cardiac comorbidities and signs of more severe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (radiological lung involvement, laboratory findings and oxygenation status) compared with those without PH. Conversely, patients with RVD had a higher burden of pre-existing cardiac comorbidities but no evidence of more severe SARS-CoV-2 infection compared with those without RVD. The presence of PH was associated with a higher rate of in-hospital death or ICU admission (41.7 vs 8.5%, p<0.001), while the presence of RVD was not (17.2 vs 11.7%, p=0.404).ConclusionsAmong hospitalised non-ICU patients with COVID-19, PH (and not RVD) was associated with signs of more severe COVID-19 and with worse in-hospital clinical outcome.Trial registration number NCT04318366