Impact of acute TTE-evidenced cardiac dysfunction on in-hospital and outpatient mortality: A multicenter NYC COVID-19 registry study

Homan, Edwin A.; Devereux, Richard B.; Tak, Katherine; Mitlak, Hannah W; Volodarskiy, Alexander; Ramasubbu, Kumudha; Zhang, David T; Kushman, Arielle; Pollie, Meridith; Agoglia, Hannah; Tafreshi, Romina; Goyal, Parag; Shaw, Leslee J.; Ndhlovu, Lishomwa C.; RoyChoudhury, Arindam; Horn, Evelyn M.; Narula, Nupoor; Safford, Monika M.; Weinsaft, Jonathan W.; Kim, Jiwon

doi:10.1371/journal.pone.0283708

Cited by 3 publications

(1 citation statement)

References 43 publications

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“…1 Various critical care cohorts demonstrate that patients with right ventricular (RV) dysfunction often have worse survival than those with isolated left ventricular (LV) dysfunction. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] No study has examined pre-and on-ECMO RV function or pulmonary artery (PA) pressures in relation to ECMO survival and duration of support. While the RV and PA directly interact anatomically and physiologically with systemic hemodynamics and ventilator parameters in cardiac support ECMO (both of which have been associated with survival 17,18 ), how they affect clinically important outcomes is unknown.…”

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confidence: 99%

Pulmonary Artery Pressures and Mortality During Venoarterial ECMO: An ELSO Registry Analysis

Owyang,

Rippon,

Teran

et al. 2024

Circ: Heart Failure

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BACKGROUND: Systemic hemodynamics and specific ventilator settings have been shown to predict survival during venoarterial extracorporeal membrane oxygenation (ECMO). How the right heart (the right ventricle and pulmonary artery) affect survival during venoarterial ECMO is unknown. We aimed to identify the relationship between right heart function with mortality and the duration of ECMO support. METHODS: Cardiac ECMO runs in adults from the Extracorporeal Life Support Organization Registry between 2010 and 2022 were queried. Right heart function was quantified via pulmonary artery pulse pressure (PAPP) for pre-ECMO and on-ECMO periods. A multivariable model was adjusted for modified Society for Cardiovascular Angiography and Interventions stage, age, sex, and concurrent clinical data (ie, pulmonary vasodilators and systemic pulse pressure). The primary outcome was in-hospital mortality. RESULTS: A total of 4442 ECMO runs met inclusion criteria and had documentation of hemodynamic and illness severity variables. The mortality rate was 55%; nonsurvivors were more likely to be older, have a worse Society for Cardiovascular Angiography and Interventions stage, and have longer pre-ECMO endotracheal intubation times ( P <0.05 for all) than survivors. Increasing PAPP from pre-ECMO to on-ECMO time (ΔPAPP) was associated with reduced mortality per 2 mm Hg increase (odds ratio, 0.98 [95% CI, 0.97–0.99]; P =0.002). Higher on-ECMO PAPP was associated with mortality reduction across quartiles with the greatest reduction in the third PAPP quartile (odds ratio, 0.75 [95% CI, 0.63–0.90]; P =0.002) and longer time on ECMO per 10 mm Hg (beta, 15 [95% CI, 7.7–21]; P <0.001). CONCLUSIONS: Early on-ECMO right heart function and interval improvement from pre-ECMO values were associated with mortality reduction during cardiac ECMO. Incorporation of right heart metrics into risk prediction models should be considered.

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mentioning

confidence: 99%

Pulmonary Artery Pressures and Mortality During Venoarterial ECMO: An ELSO Registry Analysis

Owyang,

Rippon,

Teran

et al. 2024

Circ: Heart Failure

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Pulmonary Artery Pressures and Mortality during VA ECMO: An ELSO Registry Analysis

Owyang

Rippon

Teran

et al. 2023

Preprint

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Background: Systemic hemodynamics and specific ventilator settings have been shown to predict survival during venoarterial extracorporeal membrane oxygenation (VA ECMO). While these factors are intertwined with right ventricular (RV) function, the independent relationship between RV function and survival during VA ECMO is unknown. Objectives: To identify the relationship between RV function with mortality and duration of ECMO support. Methods: Cardiac ECMO runs in adults from the Extracorporeal Life Support Organization (ELSO) Registry between 2010 and 2022 were queried. RV function was quantified via pulmonary artery pulse pressure (PAPP) for pre-ECMO and on-ECMO periods. A multivariable model was adjusted for Society for Cardiovascular Angiography and Interventions (SCAI) stage, age, gender, and concurrent clinical data (i.e., pulmonary vasodilators and systemic pulse pressure). The primary outcome was in-hospital mortality. Results: A total of 4,442 ECMO runs met inclusion criteria and had documentation of hemodynamic and illness severity variables. The mortality rate was 55%; non-survivors were more likely to be older, have a worse SCAI stage, and have longer pre-ECMO endotracheal intubation times (P < 0.05 for all) than survivors. Improving PAPP from pre-ECMO to on-ECMO time (? PAPP) was associated with reduced mortality per 10 mm Hg increase (OR: 0.91 [95% CI: 0.86-0.96]; P=0.002). Increasing on-ECMO PAPP was associated with longer time on ECMO per 10 mm Hg (Beta: 15 [95% CI: 7.7-21]; P<0.001). Conclusions: Early improvements in RV function from pre-ECMO values were associated with mortality reduction during cardiac ECMO. Incorporation of ? PAPP into risk prediction models should be considered.

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COVID-19 Pathophysiology: Inflammation to Cardiac Injury

Fouda,

Hammond,

Donnelly

et al. 2024

Hearts

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Coronavirus disease 19 (COVID-19) is responsible for one of the worst pandemics in human history. The causative virus, the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), can invade host cells in multiple organs by binding the angiotensin-converting enzyme (ACE) II expressed on the cell surface. Once inside the host cell, viral replication takes place, leading to cellular disruption and the release of signal molecules that are recognised by the innate immune system. Innate immunity activation leads to the release of proinflammatory cytokines and primes the adaptive immune system. The proinflammatory environment defends against further viral entry and replication. SARS-CoV-2 infection is thought to lead to myocardial injury through several mechanisms. Firstly, direct viral-mediated cellular invasion of cardiomyocytes has been shown in in vitro and histological studies, which is related to cellular injury. Secondly, the proinflammatory state during COVID-19 can lead to myocardial injury and the release of protein remnants of the cardiac contractile machinery. Thirdly, the hypercoagulable state of COVID-19 is associated with thromboembolism of coronary arteries and/or other vascular systems. COVID-19 patients can also develop heart failure; however, the underlying mechanism is much less well-characterised than for myocardial injury. Several questions remain regarding COVID-19-related heart failure, including its potential reversibility, the role of anti-viral medications in its prevention, and the mechanisms underlying heart failure pathogenesis in long COVID-19. Further work is required to improve our understanding of the mechanism of cardiac sequelae in COVID-19, which may enable us to target SARS-CoV-2 and protect patients against longer-lasting cardiovascular complications.

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Impact of acute TTE-evidenced cardiac dysfunction on in-hospital and outpatient mortality: A multicenter NYC COVID-19 registry study

Cited by 3 publications

References 43 publications

Pulmonary Artery Pressures and Mortality During Venoarterial ECMO: An ELSO Registry Analysis

Pulmonary Artery Pressures and Mortality During Venoarterial ECMO: An ELSO Registry Analysis

Pulmonary Artery Pressures and Mortality during VA ECMO: An ELSO Registry Analysis

COVID-19 Pathophysiology: Inflammation to Cardiac Injury

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