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Background Methods Results Conclusions Left ventricular stroke work index (LVSWI) and cardiac power index (CPI) account for the haemodynamic load of the left ventricle and are promising prognostic values in cardiogenic shock. However, accurately and non‐invasively measuring these parameters during veno‐arterial extracorporeal membrane oxygenation (V‐A ECMO) is challenging and potentially biased by the extracorporeal circulation. This study aimed to investigate, in an ovine model of cardiogenic shock, whether Pressure‐Strain Product (PSP), a novel speckle‐tracking echocardiography parameter, (1) can correlate with pressure‐volume catheter‐based LVSWI and CPI, and (2) can be load‐independent during the flow modification of V‐A ECMO.Nine Dorset‐cross ewes (51 ± 4 kg) were included. After cardiogenic shock was induced, full support V‐A ECMO (X L/min based on 60 mL/kg/min) commenced. At seven time points during 24‐h observation, echocardiographic parameters as well as pressure‐volume catheter‐based LVSWI and CPI were simultaneously measured with X and following X‐1 L/min of ECMO flow. PSP was calculated by multiplying global circumferential strain or global radial strain, and mean arterial pressure, for PSPcirc or PSPrad, respectively.PSPcirc showed a stronger correlation with LVSWI (correlation coefficient, CC = .360, p < .001) and CPI (CC = .283, p < .001) than other echocardiographic parameters. The predictability of PSPcirc for pressure‐volume catheter‐based LVSWI (AUC .82) and CPI (AUC .80) was also higher than other echocardiographic parameters. No statistically significant differences were identified between the two ECMO flow variations in PSPcirc (p = .558).A novel echocardiographic parameter, PSP, may non‐invasively predict pressure‐volume catheter‐based LVSWI and CPI in a load‐independent manner in a cardiogenic shock supported by V‐A ECMO. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions The commonest echocardiographic measurement, left ventricular ejection fraction, can not necessarily predict mortality of recipients following heart transplantation potentially due to afterload dependency. Afterload‐independent left ventricular stroke work index (LVSWI) is alternatively recommended by the current guideline; however, pulmonary artery catheters are rarely inserted in organ donors in most jurisdictions. We propose a novel non‐invasive echocardiographic parameter, Pressure‐Strain Product (PSP), as a potential surrogate of catheter‐based LVSWI. This study aimed to investigate if PSP could correlate with catheter‐based LVSWI in an ovine model of brain stem death (BSD) donors. The association between PSP and myocardial mitochondrial function in the post‐transplant hearts was also evaluated.Thirty‐one female sheep (weight 47 ± 5 kg) were divided into two groups; BSD (n = 15), and sham neurologic injury (n = 16). Echocardiographic parameters including global circumferential strain (GCS) and global radial strain (GRS) and pulmonary artery catheter‐based LVSWI were simultaneously measured at 8‐timepoints during 24‐h observation. PSP was calculated as a product of GCS or GRS, and mean arterial pressure for PSPcirc or PSPrad, respectively. Myocardial mitochondrial function was evaluated following 6‐h observation after heart transplantation.In BSD donor hearts, PSPcirc (n = 96, rho = .547, p < .001) showed the best correlation with LVSWI among other echocardiographic parameters. PSPcirc returned AUC of .825 to distinguish higher values of cardiomyocyte mitochondrial function (cut‐off point; mean value of complex 1,2 O2 Flux) in post‐transplant hearts, which was greater than other echocardiographic parameters.PSPcirc could be used as a surrogate of catheter‐based LVSWI reflecting mitochondrial function. [ABSTRACT FROM AUTHOR]

Background: Left ventricular stroke work index (LVSWI) and afterload‐related cardiac performance (ACP) consider left ventricular (LV) afterload and could be better prognosticators in septic cardiomyopathy. However, their invasive nature prevents their routine clinical applications. This study aimed to investigate (1) whether a proposed speckle‐tracking echocardiography parameter, Pressure‐Strain Product (PSP), can non‐invasively predict catheter‐based LVSWI, ACP and serum lactate in an ovine model of septic cardiomyopathy; and (2) whether PSP can distinguish the sub‐phenotypes of acute respiratory distress syndrome (ARDS) with or without sepsis‐like conditions. Methods: Sixteen sheep with ARDS were randomly assigned to either (1) sepsis‐like (n = 8) or (2) non‐sepsis‐like (n = 8) group. Each ARDS and sepsis‐like condition was induced by intravenous infusion of oleic acid and lipopolysaccharide, respectively. Pulmonary artery catheter‐based LVSWI (the product of stroke work index, mean arterial pressure and.0136), ACP (the percentage of cardiac output measured to cardiac output predicted as normal) and serum lactate were measured simultaneously with transthoracic echocardiography. Two PSP indices were calculated by multiplying the mean arterial blood pressure and either global circumferential strain (PSPcirc) or radial strain (PSPrad). Results: PSPcirc showed a significant correlation with LVSWI (r2 =.66, p <.001) and ACP (r2 =.82, p <.001) in the sepsis‐like group. Although PSP could not distinguish subphenotypes, PSPcirc predicted LVSWI (AUC.86) and ACP (AUC.88), and PSPrad predicted serum lactate (AUC.75) better than LV ejection fraction, global circumferential and radial strain. Conclusions: A novel PSP has the potential to non‐invasively predict catheter‐based LVSWI and ACP, and was associated with serum lactate in septic cardiomyopathy. [ABSTRACT FROM AUTHOR]

R3270 --> 701.5 --> Introduction: Heart transplantation (HTx) is the primary therapy for end‐stage heart failure. For HTx, donor hearts are typically preserved on ice in a cooler (devoid of oxygen), termed cold static storage (CSS). CSS beyond 4 hrs increases the risk of primary graft dysfunction (PGD), the leading cause of early death post‐HTx. Hypothermic ex vivo perfusion (HEVP) of donor hearts allows oxygen delivery during preservation, and we hypothesise, may safely extend donor heart preservation time without increasing PGD risk. We sought to compare post‐HTx recipient survival, cardiac contractility, mitochondrial function, and injury following donor heart preservation by CSS (2 hrs) or HEVP (2 and 8 hrs). Methods: Brain death was induced in donor sheep for 24 hrs, hearts were then preserved by a) CSS for 2 hrs (n=8), b) HEVP for 2 hrs (n=6), or c) HEVP for 8 hrs (n=7). Orthotopic HTx was performed in matched recipients, with progressive hemodynamic management and monitoring for 6 hrs post‐HTx. Recipient cardiac function was assessed by echocardiography, and troponin I levels were measured in plasma. Mitochondrial function, in vitro contractile responses to noradrenaline (trabeculae), and histopathological changes were determined in cardiac tissue collected at end‐study. Results: All HEVP recipients survived to 6 hrs post‐HTx, compared to 6/8 CSS recipients. HEVP (2 and 8 hrs) recipients required less vasoactive support for adequate hemodynamic function, and exhibited reduced blood lactate levels compared to CSS. Post‐HTx cardiac function and troponin I levels were comparable between groups over time, however improved contractile responses to noradrenaline were observed in isolated trabeculae from 2 and 8 hr HEVP hearts. Cardiac mitochondrial function was similar between all groups, except for the 2 hrs HEVP left ventricle, where greater improvements in mitochondrial membrane potential generation were observed. Regardless of preservation technique, histological scores revealed widespread cardiac injury (e.g. myocytolysis and neutrophil infiltration). Conclusion: Donor heart preservation by HEVP shows promising post‐HTx outcomes in comparison to CSS in a sheep HTx model. HEVP can be safely extended up to 8 hrs, without compromising post‐HTx recipient survival, cardiac contractile or mitochondrial function. HEVP may assist in overcoming limitations in preservation time associated with HTx, without increasing PGD risk. The Australian Non‐Ischemic Heart Preservation (NIHP) trial is currently assessing extended HEVP in clinical HTx (ACTRN12620000595910p). [ABSTRACT FROM AUTHOR]