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Background: Although there is some support for visual estimation (VE) as an accurate method to estimate left ventricular ejection fraction (LVEF), it is also scrutinized for its subjectivity. Therefore, more objective assessments, such as fractional shortening (FS) or e-point septal separation (EPSS), may be useful in estimating LVEF among patients in the emergency department (ED)., Objective: Our aim was to compare the real-world accuracy of VE, FS, and EPSS using a sample of point-of-care cardiac ultrasound transthoracic echocardiography (POC-TTE) images acquired by emergency physicians (EPs) with the gold standard of Simpson's method of discs, as measured by comprehensive cardiology-performed echocardiography., Methods: We conducted a single-site prospective observational study comparing VE, FS, and EPSS to assess LVEF. Adult patients in the ED receiving both POC-TTE and comprehensive cardiology TTE were included. EPs acquired POC-TTE images and videos that were then interpreted by 2 blinded EPs who were fellowship-trained in emergency ultrasound. EPs estimated LVEF using VE, FS, and EPSS. The primary outcome was accuracy., Results: Between April and May 2018, 125 patients were enrolled and 113 were included in the final analysis. EP1 and EP2 had a κ of 0.94 (95% confidence interval [CI] 0.87-1.00) and 0.97 (95% CI 0.91-1.00), respectively, for VE compared with gold standard, a κ of 0.40 (95% CI 0.23-0.57) and 0.38 (95% CI 0.18-0.57), respectively, for EPSS compared with gold standard, and a κ of 0.70 (95% CI 0.54-0.85) and 0.66 (95% CI 0.50-0.81), respectively, for FS compared with gold standard. Sensitivity of severe dysfunction was moderate to high in VE (EP1 85% and EP2 93%), poor to moderate in FS (EP1 73% and EP2 50%), and poor in EPSS (EP1 11% and EP2 18%)., Conclusions: Using a real-world sample of POC-TTE images, the quantitative measurements of EPSS and FS demonstrated poor accuracy in estimating LVEF, even among experienced sonographers. These methods should not be used to determine cardiac function in the ED. VE by experienced physicians demonstrated reliable accuracy for estimating LVEF compared with the gold standard of cardiology-performed TTE., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Introduction: Alterations in cardiac contractility can have significant clinical implications, highlighting the need for early detection of potential liabilities. Pre-clinical methods to assess contractility are typically invasive and their translation to human measures of cardiac function are not well defined. Clinically, cardiac function is most often measured non-invasively using echocardiography. The objective of these studies was to introduce echocardiography into standard large animal cardiovascular safety pharmacology studies and determine the feasibility of this combination., Methods: A consortia of laboratories combined their data sets for evaluation. At each site, telemetered beagle dogs, in a 4 × 4 Latin square crossover study design (n = 4), were administered either pimobendan (positive inotrope) or atenolol (negative inotrope) orally at clinically relevant dose levels. Standard telemetry parameters were collected (heart rate, mean arterial blood pressure, etc.) continuously over 24 h, as well as derived contractility endpoints: QA interval and LV +dP/dt max . At T max , echocardiography was performed in conscious dogs with minimal restraint to collect contractility parameters: ejection fraction (EF) and fractional shortening (FS)., Results: Correlations between telemetry and echo contractility endpoints showed that, in general, a change in LV +dP/dt max of 1000 mmHg/s translates to a 5.2% change in EF and a 4.2% change in FS. Poor correlations were shown between QA interval derived simultaneously, to both EF and FS., Discussion: Comparing data from telemetry-only groups to those that included echocardiography collections showed no effect in the ability to interpret test article-related effects, providing the foundation for the inclusion of echocardiography without compromising standard telemetry data quality., Competing Interests: Declaration of Competing Interest Unless otherwise specified, the authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Introduction: Cardiac contractility was evaluated using standard inotropic agents in rats. We compared indices of cardiac contractility, i.e. LV dP/dt max from telemetry while simultaneously collecting EF (ejection fraction) and FS (fractional shortening) measures from echocardiography., Methods: Male Wistar rats were instrumented with telemetry devices for measurements of blood pressure and left ventricular pressure. Milrinone (PDE III inhibitor) and verapamil (L-type calcium channel blocker) at doses of 0, 3, 10, and 30 mg/kg were administered orally using a 4 × 4 Latin square crossover study design. Telemetry data were recorded at predose and continuously for 24h post-dose. Echocardiographic evaluations were conducted once at predose and at 1 and 2h after milrinone or verapamil administration, respectively. During the recording of echocardiograms, telemetry data were collected simultaneously. Blood samples were also collected to confirm plasma drug exposure., Results: As expected, milrinone increased LV dP/dt max, EF and FS while verapamil decreased LV dP/dt max, EF and FS. Linear regression analysis showed a positive correlation between LV dP/dt max and EF or FS (P<0.001) with both test agents. A change in LV dP/dt max of 1000 mmHg/s was found to correspond with a change in EF and FS of 13 and 16%, respectively, in the telemetered rat., Discussion: The correlation between contractility indices assessed by telemetry and echocardiographic methods in rat models has not received much attention to date. Our results with two reference compounds demonstrate that both methods are sensitive to alterations in contractility induced by inotropic agents administered to rats. The high degree of correlation between changes in LV dP/dt max and EF or FS in the rat enables a translational-element of clinical relevance following changes in contractility indices when measured with telemetry devices in preclinical studies., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Introduction: Regarding evaluation of drug-induced changes in left ventricular contractility in safety pharmacology there is still a gap in knowledge between preclinically and clinically used measurements., Methods: As a step towards translation of preclinical to clinical outcomes, this study in telemetered dogs was initiated to compare indexes of contractility, such as LV dP/dt(max) (contractility measured as the maximum raise of pressure in the left ventricle) and LV dP/dt(max)/P (contractility measured as the maximum raise of pressure in the left ventricle, corrected for pressure) (telemetry; both commonly preclinically used) and EF (ejection fraction) and FS (fractional shortening) (echocardiography; both commonly clinically used). Different inotropic states were induced by minoxidil, milrinone, isoprenaline, clonidine, atenolol and verapamil., Results: Both techniques demonstrated reproducible changes in contractility which showed a clear linear association. A change in LV dP/dt(max) of 1000 mmHg/s (in the range of 2500 to 7500 mmHg/s; in healthy dogs) corresponded with a change in ejection fraction of approximately 7% and a fractional shortening of approximately 6%. A change of 10/s LV dP/dt(max)/P (in the range of 35 to 85/s; in healthy dogs) corresponded with a change in ejection fraction of approximately 7% and a fractional shortening of 7%., Discussion: The correlation found in this study could potentially enable a better--translational--assessment of the clinical relevance of changes in contractility indices measured with telemetry devices in preclinical safety studies., (© 2013.)

Cardiac hypertrophy occurs in response to a variety of stresses as a compensatory mechanism to maintain cardiac output and normalize wall stress. Prevention or regression of cardiac hypertrophy can be a major therapeutic target. Although regression of cardiac hypertrophy occurs after control of etiological factors, the molecular mechanisms remain to be clarified. In the present study, we investigated the role of autophagy in regression of cardiac hypertrophy. Wild-type mice showed cardiac hypertrophy after continuous infusion of angiotensin II for 14 days using osmotic minipumps, and regression of cardiac hypertrophy was observed 7 days after removal of the minipumps. Autophagy was induced during regression of cardiac hypertrophy, as evidenced by an increase in microtubule-associated protein 1 light chain 3 (LC3)-II protein level. Then, we subjected cardiac-specific Atg5-deficient (CKO) and control mice (CTL) to angiotensin II infusion for 14 days. CKO and CTL developed cardiac hypertrophy to a similar degree without contractile dysfunction. Seven days after removal of the minipumps, CKO showed significantly less regression of cardiac hypertrophy compared with CTL. Regression of pressure overload-induced cardiac hypertrophy after unloading was also attenuated in CKO. These results suggest that autophagy is necessary for regression of cardiac hypertrophy during unloading of neurohumoral and hemodynamic stress., (Copyright © 2013. Published by Elsevier Inc.)

Objectives: This study was designed to evidence the protective effect of glucocorticoid therapy on cardiac dysfunction after coronary microembolization (CME), and to clarify its mechanism with the expression of transforming growth factor-beta 1 (TGF-β1)/Smad3 and connective tissue growth factor (CTGF)., Methods: Eighteen mini-pigs were studied, including Sham-operation group (n=4), CME group (n=8) and Glucocorticoid therapy group (n=6, received methylprednisolone 25mg/kg intravenously 30 min before CME). Magnetic resonance imaging (3.0-T) was performed at baseline, 6th hour and one week after operation to evaluate cardiac function. Serum TGF-β1, CTGF and troponin T were also detected. Myocardial expressions of TGF-β1, CTGF and Smad3 were detected by western blot and immunohistochemistry. Total collagen expression was demonstrated by Masson Trichrome stain., Results: Compared with Sham-operation group, left ventricular end-systolic volume (LVESV) and left ventricular end-diastolic volume (LVEDV) in CME group were increased at 6th hour after CME, while left ventricular ejection fraction (LVEF) was decreased significantly. Compared with CME group, methylprednisolone greatly improved LVEF after CME (6th hour: 56.0 ± 3.2% vs. 51.8 ± 3.8%, P=0.030; one week: 57.8 ± 3.2% vs. 54.6 ± 2.6%, P=0.053). We found that methylprednisolone not only significantly decreased serum TGF-β1, CTGF and troponin T, but also reduced myocardial expressions of TGF-β1, CTGF and Smad3 after CME. In addition, collagen volume fraction in glucocorticoid therapy group was markedly lower than that in CME group., Conclusions: Glucocorticoid therapy could improve early cardiac function after CME, and its mechanism could be associated with TGF-β1/Smad3 and CTGF suppression., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: Within the group of patients undergoing coarctectomy today, two subgroups can be identified: neonates with a critical coarctation and nonneonatal patients. We hypothesize that patients who have to undergo repair in the neonatal period will have more persistent impairment of ventricular performance postoperatively. Accordingly, we aimed to characterize biventricular performance after coarctectomy in neonatal and nonneonatal patients., Methods: Children (aged 0 to 17 years) undergoing a coarctectomy were prospectively included and classified as neonatal (<1 month old) or nonneonatal patients. Age-matched controls were included for each measurement occasion. To evaluate left (LV) and right ventricular (RV) performance, fractional shortening, peak systolic (S') and early diastolic (E') tissue Doppler imaging velocities, and E/E' were assessed preoperatively, at discharge, and 1 year postoperatively (11.4 ± 8.3 months)., Results: In neonatal (n = 18) and nonneonatal (n = 19) patients LV performance significantly improved within the first postoperative year. Yet 1 year postoperatively, LV S' was still lower in neonatal patients vs controls (4.8 ± 1.1 vs 6.1 ± 1.6 cm/s; p = 0.036), whereas comparable results were observed in nonneonatal patients and controls. One year postoperatively, LV diastolic performance was impaired in neonatal (LV E' 8.7 ± 3.1 vs 13.2 ± 3.9 cm/s, p = 0.005) and nonneonatal patients (LV E' 12.1 ± 3.5 vs 15.1 ± 2.4 cm/s, p = 0.008) vs controls. In RV performance variables, no differences were observed 1 year postoperatively between neonatal and nonneonatal patients and controls., Conclusions: In both subgroups, LV diastolic performance does not recover to normal values within the first postoperative year. However, LV systolic performance remains more persistently impaired in patients who have to undergo repair in the neonatal period vs nonneonatal repair., (Copyright © 2013 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)