Carbon monoxide improves haemodynamics during extracorporeal resuscitation in pigs

2019 ◽  
Vol 116 (1) ◽  
pp. 158-170 ◽  
Author(s):  
Jakob Wollborn ◽  
Christoph Steiger ◽  
Eva Ruetten ◽  
Christoph Benk ◽  
Fabian A Kari ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Myocardial Dysfunction ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Flow Index ◽  
Protective Effects ◽  
Ventricular Ejection Fraction ◽  
Sublingual Microcirculation ◽  
Extracorporeal Resuscitation

Abstract Aims Heart disease of different aetiology remains the leading cause of cardiac arrest (CA). Despite efforts to improve the quality of cardiopulmonary resuscitation (CPR), subsequent myocardial and systemic damage after CA still present a major long-term burden. Low-dose carbon monoxide (CO) is known to exert protective effects in cardiovascular pathophysiology but clinical applications are challenged by unfavourable delivery modes. We tested the hypothesis that extracorporeal resuscitation (E-CPR) in combination with controlled fast onset CO delivery results in improved cardiac physiology and haemodynamics. Damage-associated molecular pattern (DAMP) signalling may be part of the molecular mechanism. Methods and results In an established porcine model, E-CPR was performed. While E-CPR leads to similar results as compared to a conventional CPR strategy, CO delivery in combination with E-CPR demonstrated significant cardioprotection. Cardiac performance analysis using echocardiography and thermodilution techniques showed a CO-dependent improved cardiac function compared to severe myocardial dysfunction in CPR and E-CPR (left ventricular ejection fraction: Sham 49 ± 5; CPR 26 ± 2; E-CPR 25 ± 2; CO-E-CPR 31 ± 4; P < 0.05). While sublingual microcirculation was significantly compromised in CPR and E-CPR, CO delivery demonstrated a significant improvement in microvascular function (microvascular flow index: Sham 2.9 ± 0.1; CPR 2.2 ± 0.1; E-CPR 1.8 ± 0.1; CO-E-CPR 2.7 ± 0.1; P < 0.01). Histological and serological myocardial damage markers were significantly reduced (hsTroponin-T Sham 0.01 ± 0.001; CPR 1.9 ± 0.2; E-CPR 3.5 ± 1.2; CO-E-CPR 0.5 ± 0.2 ng/mL; P < 0.05). DAMP signalling was decreased ipse facto leading to influence of cardioprotective heat shock and cyclooxygenase response. Conclusions CO treatment restores myocardial function and improves systemic macro- and microhaemodynamics in E-CPR through a reduction in DAMPs.

Electrophysiologic properties and ventricular fibrillation in normal and myopathic hearts

1999 ◽  
Vol 77 (7) ◽  
pp. 510-519 ◽  
Author(s):  
Katherine M Kavanagh ◽  
Patricia A Guerrero ◽  
Bodh I Jugdutt ◽  
Francis X Witkowski ◽  
Jeffrey E Saffitz
Keyword(s):  
Ventricular Fibrillation ◽  
Myocardial Dysfunction ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Functional Abnormality ◽  
Ventricular Ejection Fraction ◽  
Anisotropic Properties

This study tests the hypothesis that moderate myocardial dysfunction is associated with altered myocardial anisotropic properties and structurally altered ventricular fibrillation (VF). Mongrel dogs were randomized to either a control group or a group that was rapidly paced at 250 beats/min until the left ventricular ejection fraction was [Formula: see text] 40%. Changes in anisotropic properties and the electrical characteristics of VF associated with the development of moderate myocardial dysfunction were assessed by microminiature epicardial mapping studies. In vivo conduction, refractory periods, and repolarization times were prolonged in both longitudinal and transverse directions in myopathic animals versus controls. VF was different in myopathic versus control animals. There were significantly more conducted deflections during VF in normal hearts compared with myopathic hearts. Propagated deflection-to-deflection intervals during VF were significantly longer in myopathic hearts compared with controls (125.5 ± 49.06 versus 103.4 ± 32.9 ms, p = 0.009). There were no abnormalities in cell size, cell shape, or the number of intercellular gap junctions and there was no detectable change in the expression of the gap junction proteins Cx43 and Cx45. Moderate myocardial dysfunction is associated with significant electrophysiological abnormalities in the absence of changes in myocardial cell morphology or intercellular connections, suggesting a functional abnormality in cell-to-cell communication.Key words: cardiomyopathy, anisotropy, fibrillation, defibrillation.

Abstract 96: Thioredoxin-1 Is Essential for Hydrogen Sulfide-Mediated Cardioprotection in the Setting of Ischemic-Induced Heart Failure

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Chad K Nicholson ◽  
Bridgette F Moody ◽  
Rebecca L Hood ◽  
Junichi Sadoshima ◽  
John W Calvert
Keyword(s):  
Heart Failure ◽  
Hydrogen Sulfide ◽  
Left Ventricular ◽  
Dominant Negative ◽  
Left Ventricular Ejection ◽  
Protective Effects ◽  
Ventricular Ejection Fraction ◽  
Left Ventricular Dimensions ◽  
Thioredoxin 1 ◽  
And Function

Background: Numerous studies have reported the cytoprotective effects of hydrogen sulfide (H2S) in various models of myocardial injury. Here we examined the role that thioredoxin-1 (Trx1) plays in mediating the protective effects of H2S in a model of heart failure. Methods and Results: Mice were subjected to 60 min of left coronary artery ischemia followed by 4 wks of reperfusion (R) at which time left ventricular dimensions and function were assessed. Mice received saline (Veh) or H2S in the form of sodium sulfide (Na2S, 100 μ g/kg) at the time of R followed by daily i.v. injections for the first 7 days of R. Mice treated with Na2S experienced less left ventricular dilatation and hypertrophy, displayed improved left ventricular ejection fraction, and displayed improved contractility and relaxation when compared to Veh-treated mice. Studies aimed at evaluating the underlying cardioprotective mechanisms found that Na2S treatment increased the expression of Trx1. Further analysis revealed that this was accompanied by an increase in phosphorylation of apoptosis signaling kinase-1 (ASK1) at serine residue 966 (inhibitory site), as well as a decrease in the phosphorylation of JNK and p38 (downstream targets of ASK1). We also found that Na2S treatment did not improve cardiac dilatation, cardiac dysfunction, or cardiac hypertrophy in cardiac specific Trx1 dominant negative transgenic (Trx1 dnTg) mice when compared to Veh-treated mice. Conclusion: These findings provide important information that the upregulation of cardiac Trx1 by H2S in the setting of ischemic-induced heart failure sets into motion events, including ASK1 inhibition, which ultimately leads to cardioprotection.

scholarly journals Intra-Arrest Administration of Cyclosporine and Methylprednisolone Does Not Reduce Postarrest Myocardial Dysfunction

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Meshe Chonde ◽  
Katharyn L. Flickinger ◽  
Matthew L. Sundermann ◽  
Allison C. Koller ◽  
David D. Salcido ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Myocardial Dysfunction ◽  
Spontaneous Circulation ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Sampled Data ◽  
Ventricular Ejection Fraction

Objective. To determine whether the administration of intra-arrest cyclosporine (CCY) and methylprednisolone (MP) preserves left ventricular ejection fraction (LVEF) and cardiac output (CO) after return of spontaneous circulation (ROSC). Methods. Eleven, 25-30kg female swine were randomized to receive 10mg/kg CCY + 40mg MP or placebo, anesthetized and given a transthoracic shock to induce ventricular fibrillation. After 8 minutes, standard CPR was started. After two additional minutes, the experimental agent was administered. Animals with ROSC were supported for up to 12h with norepinephrine as needed. Echocardiography was performed at baseline, and 1, 2, 6 and 12h post-ROSC. Analysis was performed using generalized estimating equations (GEE) after downsampling continuously sampled data to 5 minute epochs. Results. Eight animals (64%) achieved ROSC after a median of 7 [IQR 5-13] min of CPR, 2 [ IQR 1-3] doses of epinephrine and 2 [IQR 1-5] defibrillation shocks. Animals receiving CCY+MP had higher post ROSC MAP (GEE coefficient -10.2, P = <0.01), but reduced cardiac output (GEE coefficient 0.8, P = <0.01) compared to placebo. There was no difference in LVEF or vasopressor use between arms. Conclusions. Intra-arrest cyclosporine and methylprednisolone decreased post-arrest cardiac output and increased mean arterial pressure without affecting left ventricular ejection fraction.

Sequential Extracorporeal Therapy Collaborative Device and Timely Support for Endotoxic, Septic, and Cardiac Shock: A Case Report

2019 ◽  
Vol 49 (4) ◽  
pp. 502-508 ◽  
Author(s):  
Silvia De Rosa ◽  
Sara Samoni ◽  
Claudio Ronco
Keyword(s):  
Septic Shock ◽  
Myocardial Dysfunction ◽  
Endotoxic Shock ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Septic Cardiomyopathy ◽  
Ventricular Ejection Fraction ◽  
Circulatory Insufficiency ◽  
Extracorporeal Therapy ◽  
Va Ecmo

We report a 49-year-old man, without prior medical history, consulted in the emergency department with a 5 day history of cough, fever, and dysuria. He was admitted to the intensive care unit due to septic shock. Critical care management was initiated, including mechanical ventilation and vasopressors. Endotoxic shock was suspected (endotoxin activity assay [EAA] 0.75), and 2 treatments with Polymyxin B hemoperfusion (Toraymyxin®, Toray Medical Co., Ltd., Tokyo, Japan) were performed in 48 h, alternate with high-volume hemofiltration sessions. Initial blood cultures were positive for Neisseria meningitidis (serogroup B), and a lumbar puncture was deferred because of the coagulopathy and a bleeding risk. The circulatory efficiency significantly improved after the second procedure of hemoperfusion, and the treatment resulted in a marked decrease in the serum endotoxin level (EAA <0.4). However, after 48 h, tachycardia did not improve, left ventricular ejection fraction was 20%, and circulatory insufficiency progressed. Therefore, considering the involvement of septic cardiomyopathy and cardiogenic shock, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) was initiated for circulation assistance on day 3 from admission. Continuous cytokine hemoadsorption (Cytosorb®, Cytosorbent Corporation, Monmouth Junction, NJ, USA) was incorporated into a VA-ECMO circuit for 48 h without a considerable improvement. For this reason, a 72-h continuous veno-venous hemodialysis session was started in which a high cutoff filter was used. Tachycardia and myocardial dysfunction improved by day 6, and VA-ECMO was withdrawn on the tenth day. Subsequently, nutrition management and rehabilitation were performed, and the patient was transferred to the department of respiratory medicine on day 80, he was discharged from our hospital on day 113. Sequential extracorporeal therapy may be beneficial when concomitant with circulatory assistance in uncontrollable cases of septic shock using catecholamines and blockers.

scholarly journals P818 Association between baseline left ventricular longitudinal strain and follow-up left ventricular ejection fraction in patients with dilated cardiomyopathy

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
I H Jung ◽  
Y S Byun ◽  
J H Park
Keyword(s):  
Ejection Fraction ◽  
Longitudinal Strain ◽  
Myocardial Dysfunction ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Reverse Remodeling ◽  
Lv Function ◽  
Ventricular Ejection Fraction

Abstract Funding Acknowledgements no Background Left ventricular global longitudinal strain (LV GLS) offers sensitive and reproducible measurement of myocardial dysfunction. The authors sought to evaluate whether LV GLS at the time of diagnosis may predict LV reverse remodeling (LVRR) in DCM patients with sinus rhythm and also investigate the relationship between baseline LV GLS and follow-up LVEF. Methods We enrolled patients with DCM who had been initially diagnosed, evaluated, and followed at our institute. Results During the mean follow-up duration of 37.3 ± 21.7 months, LVRR occurred in 28% of patients (n = 45) within 14.7 ± 10.0 months of medical therapy. The initial LV ejection fraction (LVEF) of patients who recovered LV function was 26.1 ± 7.9% and was not different from the value of 27.1 ± 7.4% (p = 0.49) of those who did not recover. There was a moderate and highly significant correlation between baseline LV GLS and follow-up LVEF (r = 0.717; p &lt;0.001). Conclusion There was a significant correlation between baseline LV GLS and follow-up LVEF in this population. Baseline Follow-up Difference (95% CI) p-value All patients (n = 160) LVEDDI, mm/m2 35.6 ± 6.6 35.6 ± 6.6 -2.7 (-3.4 to -2.0) &lt;0.001 LVESDI, mm/m2 30.3 ± 6.1 26.6 ± 6.6 -3.7 (-4.6 to -2.8) &lt;0.001 LVEDVI, mL/m2 95.0 ± 30.7 74.3 ± 30.2 -20.7 (-25.6 to -15.8) &lt;0.001 LVESVI, mL/m2 70.0 ± 24.8 50.2 ± 26.8 -19.8 (-24.2 to -15.4) &lt;0.001 LVEF, % 26.8 ± 7.5 33.9 ± 12.6 7.2 (5.2 to 9.2) &lt;0.001 LV GLS (-%) 9.2 ± 3.1 11.0 ± 4.8 1.8 (1.3 to 2.2) &lt;0.001 Patients without LVRR (n = 115) LVEDDI, mm/m2 34.9 ± 6.8 34.1 ± 6.8 -0.8 (-1.3 to -0.3) 0.002 LVESDI, mm/m2 29.5 ± 6.1 28.4 ± 6.4 -1.4 (-1.8 to -0.4) 0.002 LVEDVI, mL/m2 92.0 ± 30.5 83.4 ± 29.8 -8.6 (-12.4 to -4.8) &lt;0.001 LVESVI, mL/m2 67.1 ± 24.4 59.5 ± 25.3 -7.6 (-10.9 to -4.3) &lt;0.001 LVEF, % 27.1 ± 7.4 27.8 ± 7.4 0.7 (-0.2 to 1.6) 0.126 LV GLS (-%) 8.2 ± 2.9 8.7 ± 3.2 0.5 (0.7 to 3.6) &lt;0.001 Patients with LVRR (n = 45) LVEDDI, mm/m2 37.4 ± 5.5 29.8 ± 5.2 -7.5 (-9.1 to -6.0) &lt;0.001 LVESDI, mm/m2 32.2 ± 5.7 21.9 ± 4.4 -10.3 (-11.9 to -8.6) &lt;0.001 LVEDVI, mL/m2 102.7 ± 30.2 51.1 ± 15.0 -51.7 (-61.6 to -41.7) &lt;0.001 LVESVI, mL/m2 77.3 ± 24.5 26.4 ± 11.3 -50.9 (-58.8 to -43.1) &lt;0.001 LVEF, % 26.1 ± 7.9 49.4 ± 9.5 23.9 (20.4 to 27.5) &lt;0.001 LV GLS (-%) 11.9 ± 1.6 16.9 ± 2.7 5.1 (4.2 to 5.9) &lt;0.001 Baseline and Follow-up LV Functional Echocardiographic Data Abstract P818 Figure.

scholarly journals Myocardial Work Efficiency, A Novel Measure of Myocardial Dysfunction, Is Reduced in COVID-19 Patients and Associated With In-Hospital Mortality

2021 ◽  
Vol 8 ◽  
Author(s):  
Anum S. Minhas ◽  
Nisha A. Gilotra ◽  
Erin Goerlich ◽  
Thomas Metkus ◽  
Brian T. Garibaldi ◽  
...  
Keyword(s):  
Hospital Mortality ◽  
Systemic Inflammation ◽  
Interleukin 6 ◽  
Myocardial Dysfunction ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Work Efficiency ◽  
Ventricular Ejection Fraction ◽  
Adjusted Logistic Regression

Background: Although troponin elevation is common in COVID-19, the extent of myocardial dysfunction and its contributors to dysfunction are less well-characterized. We aimed to determine the prevalence of subclinical myocardial dysfunction and its association with mortality using speckle tracking echocardiography (STE), specifically global longitudinal strain (GLS) and myocardial work efficiency (MWE). We also tested the hypothesis that reduced myocardial function was associated with increased systemic inflammation in COVID-19.Methods and Results: We conducted a retrospective study of hospitalized COVID-19 patients undergoing echocardiography (n = 136), of whom 83 and 75 had GLS (abnormal &gt;−16%) and MWE (abnormal &lt;95%) assessed, respectively. We performed adjusted logistic regression to examine associations of GLS and MWE with in-hospital mortality. Patients were mean 62 ± 14 years old (58% men). While 81% had normal left ventricular ejection fraction (LVEF), prevalence of myocardial dysfunction was high by STE; [39/83 (47%) had abnormal GLS; 59/75 (79%) had abnormal MWE]. Higher MWE was associated with lower in-hospital mortality in unadjusted [OR 0.92 (95% CI 0.85–0.99); p = 0.048] and adjusted models [aOR 0.87 (95% CI 0.78–0.97); p = 0.009]. In addition, increased systemic inflammation measured by interleukin-6 level was associated with reduced MWE.Conclusions: Subclinical myocardial dysfunction is common in COVID-19 patients with clinical echocardiograms, even in those with normal LVEF. Reduced MWE is associated with higher interleukin-6 levels and increased in-hospital mortality. Non-invasive STE represents a readily available method to rapidly evaluate myocardial dysfunction in COVID-19 patients and can play an important role in risk stratification.

scholarly journals Case Report: Takotsubo Syndrome Associated With Novel Coronavirus Disease 2019

2021 ◽  
Vol 8 ◽  
Author(s):  
Sofia Ortuno ◽  
Mathieu Jozwiak ◽  
Jean-Paul Mira ◽  
Lee S. Nguyen
Keyword(s):  
Cardiac Function ◽  
Takotsubo Cardiomyopathy ◽  
Viral Infections ◽  
Troponin T ◽  
Myocardial Dysfunction ◽  
Apical Ballooning ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Novel Coronavirus

Background: Takotsubo cardiomyopathy is triggered by emotional or physical stress. It is defined as a reversible myocardial dysfunction, usually with apical ballooning aspect due to apical akinesia associated with hyperkinetic basal left ventricular contraction. Described in cases of viral infections such as influenza, only few have been reported associated with novel coronavirus disease 2019 (COVID-19) in the recent pandemic.Case summary: A 79-years-old man, with cardiovascular risk factors (type 2 diabetes and hypertension) and chronic kidney disease, presented to the emergency room for severe dyspnea after 8 days of presenting respiratory symptoms and fever. Baseline electrocardiogram (ECG) was normal, but he presented marked inflammatory syndrome. He was transferred to an intensive care unit to receive mechanical ventilation within 6 h, due to acute respiratory distress syndrome. He presented circulatory failure 2 days after, requiring norepinephrine support (up to up to 1.04 μg/kg/min). Troponin T was elevated (637 ng/l). ECG showed diffuse T wave inversion. Echocardiography showed reduced left ventricular ejection fraction (LVEF 40%), with visual signs of Takotsubo cardiomyopathy. Cardiac failure resolved after 24 h with troponin T decrease (433 ng/l) and restoration of cardiac function (LVEF 60% with regression of Takotsubo features). Patient died after 15 days of ICU admission, due to septic shock from ventilator-acquired pneumonia. Cardiac function was then normal.Conclusion: Mechanisms of Takotsubo cardiomyopathy in viral infections include catecholamine-induced myocardial toxicity and inflammation related to sepsis. Differential diagnoses include myocarditis and myocardial infarction. Evidence of the benefit of immunomodulatory drugs and dexamethasone are growing to support this hypothesis in COVID-19.

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