Abstract 2629: High Dose Erythropoietin Improves the Postresuscitation Myocardial Dysfunction and Survival in an Appropriate Therapeutic Time Window

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Chien-Hua Huang ◽  
Chiung-Yuan Hsu ◽  
Huei-Wen Chen ◽  
Wei-Tien Chang ◽  
Wen-Jone Chen
Keyword(s):  
Cardiac Arrest ◽  
Time Window ◽  
Myocardial Dysfunction ◽  
Treated Group ◽  
Left Ventricular ◽  
Control Group ◽  
Male Adult ◽  
Term Survival ◽  
Therapeutic Time Window ◽  
Induced Cardiac Arrest

Introduction: The myocardial dysfunction carries high mortality rate in the postresuscitation period. Interventions for improving myocardial dysfunction may improve the outcomes of resuscitated victims. The erythropoietin (EPO) provides protective effects for the myocardium with ischemia-reperfusion injuries. However, its effects on the treatment of cardiopulmonary arrest and post-resuscitation myocardial dysfunction remain unknown. Hypothesis: EPO can improve the postresuscitation myocardial dysfunction in an appropriate therapeutic time window. Methods: Asphyxia-induced cardiac arrest was performed in male adult Wistar rats. Cardiopulmonary resuscitation including chest compressions, mechanical ventilation and epinephrine (0.01 mg/kg) was begun after 6.5 or 9.5 minutes of asphyxia. Animals were randomized to undergo treatment with intravenous EPO (5000 U/kg) or equivalent volume of 0.9% saline placebo. These agents were administrated 3 minutes after the return of spontaneous circulation. Results: The better left ventricular dP/dt 40 (2958±827 vs. 1321±1200 mmHg/s, P<0.05) and maximal -dP/dt (2562±546 vs. 745±877 mmHg/s, P<0.05) at 120 minutes after cardiac arrest, and better left ventricular fraction shortening (32.0 ± 2.0 vs. 24 ± 6.7 %, P<0.05) by echocardiography at 90 minutes after cardiac arrest were noted in the EPO-treated group compared to the control group in the condition of 6.5 minutes of asphyxia. The EPO treated group had better neurological recovery at 24 hours after resuscitation. Survival rate at 72 hours after 6.5 minutes of asphyxia was better in the EPO-treated group (50% vs. 20 %, P=0.02). No animal survived 72 hours after 9.5 minutes of asphyxia either in EPO-treated or control group. More activation of cardiac Akt and ERK 42/44 signaling pathways were noted in the EPO-treated group than the control group. Conclusions: EPO has the potential to improve postresuscitation myocardial dysfunction and short term survival in rats after asphyxia-induced cardiac arrest in an appropriate therapeutic time window.

Cardiopulmonary resuscitation in a rat model of chronic myocardial ischemia

2006 ◽  
Vol 101 (4) ◽  
pp. 1091-1096 ◽  
Author(s):  
Xiangshao Fang ◽  
Wanchun Tang ◽  
Shijie Sun ◽  
Lei Huang ◽  
Yun-Te Chang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Coronary Artery ◽  
Cardiopulmonary Resuscitation ◽  
Myocardial Ischemia ◽  
Rat Model ◽  
Myocardial Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Chronic Myocardial Ischemia

Our group has developed a rat model of cardiac arrest and cardiopulmonary resuscitation (CPR). However, the current rat model uses healthy adult animals. In an effort to more closely reproduce the event of cardiac arrest and CPR in humans with chronic coronary disease, a rat model of coronary artery constriction was investigated during cardiac arrest and CPR. Left coronary artery constriction was induced surgically in anesthetized, mechanically ventilated Sprague-Dawley rats. Echocardiography was used to measure global cardiac performance before surgery and 4 wk postsurgery. Coronary constriction provoked significant decreases in ejection fraction, increases in left ventricular end-diastolic volume, and increases left ventricular end-systolic volume at 4 wk postintervention, just before induction of ventricular fibrillation (VF). After 6 min of untreated VF, CPR was initiated on three groups: 1) coronary artery constriction group, 2) sham-operated group, and 3) control group (without preceding surgery). Defibrillation was attempted after 6 min of CPR. All the animals were resuscitated. Postresuscitation myocardial function as measured by rate of left ventricular pressure increase at 40 mmHg and the rate of left ventricular pressure decline was more significantly impaired and left ventricular end-diastolic pressure was greater in the coronary artery constriction group compared with the sham-operated group and the control group. There were no differences in the total shock energy required for successful resuscitation and duration of survival among the groups. In summary, this rat model of chronic myocardial ischemia was associated with ventricular remodeling and left ventricular myocardial dysfunction 4 wk postintervention and subsequently with severe postresuscitation myocardial dysfunction. This model would suggest further clinically relevant investigation on cardiac arrest and CPR.

Abstract 11: Beneficial Effects of Hcn Inhibitor on Post-Resuscitation Myocardial Dysfunction in a Porcine Model of Cardiac Arrest

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Min Yang ◽  
Tianfeng Hua ◽  
Limin Chen ◽  
Yangyang Zou
Keyword(s):  
Heart Rate ◽  
Cardiac Arrest ◽  
Placebo Group ◽  
Porcine Model ◽  
Troponin I ◽  
Myocardial Dysfunction ◽  
Velocity Ratio ◽  
Left Ventricular ◽  
Control Group ◽  
Histopathological Analysis

Introduction: Previous studies have demonstrated that β-adrenergic blocking agents improved neurologic function and the rate of survival. However, its negative inotrope effects that increased the severity of PRMD (post-resuscitation myocardial dysfunction). We studied whether ivabradine (IVA) improves PRMD in a cardiac arrest model. Hypothesis: we hypothesized that the rational use of IVA would improve severity of PRMD and prognosis in a porcine model of CA. Methods: Ventricular fibrillation was induced and untreated for 8 minutes in anesthetized domestic swine while defibrillation was attempted after 6 minutes of cardiopulmonary resuscitation. Hemodynamic parameters were monitored continuously after ROSC. Mitral E/A ratio and E/e′ velocity ratio were assessed by echocardiography at Baseline, PR 1, 2, 4, 8 and 24hours after ROSC. The levels of cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured by ELISA method at Baseline, PR 1, 4 and 24hours. The animals were euthanized 24h after ROSC, and the cardiac tissue was removed for histopathological analysis. Results: Heart rate in the IVA group reduced significantly compared with the control group (all P < 0.05) at PR 1, 2, 4, 8hours. Animals subjected to IVA groups presented significantly better post-resuscitation relaxation function (E/A, E/e′) than those in the Placebo groups (all P < 0.05) (Figure1). IVA group had a lower cTnI and NT-proBNP levels than Placebo group at PR 1, 4 and 24hours (all P < 0.05) (Figure1). Biopsy score in the IVA group was significantly lower at PR 24hours when compared with the Placebo group (all P < 0.05) (Figure2). Conclusions: Heart rate reduction with IVA, improved left ventricular diastolic function and reduced myocardial injury.

ERYTHROPOIETIN IMPROVES THE POSTRESUSCITATION MYOCARDIAL DYSFUNCTION AND SURVIVAL IN THE ASPHYXIA-INDUCED CARDIAC ARREST MODEL

Shock ◽  
2007 ◽  
Vol 28 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Chien-Hua Huang ◽  
Chiung-Yuan Hsu ◽  
Huei-Wen Chen ◽  
Min-Shan Tsai ◽  
Hsiao-Ju Cheng ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Myocardial Dysfunction ◽  
Induced Cardiac Arrest

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 87: Cyclosporin A does not Prevent Myocardial Dysfunction after Resuscitation from Cardiac Arrest in Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Iyad M Ayoub ◽  
Jeejabai Radhakrishnan ◽  
Raúl J Gazmuri
Keyword(s):  
Cardiac Arrest ◽  
Cyclosporin A ◽  
Chest Compression ◽  
Rat Model ◽  
Mitochondrial Permeability Transition ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
List Type ◽  
Ischemia And Reperfusion ◽  
Biphasic Waveform

Objective: We have previously reported in a rat model of VF and closed-chest resuscitation that cytochrome c is released into the bloodstream after resuscitation from cardiac arrest attaining plasma levels inversely proportional to survival. Recent evidence indicates that release of cytochrome c during ischemia and reperfusion may be a manifestation of prolonged opening of the mitochondrial permeability transition pore (mPTP). In this study, we investigated whether cyclosporin A (CsA, an inhibitor of mPTP opening) can prevent post-resuscitation (PR) myocardial dysfunction and improve survival. Methods: VF was electrically induced and left untreated for 10 mins. Resuscitation was attempted by 8 mins of chest compression followed by biphasic waveform defibrillation. Rats were randomized to received a bolus CsA (10 mg/kg) five minutes before inducing VF (n=6), immediately before starting chest compression (n=6), or to receive vehicle control before inducing VF (n=3) or before starting chest compression (n=3). CsA-treated (n=12) and vehicle-treated (n=6) rats were pooled for this analysis after noticing no differences between subgroups. Resuscitated rats were monitored for up to 6 hours. Results: All rats were successfully resuscitated. Treatment with CsA did not improve PR myocardial function (Table ). Survival time was comparable between CsA-treated (321±67 mins) and vehicle-treated (331±67 mins) rats. Conclusions: In our rat model of VF and resuscitation, CsA failed to prevent PR myocardial dysfunction and improve survival. These data contrast with numerous studies demonstrating a protective effect in isolated heart models of ischemia and reperfusion. Two possible explanations are the mPTP does not open in this unique setting of cardiac arrest and resuscitation, and the optimal in vivo dose of CsA needs to be determined as the protective effects of CsA are dose dependent. Hemodynamic and Left Ventricular Function

Abstract 14632: Effect of Obesity on Myocardial Strain Determined by Speckle Tracking Imaging

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Meihua Zhu ◽  
Cole Streiff ◽  
Tao He ◽  
Muhammad Ashraf ◽  
Jiahui Zhang ◽  
...  
Keyword(s):  
Speckle Tracking ◽  
Myocardial Dysfunction ◽  
Global Longitudinal Strain ◽  
Myocardial Strain ◽  
Left Ventricular ◽  
Control Group ◽  
Speckle Tracking Imaging ◽  
Initial Weight ◽  
Newborn Mice ◽  
2D Speckle Tracking

Introduction: Obesity may affect cardiac function, which is hard to detect by traditional echocardiography in the early stages. Speckle tracking imaging (STI) is sensitive to subtle myocardial dysfunction. The aim of this study was to determine the influence of obesity on left ventricular (LV) myocardial function in diet-induced obesity (DIO) mice using two-dimensional (2D) speckle tracking echocardiography (STE). Hypothesis: 2D STE is useful to detect obesity-caused myocardial dysfunction. Methods: Twenty newborn mice were divided into two groups: a DIO group (high-fat diet) and a control group (regular-fat diet). 2D image loops were acquired at the end of each month for 6 months. Global longitudinal strain (GLS) and global circumferential strain (GCS) were analyzed at feeding periods over 3 months and 6 months, and compared between the two groups. Results: The control group gained 64% of its initial weight, while the DIO group gained 82% of its initial weight at the 3 month feeding period; and the two groups gained 88% (control) and 125% (DIO) respectively at 6 months. STE analysis revealed an insignificant decrease in strain values in the DIO mice after 3 months; however, after 6 months, the DIO group demonstrated a significant decrease in strain values (P<0.05) despite normal ejection fractions in both groups. Conclusions: 2D STE is highly feasible to detect the myocardial dysfunction caused by obesity in earlier stage. These strain values appear to be related to the severity of obesity.

scholarly journals P321 Cardiotoxicity related to cancer therapy. is the study of mechanical dispersion an additional value?

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
F Privitera ◽  
V Losi ◽  
I P Monte
Keyword(s):  
Ventricular Dysfunction ◽  
Myocardial Dysfunction ◽  
Global Longitudinal Strain ◽  
Treated Group ◽  
Left Ventricular ◽  
Lv Function ◽  
Breast Cancer Chemotherapy ◽  
Mechanical Dispersion ◽  
Group 2 ◽  
Group 1

Abstract Myocardial dysfunction are the most concerning cardiovascular complications of cancer therapies with a poor prognosis, so it’s critical to detect subclinical cardiac abnormalities in order to start cardioprotective therapy early or increased surveillance frequency. Global longitudinal strain (GLS) by echocardiography is an excellent tool for assessing regional and global left ventricular (LV) function. Mechanical dispersion (MD) reflects heterogeneous myocardial contraction, evaluated in many cardiopathies. We evaluated subclinical myocardial dysfunction by GLS and MD using 2D Speckle-tracking Echo, in order to established if MD could be a predictor of ventricular dysfunction in the field of Cardiotoxicity (CTX). Were enrolled 42 women with breast cancer chemotherapy-treated and underwent to Echo evaluation during 3- and 6-months follow-up, compared to evaluation performed before starting chemotherapy (T0). Depending on chemotherapy type were identified 2 groups: Anthracyclines ± Taxol treated (group 1) and Anti-HER2 treated (group 2). CTX diagnosis was made according ESC criteria: LVEF &lt; 50%, LVEF decrease &gt;10% or GLS decrease &gt;15% compared to previous check. At three months, 28% patients (p &lt; 0,009) developed CTX and, in this group, MD was significantly increased compared to T0 (64,4ms ± 18,6 vs 43,48ms ± 7.88 p &lt; 0,001). This finding was consistent regardless treatment group: 65,2 ms ± 5,30 (p &lt; 0.0001) in group 1 and 63,14 ms ± 36,40 (p 0.02) in group 2. Also, GLS was significantly changed: in CTX patients decreased of 9% compared to T0 (p 0.02), but this finding was consistent in group 1 in which GLS decreased of 18% (p 0,01), while in group 2 decrease only of 5% and wasn’t statistically significant compared to T0 (p = 0,3). These patients were treated by beta-blockers or ACE-inhibitors. At six months there was a normalization of MD value (47.7 ± 15.97 ms in CTX group) that was not statistically significant compared to T0 (p = 0,2) and we have interpreted as consequence of positive effect induced by cardioprotective therapy. We believe that MD is a predictor of ventricular dysfunction earlier than GLS during Anti-HER2 treatment, so in this field MD could integrates information obtained from GLS about subclinical dysfunction.

scholarly journals Speckle Tracking Echocardiography and All-Cause and Cardiovascular Mortality Risk in Chronic Kidney Disease Patients

2019 ◽  
Vol 44 (4) ◽  
pp. 690-703 ◽  
Author(s):  
Laura Jahn ◽  
Rafael Kramann ◽  
Nikolaus Marx ◽  
Jürgen Floege ◽  
Michael Becker ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mortality Risk ◽  
Speckle Tracking ◽  
Speckle Tracking Echocardiography ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Control Group ◽  
Increased Risk ◽  
All Cause Mortality

Background and Objectives: Patients with chronic kidney disease (CKD) exhibit a highly increased risk of cardiovascular (CV) morbidity and mortality. Subtle changes in left ventricular function can be detected by two-dimensional (2D) speckle tracking echocardiography (STE). This study investigated whether myocardial dysfunction detected by 2D STE may aid in CV and all-cause mortality risk assessment in patients with CKD stages 3 and 4. Method: A study group of 285 patients (CKD 3: 193 patients; CKD 4: 92 patients) and a healthy control group (34 participants) were included in the retrospective study. 2D STE values as well as early and late diastolic strain rates were measured in ventricular longitudinal, circumferential and radial directions. Patients’ CV and all-cause outcome was determined. Results: In the CKD group all measured longitudinal STE values and radial strain were significantly reduced compared to the control group. Cox proportional hazards regression revealed global longitudinal strain to predict CV and all-cause mortality (hazard ratio [HR] 1.15, 95% CI 1.06–1.25; p = 0.0008 and HR 1.09, 95% CI 1.04–1.14; p = 0.0003). After adjustment for sex, age, diabetes, estimated glomerular filtration rate, and preexisting CV disease, this association was maintained for CV mortality and all-cause mortality (HR 1.16, 95% CI 1.06–1.27; p = 0.0019 and HR 1.08, 95% CI 1.03–1.14; p = 0.0026, respectively). Conclusions: The present study shows that 2D STE detects reduced left ventricular myocardial function and allows the prediction of CV and all-cause mortality in patients at CKD stages 3 and 4.

scholarly journals Insulin Preconditioning Elevates p-Akt and Cardiac Contractility after Reperfusion in the Isolated Ischemic Rat Heart

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Tamaki Sato ◽  
Hiroaki Sato ◽  
Takeshi Oguchi ◽  
Hisashi Fukushima ◽  
George Carvalho ◽  
...  
Keyword(s):  
Myocardial Dysfunction ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Control Group ◽  
Optimal Timing ◽  
Insulin Administration ◽  
Rat Hearts ◽  
Reperfusion Period ◽  
Pressure Development ◽  
And Control

Insulin induces cardioprotection partly via an antiapoptotic effect. However, the optimal timing of insulin administration for the best quality cardioprotection remains unclear. We tested the hypothesis that insulin administered prior to ischemia provides better cardioprotection than insulin administration after ischemia. Isolated rat hearts were prepared using Langendorff method and divided into three groups. The Pre-Ins group (Pre-Ins) received 0.5 U/L insulin prior to 15 min no-flow ischemia for 20 min followed by 20 min of reperfusion. The Post-Ins group (Post-Ins) received 0.5 U/L insulin during the reperfusion period only. The control group (Control) was perfused with KH buffer throughout. The maximum of left ventricular derivative of pressure development (dP/dt(max)) was recorded continuously. Measurements of TNF-αand p-Akt in each time point were assayed by ELISA. After reperfusion, dP/dt(max) in Pre-Ins was elevated, compared with Post-Ins at 10 minutes after reperfusion and Control at all-time points. TNF-αlevels at 5 minutes after reperfusion in the Pre-Ins were lower than the others. After 5 minutes of reperfusion, p-Akt was elevated in Pre-Ins compared with the other groups. Insulin administration prior to ischemia provides better cardioprotection than insulin administration only at reperfusion. TNF-αsuppression is possibly mediated via p-Akt leading to a reduction in contractile myocardial dysfunction.

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