Severe Myocardial Dysfunction after Non-Ischemic Cardiac Arrest: Effectiveness of Percutaneous Assist Devices.
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ABSTRACT: Introduction
Despite the improvements in standardized cardiopulmonary resuscitation, survival remains low, mainly due to initial myocardial dysfunction and hemodynamic instability. Our goal was to compare the efficacy of two left ventricular assist devices on resuscitation and hemodynamic supply in a porcine model of ventricular fibrillation (VF) cardiac arrest.Methods
Seventeen anaesthetized pigs had 12 min of untreated VF followed by 6 min of chest compression and boluses of epinephrine. Next, a first defibrillation was attempted and pigs were randomized to any of the three groups: control (n = 5), implantation of an percutaneous left ventricular assist device (Impella, n = 5) or extracorporeal membrane oxygenation (ECMO, n = 7). Hemodynamic and myocardial functions were evaluated invasively at baseline, at return of spontaneous circulation (ROSC), after 10-30-60-120-240 min post-resuscitation. The primary endpoint was the rate of ROSC.Results
Only one of 5 pigs in the control group, 5 of 5 pigs in the Impella group, and 5 of 7 pigs in the ECMO group had ROSC (p < 0.05). Left ventricular ejection fraction at 240 min post-resuscitation was 37.5 ± 6.2% in the ECMO group vs. 23 ± 3% in the Impella group (p = 0.06). No significant difference in hemodynamic parameters was observed between the two ventricular assist devices.Conclusion
Early mechanical circulatory support appeared to improve resuscitation rates in a shockable rhythm model of cardiac arrest. This approach appears promising and should be further evaluated.
SUBMITTER: Manzo-Silberman S
PROVIDER: S-EPMC8396996 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundPercutaneous ventricular assist devices (PVADs) have been replacing intra-aortic balloon pumps for hemodynamic support during percutaneous coronary intervention (PCI), even though data supporting a benefit for hard clinical end points remain limited. We evaluated diffusion of PVADs across US markets and examined the association of market utilization of PVAD with mortality and cost.MethodsUsing the 2013 to 2019 Medicare data, we identified all patients aged ≥65 years who underwent PCI with either a PVAD or intra-aortic balloon pump. We used hospital referral region to define regional health care markets and categorized them in quartiles based on the proportional use of PVADs during PCI. Multilevel models were constructed to determine the association of patient, hospital, and market factors with utilization of PVADs and the association of PVAD utilization with 30-day mortality and cost.ResultsA total of 79 176 patients underwent PCI with either intra-aortic balloon pump (47 514 [60.0%]) or PVAD (31 662 [40.0%]). The proportion of PCI procedures with PVAD increased over time (17% in 2013 to 57% in 2019; P for trend, <0.001), such that PVADs overtook intra-aortic balloon pump for hemodynamic support during PCI in 2018. There was a large variation in PVAD utilization across markets (range, 0%-85%), which remained unchanged after adjustment of patient characteristics (median odds ratio, 2.05 [95% CI, 1.91-2.17]). The presence of acute myocardial infarction, cardiogenic shock, and emergent status was associated with a 45% to 50% lower odds of PVAD use suggesting that PVADs were less likely to be used in the sickest patients. Greater utilization of PVAD at the market level was not associated with lower risk mortality but was associated with higher cost.ConclusionsAlthough utilization of PVADs for PCI continues to increase, there is large variation in PVAD utilization across markets. Greater market utilization of PVADs was not associated with lower mortality but was associated with higher cost.
| S-EPMC10797917 | biostudies-literature
Project description:BackgroundThere are limited data on the complications with a percutaneous left ventricular assist device (pLVAD) vs. intra-aortic balloon pump (IABP) in acute myocardial infarction-cardiogenic shock (AMI-CS).ObjectiveTo assess the trends, rates and predictors of complications.MethodsUsing a 17-year AMI-CS population from the National Inpatient Sample, AMI-CS admissions receiving pLVAD and IABP support were evaluated for vascular, lower limb amputation, hematologic, neurologic and acute kidney injury (AKI) complications. In-hospital mortality, hospitalization costs and length of stay in pLVAD and IABP cohorts with complications was studied.ResultsOf 168,645 admissions, 7,855 (4.7%) receiving pLVAD support. The pLVAD cohort had higher comorbidity, cardiac arrest (36.1% vs. 29.7%) and non-cardiac organ failure (74.7% vs. 56.9%) rates. Complications were higher in pLVAD compared to IABP cohort-overall 69.0% vs. 54.7%; vascular 3.8% vs. 2.1%; lower limb amputation 0.3% vs. 0.3%; hematologic 36.0% vs. 27.7%; neurologic 4.9% vs. 3.5% and AKI 55.4% vs. 39.1% (all p<0.001 except for amputation). Non-White race, higher comorbidity, organ failure, and extracorporeal membrane oxygen use were predictors of complications for both cohorts. The pLVAD cohort with complications had higher in-hospital mortality (45.5% vs. 33.1%; adjusted odds ratio 1.65 [95% confidence interval 1.55-1.75]), shorter duration of hospital stay, and higher hospitalization costs compared to the IABP cohort with complications (all p<0.001). These results were consistent in propensity-matched pairs.ConclusionsAMI-CS admissions receiving pLVAD had higher rates of complications compared to the IABP, with worse in-hospital outcomes in the cohort with complications.
| S-EPMC7444810 | biostudies-literature
Project description:Data on relative safety, efficacy, and role of different percutaneous left ventricular assist devices for hemodynamic support during the ventricular tachycardia (VT) ablation procedure are limited.We performed a multicenter, observational study from a prospective registry including all consecutive patients (N=66) undergoing VT ablation with a percutaneous left ventricular assist devices in 6 centers in the United States. Patients with intra-aortic balloon pump (IABP group; N=22) were compared with patients with either an Impella or a TandemHeart device (non-IABP group; N=44). There were no significant differences in the baseline characteristics between both the groups. In non-IABP group (1) more patients could undergo entrainment/activation mapping (82% versus 59%; P=0.046), (2) more number of unstable VTs could be mapped and ablated per patient (1.05±0.78 versus 0.32±0.48; P<0.001), (3) more number of VTs could be terminated by ablation (1.59±1.0 versus 0.91±0.81; P=0.007), and (4) fewer VTs were terminated with rescue shocks (1.9±2.2 versus 3.0±1.5; P=0.049) when compared with IABP group. Complications of the procedure trended to be more in the non-IABP group when compared with those in the IABP group (32% versus 14%; P=0.143). Intermediate term outcomes (mortality and VT recurrence) during 12±5-month follow-up were not different between both groups. Left ventricular ejection fraction ?15% was a strong and independent predictor of in-hospital mortality (53% versus 4%; P<0.001).Impella and TandemHeart use in VT ablation facilitates extensive activation mapping of several unstable VTs and requires fewer rescue shocks during the procedure when compared with using IABP.
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Project description:AimsHemodynamic instability occurs following cardiac arrest and is associated with high mortality during the post-cardiac period. Urocortin is a novel peptide and a member of the corticotrophin-releasing factor family. Urocortin has the potential to improve acute cardiac dysfunction, as well as to reduce the myocardial damage sustained after ischemia reperfusion injury. The effects of urocortin in post-cardiac arrest myocardial dysfunction remain unclear.Methods and resultsWe developed a preclinical cardiac arrest model and investigated the effects of urocortin. After cardiac arrest induced by 6.5 min asphyxia, male Wistar rats were resuscitated and randomized to either the urocortin treatment group or the control group. Urocortin (10 μg/kg) was administrated intravenously upon onset of resuscitation in the experimental group. The rate of return of spontaneous circulation (ROSC) was similar between the urocortin group (76%) and the control group (72%) after resuscitation. The left ventricular systolic (dP/dt40) and diastolic (maximal negative dP/dt) functions, and cardiac output, were ameliorated within 4 h after ROSC in the urocortin-treated group compared to the control group (P<0.01). The neurological function of surviving animals was better at 6 h after ROSC in the urocortin-treated group (p = 0.023). The 72-h survival rate was greater in the urocortin-treated group compared to the control group (p = 0.044 by log-rank test). Cardiomyocyte apoptosis was lower in the urocortin-treated group (39.9±8.6 vs. 17.5±4.6% of TUNEL positive nuclei, P<0.05) with significantly increased Akt, ERK and STAT-3 activation and phosphorylation in the myocardium (P<0.05).ConclusionsUrocortin treatment can improve acute hemodynamic instability as well as reducing myocardial damage in post-cardiac arrest myocardial dysfunction.
| S-EPMC5104489 | biostudies-literature
Project description:OBJECTIVES:The PAREPET (Prediction of ARrhythmic Events with Positron Emission Tomography) study sought to test the hypothesis that quantifying inhomogeneity in myocardial sympathetic innervation could identify patients at highest risk for sudden cardiac arrest (SCA). BACKGROUND:Left ventricular ejection fraction (LVEF) is the only parameter identifying patients at risk of SCA who benefit from an implantable cardiac defibrillator (ICD). METHODS:We prospectively enrolled 204 subjects with ischemic cardiomyopathy (LVEF ?35%) eligible for primary prevention ICDs. Positron emission tomography (PET) was used to quantify myocardial sympathetic denervation ((11)C-meta-hydroxyephedrine [(11)C-HED]), perfusion ((13)N-ammonia) and viability (insulin-stimulated (18)F-2-deoxyglucose). The primary endpoint was SCA defined as arrhythmic death or ICD discharge for ventricular fibrillation or ventricular tachycardia >240 beats/min. RESULTS:After 4.1 years follow-up, cause-specific SCA was 16.2%. Infarct volume (22 ± 7% vs. 19 ± 9% of left ventricle [LV]) and LVEF (24 ± 8% vs. 28 ± 9%) were not predictors of SCA. In contrast, patients developing SCA had greater amounts of sympathetic denervation (33 ± 10% vs. 26 ± 11% of LV; p = 0.001) reflecting viable, denervated myocardium. The lower tertiles of sympathetic denervation had SCA rates of 1.2%/year and 2.2%/year, whereas the highest tertile had a rate of 6.7%/year. Multivariate predictors of SCA were PET sympathetic denervation, left ventricular end-diastolic volume index, creatinine, and no angiotensin inhibition. With optimized cut-points, the absence of all 4 risk factors identified low risk (44% of cohort; SCA <1%/year); whereas ?2 factors identified high risk (20% of cohort; SCA ?12%/year). CONCLUSIONS:In ischemic cardiomyopathy, sympathetic denervation assessed using (11)C-HED PET predicts cause-specific mortality from SCA independently of LVEF and infarct volume. This may provide an improved approach for the identification of patients most likely to benefit from an ICD. (Prediction of ARrhythmic Events With Positron Emission Tomography [PAREPET]; NCT01400334).
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Project description:BackgroundPercutaneous coronary intervention (PCI) is frequently undertaken in patients with ischemic left ventricular systolic dysfunction. The REVIVED (Revascularization for Ischemic Ventricular Dysfunction)-BCIS2 (British Cardiovascular Society-2) trial concluded that PCI did not reduce the incidence of all-cause death or heart failure hospitalization; however, patients assigned to PCI reported better initial health-related quality of life than those assigned to optimal medical therapy (OMT) alone. The aim of this study was to assess the cost-effectiveness of PCI+OMT compared with OMT alone.MethodsREVIVED-BCIS2 was a prospective, multicenter UK trial, which randomized patients with severe ischemic left ventricular systolic dysfunction to either PCI+OMT or OMT alone. Health care resource use (including planned and unplanned revascularizations, medication, device implantation, and heart failure hospitalizations) and health outcomes data (EuroQol 5-dimension 5-level questionnaire) on each patient were collected at baseline and up to 8 years post-randomization. Resource use was costed using publicly available national unit costs. Within the trial, mean total costs and quality-adjusted life-years (QALYs) were estimated from the perspective of the UK health system. Cost-effectiveness was evaluated using estimated mean costs and QALYs in both groups. Regression analysis was used to adjust for clinically relevant predictors.ResultsBetween 2013 and 2020, 700 patients were recruited (mean age: PCI+OMT=70 years, OMT=68 years; male (%): PCI+OMT=87, OMT=88); median follow-up was 3.4 years. Over all follow-ups, patients undergoing PCI yielded similar health benefits at higher costs compared with OMT alone (PCI+OMT: 4.14 QALYs, £22 352; OMT alone: 4.16 QALYs, £15 569; difference: -0.015, £6782). For both groups, most health resource consumption occurred in the first 2 years post-randomization. Probabilistic results showed that the probability of PCI being cost-effective was 0.ConclusionsA minimal difference in total QALYs was identified between arms, and PCI+OMT was not cost-effective compared with OMT, given its additional cost. A strategy of routine PCI to treat ischemic left ventricular systolic dysfunction does not seem to be a justifiable use of health care resources in the United Kingdom.RegistrationURL: https://www.clinicaltrials.gov; Unique identifier: NCT01920048.
| S-EPMC10782932 | biostudies-literature
Project description:Out-of-hospital cardiac arrest is a leading cause of death worldwide. Rapid diagnosis and initiation of cardiopulmonary resuscitation (CPR) is the cornerstone of therapy for victims of cardiac arrest. Yet a significant fraction of cardiac arrest victims have no chance of survival because they experience an unwitnessed event, often in the privacy of their own homes. An under-appreciated diagnostic element of cardiac arrest is the presence of agonal breathing, an audible biomarker and brainstem reflex that arises in the setting of severe hypoxia. Here, we demonstrate that a support vector machine (SVM) can classify agonal breathing instances in real-time within a bedroom environment. Using real-world labeled 9-1-1 audio of cardiac arrests, we train the SVM to accurately classify agonal breathing instances. We obtain an area under the curve (AUC) of 0.9993 ± 0.0003 and an operating point with an overall sensitivity and specificity of 97.24% (95% CI: 96.86-97.61%) and 99.51% (95% CI: 99.35-99.67%). We achieve a false positive rate between 0 and 0.14% over 82 h (117,985 audio segments) of polysomnographic sleep lab data that includes snoring, hypopnea, central, and obstructive sleep apnea events. We also evaluate our classifier in home sleep environments: the false positive rate was 0-0.22% over 164 h (236,666 audio segments) of sleep data collected across 35 different bedroom environments. We prototype our proof-of-concept contactless system using commodity smart devices (Amazon Echo and Apple iPhone) and demonstrate its effectiveness in identifying cardiac arrest-associated agonal breathing instances played over the air.
| S-EPMC6584582 | biostudies-literature
Project description:BackgroundST-segment elevation myocardial infarction (STEMI) is a frequent cause of sudden cardiac arrest (SCA) and early percutaneous coronary intervention (PCI) is associated with increased survival. Despite constant improvements in SCA management, survival remains poor. We aimed to assess pre-PCI SCA incidence and related outcomes in patients admitted with STEMI.MethodsThis was a prospective cohort study of patients admitted with STEMI in a tertiary university hospital over 11 years. All patients were submitted to emergency coronary angiography. Baseline characteristics, details of the procedure, reperfusion strategies, and adverse outcomes were assessed. The primary outcome was in-hospital mortality. The secondary outcome was 1-year mortality after hospital discharge. Predictors of pre-PCI SCA was also assessed.ResultsDuring the study period 1,493 patients were included; the mean age was 61.1 years (±12), and 65.3% were male. Pre-PCI SCA was present in 133 (8.9%) patients. In-hospital mortality was higher in the pre-PCI SCA group (36.8% vs. 8.8%, p < 0.0001). In multivariate analysis, anterior MI, cardiogenic shock, age, pre-PCI SCA and lower ejection fraction remained significantly associated with in-hospital mortality. When we analyzed the interaction between pre-PCI SCA and cardiogenic shock upon admission there is a further increase in mortality risk when both conditions are present. For predictors of pre-PCI SCA, only younger age and cardiogenic shock remained significantly associated after multivariate analysis. Overall 1-year mortality rates were similar between pre-PCI SCA survivors and non-pre-PCI SCA group.ConclusionIn a cohort of consecutive patients admitted with STEMI, pre-PCI SCA was associated with higher in-hospital mortality, and its association with cardiogenic shock further increases mortality risk. However, long-term mortality among pre-PCI SCA survivors was similar to non-SCA patients. Understanding characteristics associated with pre-PCI SCA may help to prevent and improve the management of STEMI patients.
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Project description:Purpose:We investigated the protective effects and the underlying mechanisms through which recombinant human brain natriuretic peptide (rhBNP) acts on postresuscitation myocardial dysfunction (PRMD) in the cardiac arrest (CA) model. Methods:Ventricular fibrillation was induced and untreated for 6?min. And the time of cardiopulmonary resuscitation was 8?min, after which defibrillation was attempted in this rat model. 24 Sprague Dawley rats (450-550g) were randomized into cardiopulmonary resuscitation (CPR)?+?rhBNP and CPR?+?placebo groups after restoration of spontaneous circulation (ROSC). rhBNP was infused at PR 30?min (loading dose: 1.5?µg/kg, 3?min; maintenance dose: 0.01?µg/kg, 3?min; maintenance dose: 0.01?? (TNF-? (TNF-? (TNF-?B (NF-?B (NF. Results:The administration of rhBNP attenuated the severity of PRMD and myocardial tissue injuries, with improvement of MAP (mean arterial blood pressure), ETCO2 (end-tidal CO2), serum level of NT-proBNP, EF, CO, and MPI values. The serum levels and protein expression levels in myocardial tissue of IL-6 and TNF-? (TNF-?B (NF. Conclusion:Our research demonstrated that the administration of rhBNP attenuated the severity of PRMD and myocardial tissue injuries and increased the 24?h survival rate in this CA model. rhBNP administration also reduced the serum and myocardial tissue levels of IL-6 and TNF-? after ROSC, likely due to the suppression of the TLR4/NF-?B signaling pathway and the regulation of inflammatory mediator secretion.? (TNF-?B (NF.
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Project description:Post‑cardiac arrest myocardial dysfunction (PAMD) is a leading cause of death in patients undergoing resuscitation patients following cardiac arrest (CA). Although prostaglandin E1 (PGE1) is a clinical drug used to mitigate ischemia injury, its effect on PAMD remains unknown. In the present study, the protective effects of PGE1 on PAMD were evaluated in a rat model of CA and in a hypoxia‑reoxygenation (H/R) in vitro model. Rats were randomly assigned to CA, CA+PGE1 or sham groups. Asphyxia for 8 min followed by cardiopulmonary resuscitation were performed in the CA and CA+PGE1 groups. PGE1 was intravenously administered at the onset of return of spontaneous circulation (ROSC). PGE1 treatment significantly increased the ejection fraction and cardiac output within 4 h following ROSC and improved the survival rate, compared with the CA group. Moreover, PGE1 inactivated GSK3β, prevented mitochondrial permeability transition pore (mPTP) opening, while reducing cytochrome c and cleaved caspase‑3 expression, as well as cardiomyocyte apoptosis in the rat model. To examine the underlying mechanism, H/R H9c2 cells were treated with PGE1 at the start of reoxygenation. The changes in GSK3β activity, mPTP opening, cytochrome c and cleaved caspase‑3 expression, and apoptosis of H9c2 cells were consistent with those noted in vivo. The results indicated that PGE1 attenuated PAMD by inhibiting mitochondria‑mediated cardiomyocyte apoptosis.
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