Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction

Lévy, Bruno; Clère-Jehl, Raphaël; Legras, Annick; Morichau‐Beauchant, Tristan; Léone, Marc; Ganster, Frédérique; Quenot, Jean‐Pierre; Kimmoun, Antoine; Cariou, Alain; Lassus, Johan; Harjola, Veli‐Pekka; Meziani, Ferhat; Louis, Guillaume; Rossignol, Patrick; Duarte, Kévin; Girerd, Nicolas; Mebazaa, Alexandre; Vignon, Philippe; Mattéi, M.; Thivilier, Carine; Perez, Pierre; Auchet, Thomas; Fritz, Caroline; Boisrame-Helme, Julie; Mercier, Emmanuelle; Garot, Denis; Perny, Jessica; Gette, Sébastien; Hammad, Emmanuelle; Vigne, Coralie; Dargent, Auguste; Andreu, Pascal; Guiot, P.

doi:10.1016/j.jacc.2018.04.051

Cited by 317 publications

(252 citation statements)

References 38 publications

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“…OptimaCC is a homogeneous and severe population of CS with low cardiac index despite high doses of catecholamines at ICU admission . This presentation reflected the current definition of CS, which was associated with a high degree of inflammation and vasoplegia .…”

Section: Discussionmentioning

confidence: 59%

“…The primary outcome was the change in cardiac index and the secondary outcomes were changes in other haemodynamic variables, cardiac power index, lactate levels, lactate clearance, biomarker levels, and Sequential Organ Failure Assessment (SOFA) score evolution. A detailed description of the study design and main results have been previously published . Of note, in 2015 the safety monitoring board reported a significant imbalance between the epinephrine and norepinephrine groups for the occurrence of refractory CS.…”

Section: Methodsmentioning

confidence: 99%

“…Non‐inclusion criteria were mainly: shock of other origin; immediate indication for MCS; cardiac arrest with early signs of cerebral anoxia; and septic, toxic, and obstructive cardiomyopathy. Refractory CS was previously defined as a CS with major cardiac dysfunction assessed according to echocardiography, elevated lactate level, acute deterioration of organ function despite the use of >1 μg/kg/min of epinephrine/norepinephrine or dobutamine >10 μg/kg/min and/or intra‐aortic balloon support and sustained hypotension (systolic arterial pressure <90 mmHg or mean arterial pressure <65 mmHg) despite adequate intravascular volume.…”

Section: Methodsmentioning

confidence: 99%

“…The initial protocol was detailed in the princeps paper. 21 In summary, patients with CS already treated by a vasopressor had to be randomized in the 6 h following the initiation of this vasopressor. After initiation of the study drug, the initial open-label vasopressor was discontinued.…”

Section: Study Treatment and Protocolmentioning

confidence: 99%

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Circulating dipeptidyl peptidase 3 and alteration in haemodynamics in cardiogenic shock: results from the OptimaCC trial

Takagi

Blet

Lévy

et al. 2019

European J of Heart Fail

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Aims Dipeptidyl peptidase 3 (DPP3) is a protease involved in the degradation of cardiovascular mediators. Its administration has been shown to be associated with impaired cardiac contraction and kidney haemodynamics while its inhibition restored cardiac contraction in a pre‐clinical model of severe heart failure in mice. Circulating DPP3 (cDPP3) was found to be elevated in shock. The present study aims to assess the association between cDPP3 and worsening haemodynamics, namely refractory shock, in a cohort of cardiogenic shock (CS). Methods and results This is an ancillary study of OptimaCC, a prospective, double‐blind, multicentre, randomized study assessing efficacy and safety of catecholamines in 57 patients with CS after acute myocardial infarction. cDPP3 was measured in plasma at inclusion, 24 h, 48 h, and 72 h, and haemodynamic and biological parameters were recorded at inclusion. cDPP3 values were higher in refractory CS than non‐refractory CS at inclusion (median [interquartile range]; 76.1 [37.9–238.7] ng/mL vs. 32.8 [23.9–47.6] ng/mL, P = 0.014), at 24 h (P < 0.001) and up to 48 h (P = 0.027). Furthermore, cDPP3 at inclusion discriminated CS patients who did develop refractory shock vs. non‐refractory with an area under the curve of 0.73 (95% confidence interval [CI] 0.55–0.92). The high cDPP3 group (cDPP3 ≥59.1 ng/mL) at inclusion had a higher Simplified Acute Physiology Score II (SAPS II), lower cardiac index and lower estimated glomerular filtration rate. More importantly, in CS patients with high cDPP3 at inclusion, those who rapidly decreased cDPP3 at 24 h exhibited a striking reduction in the occurrence of refractory shock and death. Conclusion In CS patients, cDPP3 gives an early prediction of outcome, including development of refractory status and/or survival. Clinical Trial Registration: http://clinicaltrials.gov Identifier NCT01367743

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Section: Discussionmentioning

confidence: 59%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Study Treatment and Protocolmentioning

confidence: 99%

See 2 more Smart Citations

Circulating dipeptidyl peptidase 3 and alteration in haemodynamics in cardiogenic shock: results from the OptimaCC trial

Takagi

Blet

Lévy

et al. 2019

European J of Heart Fail

Self Cite

View full text Add to dashboard Cite

show abstract

“…This is an ancillary study of the OptimaCC trial, which was a randomized controlled trial designed to assess the efficacy of different vasopressors in cardiogenic shock after AMI . cDPP3 levels were measured at 24, 48 and 72 h after the initiation of vasopressors.…”

mentioning

confidence: 99%

Circulating plasma dipeptidyl dipeptidase 3 and the prognosis of cardiogenic shock

Raju

McCullough

2019

European J of Heart Fail

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Cardiogenic Shock After Acute Myocardial Infarction

Samsky

Morrow

Proudfoot

et al. 2021

JAMA

179

101

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ardiogenic shock (CS) is defined by systemic hypoperfusion and tissue hypoxia due to cardiac dysfunction. The most common etiology of CS is acute myocardial ischemia due to occlusion of an epicardial coronary artery, resulting in regional cardiac myocyte necrosis (acute myocardial infarction [AMI]) and loss of ventricular function. 1 CS is the leading cause of in-hospital death in patients with AMI. Between 40 000 and 50 000 patients in the US have CS associated with AMI each year, which correlates to an incidence of approximately 5% to 10% of all patients with AMI. [2][3][4][5] Thirty-day mortality is nearly 40% and approaches approximately 50% at 1 year (Box). [5][6][7][8] Severe left ventricular (LV) dysfunction is the most common presentation of CS in the setting of AMI, most frequently occurring after anterior MI. Of the 686 patients included in the Percutaneous Coronary Intervention Strategies with Acute Myocardial Infarction and Cardiogenic Shock (CULPRIT-SHOCK) trial, 288 (42.0%) had a left anterior descending MI and 53 (7.7%) had a left main coronary artery MI. 7 Few treatment approaches reduce short-or long-term morbidity and mortality in patients with CS. This review describes the pathophysiology, diagnosis, and management of CS in the setting of AMI. MethodsA literature search was performed that applied the Cochrane Highly Sensitive Search Strategy for randomized clinical trials (RCTs), a string for meta-analyses and systematic reviews, and established Medical Subject Headings for "cardiogenic shock" and "treatment" to the PubMed and Cochrane databases for articles published from January 1, 1995, through August 5, 2021. The literature search identified 1552 articles. The authors prioritized RCTs, meta-analyses, and larger observational studies. A total of 46 papers were included, including 12 randomized trials, 2 metaanalyses, 1 systematic review, and 31 observational studies.

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Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction

Cited by 317 publications

References 38 publications

Circulating dipeptidyl peptidase 3 and alteration in haemodynamics in cardiogenic shock: results from the OptimaCC trial

Circulating dipeptidyl peptidase 3 and alteration in haemodynamics in cardiogenic shock: results from the OptimaCC trial

Circulating plasma dipeptidyl dipeptidase 3 and the prognosis of cardiogenic shock

Cardiogenic Shock After Acute Myocardial Infarction

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