Epinephrine and short-term survival in cardiogenic shock : an individual data meta-analysis of 2583 patients

Correction Volume: 44 Issue: 11 Pages: 2022-2023 DOI: 10.1007/s00134-018-5372-9Catecholamines have been the mainstay of pharmacological treatment of cardiogenic shock (CS). Recently, use of epinephrine has been associated with detrimental outcomes. In the present study we aimed to evaluate the association between epinephrine use and short-term mortality in all-cause CS patients. We performed a meta-analysis of individual data with prespecified inclusion criteria: (1) patients in non-surgical CS treated with inotropes and/or vasopressors and (2) at least 15% of patients treated with epinephrine administrated alone or in association with other inotropes/vasopressors. The primary outcome was short-term mortality. Fourteen published cohorts and two unpublished data sets were included. We studied 2583 patients. Across all cohorts of patients, the incidence of epinephrine use was 37% (17-76%) and short-term mortality rate was 49% (21-69%). A positive correlation was found between percentages of epinephrine use and short-term mortality in the CS cohort. The risk of death was higher in epinephrine-treated CS patients (OR [CI] = 3.3 [2.8-3.9]) compared to patients treated with other drug regimens. Adjusted mortality risk remained striking in epinephrine-treated patients (n = 1227) (adjusted OR = 4.7 [3.4-6.4]). After propensity score matching, two sets of 338 matched patients were identified and epinephrine use remained associated with a strong detrimental impact on short-term mortality (OR = 4.2 [3.0-6.0]). In this very large cohort, epinephrine use for hemodynamic management of CS patients is associated with a threefold increase of risk of death.Peer reviewe

Characterization of the hypercoagulable phenotype in patients with acute heart failure

Malgré le bénéfice observé par de nouvelles thérapeutiques, le devenir des patients hospitalisés pour une insuffisance cardiaque aigue (ICA) reste sombre. Ce pronostic péjoratif est en partie influencé par la survenue fréquente d’événements thrombotiques qui sont à parfois directement à l’origine du décès des patients. Les mécanismes physiopathologiques de cette hypercoagulabilité pourraient être considérés comme des cibles thérapeutiques d’intérêt. L’objectif de ce travail est de démontrer qu’une défaillance des systèmes biologiques contrôlant la thrombose est impliquée dans la physiopathologie de l’ICA. Notre travail met en évidence la présence d’une hypercoagulabilité de ces patients qui se caractérise par une génération de thrombine exagérée pendant la phase aigüe de la décompensation cardiaque et qui se normalise ensuite à distance. Cette élévation de la génération de thrombine est la conséquence d’une augmentation du nombre de microparticules procoagulantes circulantes et d’une altération de l'activité d’un système naturel anticoagulant représenté par la voie de la protéine CAcute heart failure (AHF) is a syndrome with an increasing prevalence and a high mortality whose management is challenging given the incomplete understanding of its pathophysiology. This doomed prognosis is partly influenced by thromboembolic events and is often the cause of death. The present study demonstrates a significant shift towards a prothrombotic biological profile at the acute phase of decompensated heart failure. Using a comprehensive exploration of the dynamics of thrombin generation and inhibition, we found an increased overall thrombin-generating capacity in AHF patients during hospital course. Both increased in circulating procoagulant microparticles and impairment in the downregulation of thrombin generation by the anticoagulant C protein pathway represent mechanisms contributing to this hypercoagulable state in AH

Caractérisation du phénotype hypercoagulable et de ses déterminants dans l’insuffisance cardiaque aiguë

Acute heart failure (AHF) is a syndrome with an increasing prevalence and a high mortality whose management is challenging given the incomplete understanding of its pathophysiology. This doomed prognosis is partly influenced by thromboembolic events and is often the cause of death. The present study demonstrates a significant shift towards a prothrombotic biological profile at the acute phase of decompensated heart failure. Using a comprehensive exploration of the dynamics of thrombin generation and inhibition, we found an increased overall thrombin-generating capacity in AHF patients during hospital course. Both increased in circulating procoagulant microparticles and impairment in the downregulation of thrombin generation by the anticoagulant C protein pathway represent mechanisms contributing to this hypercoagulable state in AHFMalgré le bénéfice observé par de nouvelles thérapeutiques, le devenir des patients hospitalisés pour une insuffisance cardiaque aigue (ICA) reste sombre. Ce pronostic péjoratif est en partie influencé par la survenue fréquente d’événements thrombotiques qui sont à parfois directement à l’origine du décès des patients. Les mécanismes physiopathologiques de cette hypercoagulabilité pourraient être considérés comme des cibles thérapeutiques d’intérêt. L’objectif de ce travail est de démontrer qu’une défaillance des systèmes biologiques contrôlant la thrombose est impliquée dans la physiopathologie de l’ICA. Notre travail met en évidence la présence d’une hypercoagulabilité de ces patients qui se caractérise par une génération de thrombine exagérée pendant la phase aigüe de la décompensation cardiaque et qui se normalise ensuite à distance. Cette élévation de la génération de thrombine est la conséquence d’une augmentation du nombre de microparticules procoagulantes circulantes et d’une altération de l'activité d’un système naturel anticoagulant représenté par la voie de la protéine

Blocs auriculo-ventriculaires complets congénitaux isolés (suivi à long terme d' une série consécutive de 54 patients)

NANCY1-SCD Medecine (545472101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Influence de l'atteinte polyartérielle sur le devenir à long terme des patients éligibles à une revascularisation myocardique chirurgicale (à propos de 589 patients)

Le risque vasculaire global est un facteur prédictif reconnu d'évènements majeurs chez les patients coronariens. L'objectif de notre travail est d'établir dans un premier temps une cartographie globale des lésions athéromateuses des patients éligibles à une revascularisation myocardique chirurgicale. II est surtout d'étudier le devenir au long cours de ces patients en fonction de la présence ou non d'une atteinte athéromateuse extra coronarienne. Il s'agit d'une étude monocentrique rétrospective portant sur une population consécutive de 589 patients ayant bénéficié d'un pontage aorto-coronarien durant la période 2003-2005. 40% des patients de notre population présentent une atteinte athéromateuse extracoronarienne. Comparés au groupe des patients exclusivement coronariens (groupe 1), l'étude des patients du groupe 2 montre une population plus âgée (p<0,001), à prédominance masculine (p=0,04), plus hypertendus (p=0,002), ayant plus d'antécédents coronariens (p=0,03), rénaux (p<0,001) et respiratoires (p=0,005). L'évaluation des évènements cardiovasculaires au terme du suivi de 2 ans montre en analyse univariée une différence significative en termes de décès toutes causes, de décès d'origine cardio-vasculaires, d'AVC ou AIT, et d'évènements ischémiques périphériques. En analyse multivariée, l'atteinte athéromateuse extracoronarienne est un facteur prédictif indépendant de décès de toutes causes [HR= 3,2 (1.8-5.7), p<0.001]. Au delà de l'impact sur la stratégie chirurgicale et les suites opératoires, l'évaluation de l'étendue de la maladie athéromateuse est primordiale sur le devenir à long terme des patients candidats une revascularisation myocardique chirurgicale.NANCY1-SCD Medecine (545472101) / SudocSudocFranceF

Ventricular Dysfunction in Patients with Acute Coronary Syndrome Undergoing Coronary Surgical Revascularization: Prognostic Impact on Long-Term Outcomes.

Patients with non-ST elevation acute coronary syndrome complicated by left ventricular dysfunction (LVEF) are a poor prognosis group. The aim of our study was to assess the short and long term LEVF prognostic value in a cohort of NSTE-ACS patients undergoing surgical revascularization.We performed elective and isolated CABG on a cohort of 206 consecutive patients with LVEF≤0.40 complicating acute coronary syndrome. The case cohort was compared with a cohort of controls (LVEF>0.40) randomly selected (2:1) among patients who underwent the procedure during this period.The Kaplan-Meier 5-year estimated survival rates for patients in the low and normal LVEF groups were 70.8% (95% confidence interval CI: 64.2-77.4) and 81.7% (95%CI: 77.8-85.6), respectively. A low LVEF was associated with both a higher all-cause (HR [95%CI] = 1.84[1.18-2.86]) and a higher cardiovascular mortality (HR = 2.07 [1.27-3.38]) during the first 12 months of follow-up. After adjustment for potential confounders, a low LVEF remained associated with a higher cardiovascular mortality only (1.87[1.03-3.38]) during the first 12 months of follow-up. After 12 months of follow-up, a low LVEF was no more associated with all-cause, nor cardiovascular mortality.Patients with low LVEF might require more intensive care than patients with normal LVEF during the year after the surgical procedure, but once the first postoperative year over, the initial low LVEF was no more associated with long term mortality

Outcomes after acute coronary syndrome in patients with inflammatory bowel disease

International audienceBackground: Patients with chronic inflammatory conditions are at an increased risk of developing atherothrombotic events. We aimed to assess the 1-year prognosis after myocardial infarction (MI) in patients with inflammatory bowel disease (IBD).Methods: From the PMSI (Program de Medicalisation des Systèmes d'informatique) database, 246 out of 39,835 consecutive MI patients, hospitalized between 2012 and 2017, were diagnosed with IBD and followed up for 1 year after discharge. A matched cohort was built matching each MI patient with IBD to patient without IBD using age and sex (n = 1,470, matching ratio 1:5).Results: Compared with MI patients without IBD, MI patients with IBD were younger (aged 69 vs. 70.8 years, p = 0.04) with a higher rate of increased body mass index (BMI) (21.5% vs 15%, p = 0.004), previously diagnosed ischemic cardiopathy (18.3% vs 12.6%, p < 0.0008) and chronic renal disease (8.9% vs 5.6%, p = 0.02). In our age- and sex-matched cohort, we found that all-cause mortality (9% vs 8.3, p = 0.729), stroke (0.8% vs 0.6%, p = 0.656) and hospitalization resulting from heart failure (3ool, .3% vs 3.5%, p = 0.846) did not significantly differ between the IBD and non-IBD groups within the first year after initial admission whereas the risk of recurrent MI was increased by 50% (2.9% vs 1.9%, p = 0.33) in the IBD group without reaching statistical significance. Moreover, a significant increase in the blood transfusion rate at the 1-year follow-up was observed in MI patients with IBD compared with MI patients without IBD (15.1% vs 9.4%, p < 0.001).Conclusion: Our findings suggest that both residual MI risk and bleeding events should be carefully monitored in MI patients diagnosed with chronic inflammation such as that observed in IBD

Pharmacological inhibition of the triggering receptor expressed on myeloid cells-1 limits reperfusion injury in a porcine model of myocardial infarction

International audienceAIMS: Limitation of ischemia/reperfusion injury is a major therapeutic target after acute myocardial infarction (AMI). Toll-like receptors are implicated in the inflammatory response that occurs during reperfusion. The triggering receptor expressed on myeloid cells (TREM)-1 acts as an amplifier of the immune response triggered by toll-like receptor engagement. We hypothesized that administration of a TREM-1 inhibitory peptide (LR12) could limit reperfusion injury in a porcine model of AMI.METHODS AND RESULTS: AMI was induced in 15 adult minipigs by a closed-chest coronary artery occlusion-reperfusion technique. Animals were randomized to receive LR12 or vehicle before reperfusion (LR12 n = 7, vehicle n = 8), and were monitored during 18 h. AMI altered hemodynamics and cardiac function, as illustrated by a drop of mean arterial pressure, cardiac index, cardiac power index, ejection fraction, and real-time pressure-volume loop-derived parameters. TREM-1 inhibition by LR12 significantly improved these dysfunctions (P < 0.03) and limited infarct size, as assessed by lower creatine phosphokinase and troponin I concentrations (P < 0.005). Pulmonary, renal, and hepatic impairments occurred after AMI and were attenuated by LR12 administration as assessed by a better PaO2 to FiO2 ratio, a less positive fluid balance, and lower liver enzymes levels (P < 0.05).CONCLUSION: Inhibition of the TREM-1 pathway by a synthetic peptide limited myocardial reperfusion injury in a clinically relevant porcine model of AMI