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Idiopathic dilated cardiomyopathy (IDCM) is one of the most common forms of non-ischemic cardiomyopathy (NICM) worldwide, possibly leading to cardiogenic shock (CS). Despite this heavy burden, outcomes of CS in IDCM are poorly reported. Based on a large registry of unselected CS, our aim was to shed light on one-year outcomes after CS in IDCM and non-IDCM patients. FRENSHOCK was a prospective registry including 772 CS patients from 49 centers. One-year outcomes (rehospitalizations, mortality, heart transplantation [HTx], ventricular assist devices [VAD]) were analysed, adjusted on independent predictive factors. Within 772 CS included, 78 occurred in IDCM (10.1%) (Fig. 1). IDCM patients had more frequent history of chronic kidney failure and ICD implantation. No difference was found in 1-month all-cause mortality between groups (28.2 vs. 25.8% respectively for IDCM and others, aHR 1.14 [0.73–1.77], P = 0.57). Non-IDCM were more frequently treated with non-invasive ventilation and IABP. At 1-year, IDCM led to higher rates of death or cardiovascular rehospitalizations (aOR 4.77 [95% CI 1.13–20.1], P = 0.03) and higher rate of HTx or VAD for individuals under 65 years old (aOR 2.68 [1.21–5.91], P = 0.02). CS in IDCM is a very common scenario and is associated with a higher rate of 1-year death or cardiovascular rehospitalizations, and a more frequent recourse to HTx or VAD for individuals < 65 years old, encouraging to consider it as a red flag for myocardial decline, urging to closer follow-up and earlier evaluation for advanced heart failure therapies. [ABSTRACT FROM AUTHOR]

Cardiogenic shock (CS) is a life-threatening hemodynamic condition carrying a very poor prognosis. Ventricular tachycardia (VT) can be the culprit element inducing CS. Although the role of VT burden is well established in chronic heart failure, resulting in higher in-hospital and long-term mortality, whether the occurrence of VT as a trigger of CS worsens the prognosis compared to any other cause remains unclear. To evaluate 1-month and 1-year outcomes in terms of mortality, heart transplantation and ventricular assist devices (VAD) between CS triggered by VT vs. others causes. FRENSHOCK registry is a multicentric national registry including 772 patients in 49 centers. Patients were included if they met the following three criteria of CS: (1) low cardiac output defined by SB P < 90 mmHg and/or the need of amines, or a CI < 2.2L/min/m2 (TTE or Swan-Ganz); (2) elevation of left and/or right heart pressures defined by clinic/radiology/biology/echocardiography/Swan-Ganz; and (3) clinical and/or biological signs of hypoperfusion. Patients presenting with VT at admission (or during the early evolution of CS) were compared to other ones. Sustained VT (> 30 sec) or incessant non sustained VT (> 12 h per day) only were considered as VT. 769 CS patients were included, of which 94 (12%) were triggered by VT and 675 (88%) by any other cause. Ischemic and non-ischemic cardiomyopathies were equally distributed between groups. No refractory electrical storm was observed. VT-triggered CS was associated with more frequent initial cardiac arrest (29.8% vs. 7.4%, P < 0.01). Non-VT triggered CS presented poorer biological parameters such as initial Nt-proBNP (17,837.0 vs. 11,259.7, P = 0.03) or creatinine (154.3 vs. 133.7, P = 0.04) and prothrombin time (56.1 vs. 64.1, P < 0.01) 24 h after admission. There was no difference in all-cause mortality at 1 month (26.6% vs. 25.8%, HR 0.940 [0.618–1.429]) and at 1 year (42.6% vs. 45.3%, HR 1.067 [0.767–1.483]). However, VT-triggered CS resulted in more heart transplantation or need for VAD at 1 year compared to other cases (17% vs. 9%, P = 0.016) (Table 1). Ventricular tachycardia as a trigger of cardiogenic shock did not show higher short- and long-term mortality than cardiogenic shock from other cause. Yet, the presence of VT associated CS was linked to more heart transplantation and ventricular assist devices. [ABSTRACT FROM AUTHOR]

Introduction Myocardial infarction (MI) is followed by an intense inflammatory response which is necessary for the healing of the infarcted area, but which can also have deleterious effect by increasing infarct size (IS). A good knowledge of this inflammatory response is necessary to develop new treatments targeting this phase. Objective Our study aims at describing the temporal kinetic of inflammatory biomarkers in ST-elevation MI (STEMI) patients and to evaluate their correlation with IS and left ventricular ejection fraction (LVEF). Method We included 100 patients of our HIBISCUS cohort (STEMI patients cohort) with blood samples collected at admission (H0), then 4 (H4), 24 (H24), 48 hours (H48) and 1 month (M1) after reperfusion. C-reactive protein (CRP), interleukin(IL)-1β, IL-1α, IL-6, IL-8, IL-10, tumor necrosis factor (TNFα), Growth Differentiation Factor 15 (GDF15) and interleukin 1 receptor-like 1 (ST2) were assessed in the serum by ELISA. All patients underwent a cardiac magnetic resonance imaging (CMR) at 1 month. Results Patient were aged of 57 ± 10 years. Contrary to other biomarkers, IL-1β, IL-1α and TNFα were weakly detectable in the serum. CRP reached a peak at H48 with a median of 11.7 mg/L interquartile range (IQR) [2.3–29.1]. IL-6 peaked at H24 with 4.8 pg/mL IQR [1.9–14.3], IL-8 at H24 with 2.6 pg/mL IQR [1.3–4.7], IL-10 at H0 with 5.7 pg/mL IQR [2.9–11.3], GDF15 at H0 with 203.7 pg/mL IQR [106.0–301.6] and ST2 at H24 with 25.6 pg/mL IQR [16.8–37.7]. Only CRP, IL-6, IL-10 and ST2 were significantly corelated with IS (respectively r = 0.51, P < 0.0001; r = 0.57, p < 0.0001; r = 0.53, P < 0.0001; r = 0.35, P = 0.0004) and inversed correlated with LVEF (respectively r = −0.38, P = 0.0002; r = −0.50, P < 0.0001; r = −0.41, P < 0.0001; r = −0.23, P = 0.02) assessed by CMR. Conclusion During STEMI, we observed a specific kinetic for each biomarker with variable peak time. CRP, IL-6, IL-10 and ST2 were significantly correlated with IS and inversely correlated with LVEF. [ABSTRACT FROM AUTHOR]

IL-6 and IL-10 are two major cytokines secreted at the acute phase of myocardial infarction (MI). IL-6 has a pro-inflammatory effect whereas IL-10 has anti-inflammatory effect. Our objective was to assess the prognosis value of IL-6, IL-10 and IL-10/IL-6 ratio serum level at the acute phase of ST elevation MI (STEMI). We prospectively enrolled 247 patients admitted for acute STEMI from 2016 to 2019. Blood samples were collected at 5 time points: admission, 4, 24, 48 hours and 1 month (H4, H24, H48, M1). IL-6 and IL-10 were assessed using ELISA. Patients underwent cardiac magnetic resonance imaging at one month for infarct size (IS) and left ventricular ejection fraction (LVEF) assessment. Clinical outcomes were prospectively recorded over 18 months. Patient mean age was 59 ± 12 years. IL-6 reached a peak at H24 at 5.4 pg/mL interquartile range (IQR) [2.1–11.0] and IL-10 peaked as early as admission at 5.6 pg/mL IQR [8.7–29.3] followed by a decrease within the first month. Median IL-10/IL-6 ratio at admission was 4.2 [1.4–8.6] with a strong decrease at H24 (0.5 [0.2–1.3]). IL-6 and IL-10 levels at H24 were correlated with IS (respectively r = 0.44, P < 0.0001, and r = 0.29, P = 0.0001) and inversely correlated with LVEF (respectively r = −0.42, P < 0.0001 and r = −0.26, P = 0.0003). Patients with IL-10/IL-6 ratio ≥ 1 had smaller IS compared to patients with IL-10/IL-6 ratio < 1 (respectively 9.0% IQR [2.4–15.4] of LV versus 17% IQR [8.7–29.3] of LV, P < 0.0001) and they had higher LVEF (58.0% IQR [52.0–62.3] versus 49.0% IQR [41.5–56.0], P < 0.0001). Patients with IL-10/IL-6 ratio < 1 were more likely to have an adverse clinical event (MI, stroke, hospitalization for heart failure and all-cause death) during the first 18 months after STEMI compared to patients with IL-10/IL-6 ratio ≥ 1 (HR = 2.7 95% CI [1.2–5.5], P = 0.04). Serum IL-10/IL-6 > 1 was associated with a poor outcome after STEMI and might be a valuable prognostic marker. [ABSTRACT FROM AUTHOR]

White blood cell count (lymphocyte, neutrophil, eosinophil) have been shown to be independently and incrementally associated with clinical events after acute myocardial infarction (MI). However, the prognostic value of basophil has never been studied at the acute phase of MI. Our objective was to define the kinetics of basophils within the first month in patients admitted for STEMI and to assess their prognostic value. We prospectively enrolled 243 patients admitted for acute ST elevated MI (STEMI) from 2016 to 2019. Blood samples were collected at 5 time points: admission, 4, 24, 48 hours and 1 month after admission (H4, H24, H48, M1). Patients underwent cardiac magnetic resonance imaging at one month for infarct size (IS) and left ventricular ejection fraction (LVEF) assessment. Clinical outcomes were prospectively recorded over 18 months. Patient mean age was 59 ± 12 years. Basophil count significantly decreased at H24 with a median of 30.0 Mega/L (interquartile range [IQR] [20.0–50.0]) compared to admission (40.0 M/L IQR [30.0–60.0], P < 0.001) and was back to baseline level at H48. Basophils at H48 were not associated with IS assessed by CMR (r = −0.08, P = 0.32), LVEF (r = −0.12, P = 0.08) or LV end diastolic volume (r = −0.03, P = 0.68). Patients with H48 basophil level below the median value of the population were more likely to have an adverse clinical event (MI, stroke, hospitalization for heart failure and all-cause death) during the 18 months follow-up compared to patients with basophil level above the median (hazard ratio at 6.1 [2.5–15.0], P = 0.005). In a multivariable Cox regression analyses with models including peak troponin I, LVEF and age, low levels of basophils at H48 remained associated with an increased risk of adverse clinical event. Area under the receiver operating curve was 0.68 (0.57–0.78), P = 0.005 (Fig. 1). Basophil count at H48 in STEMI patients is an independent prognosis marker to predict clinical outcome. [ABSTRACT FROM AUTHOR]

Introduction The prognosis after a myocardial infarction is now importantly linked to the reperfusion injury, which consists in cellular death due to reperfusion by itself. This ischemia/reperfusion phenomenon is mediated by the inflammatory response to myocardial infarction, mainly through the secretion of pro-inflammatory and anti-inflammatory cytokines by macrophages. Many treatments has been developed to target that inflammatory response, but the effects of standard treatments of the myocardial infarction, as recommended in the guidelines, has never been studied. Objective To examine the effects of standard treatments of the myocardial infarction on the secretion of the most important ischemia/reperfusion cytokines. Method We used a murin macrophage model of inflammation (BMDM) to quantify the secretion of the main cytokines of ischemia/reperfusion (TNF-α, IL-6, IL-1α, IL-1β and IL-10). These macrophages were incubated alone, along with a treatment of each main class given after a myocardial infarction or with an association of pre-hospital phase treatments (aspirine, ticagrelor and unfractionned heparin). Secretion of the different cytokines was quantified using an ELISA testing. Results The standard treatments impact mostly IL-1β, which is known to be the most deleterious cytokine during ischemia/reperfusion. Its secretion is lowered by aspirin, the anti-Gp2b3a abciximab, and unfractionned heparin. The other treatments tested, including the low-weight molecular heparin enoxaparin, have no effect on IL-1β secretion. The standard treatments have only few effects on the secretion of the other cytokins. Conclusion Aspirin, abciximab and unfractionned heparin have an important anti-IL-1β effect, reducing its secretion. This could explain the lack of efficacy of the specific anti-IL-1β treatments during the acute phase of myocardial infarction. These results should be confirmed using an in vivo murin model and a human in vitro model. [ABSTRACT FROM AUTHOR]

Background The safety of morphine use has been questioned in the management of ST Elevation Myocardial Infarction (STEMI). Are there other analgesics that are at least as effective without adverse effects? Purpose Evaluate the non-inferiority of nitrous oxide/oxygen plus acetaminophen versus morphine in pre-hospital patients with STEMI. Method Multi-center, randomized, non-inferiority cluster study. Thirty-eight mobile intensive care unit centres were randomized. Inclusion criteria: patients with STEMI and pain intensity score ≥ 4 on the numerical rating scale (NRS). Outcome: proportion of patient with NRS ≤ 3, 30 minutes after starting analgesia without adding morphine in the nitrous oxide/oxygen group. Expected or unexpected events were measured at 30 minutes and 1 month. Estimated number of subjects: 684. Per protocol (PP) and intention to treat (ITT) statistical analyses were planned. A non-inferiority margin was specified as an absolute difference of − 10% in proportions. The cluster design of the trial was taken into account through generalised estimating equations. Results A total of 684 patients were included in ITT analysis and 644 in PP analysis. Pain relief was obtained in 73.6% patients in the morphine group versus 51.7% patients in the nitrous oxide/oxygen group in the PP analysis. The absolute risk difference was − 21.7% (95% CI − 29.6 to − 13.8) and was below the non-inferiority margin of − 10%. The incidence of expected and serious adverse events were 10.2% and 3.5% respectively in the morphine group versus 13.2% and 6.2% in the nitrous oxide/oxygen group. Conclusion Oxide/oxygen plus acetaminophen is inferior to morphine analgesia in patients with STEMI. Adverse effects were not different between the groups. [ABSTRACT FROM AUTHOR]

Introduction and objective Although early reperfusion, ST-elevation myocardial infarction (STEMI) remain a major cause of mortality and heart failure. Reperfusion is commonly associated with persistent micro-vascular obstruction (MVO), edema and intramyocardial hemorrhage (IMH) which are detected using cardiovascular magnetic resonance (CMR) imaging. Furthermore, STEMI is associated with an important inflammatory reaction. So far, the correlation between CMR parameters and inflammation remain unclear. Methods and results This study aims at deciphering the correlation between adverse events and inflammatory biomarkers. This is a prospective study including 21 STEMI patients referred for a primary percutaneous coronary intervention. Seven blood samples were collected at admission, 4, 12, 24, 48 hours, 7 and 30 days after reperfusion. The presence of inflammatory markers including fibrinogen, inteleukin-10, interleukine-6, C reactive protein (CRP), interleukine-8, and neutrophils count was assessed by enzyme-linked immunosorbent assay (ELISA) technique. At day 7 after reperfusion, CMR was performed to determine infarct size, MVO, IMH and edema. The study compares the expression level of each biomarker with CMR measures. MVO was present in 55% of patients and IMH in 33.3%. We observed a correlation between IL-6, CRP, fibrinogen, neutrophil levels and IMH (P = 0.033; P = 0.05; P = 0.0085; P = 0.0046 respectively). Patients with persistent MVO present a significantly higher rate of CRP (P = 0.0125). No significant difference was found for other markers and edema was not significantly correlated with inflammation. Conclusion Following acute myocardial infarction in human patient, IMH appears to be strongly correlated with inflammatory biomarkers. Targeting the couple IMH/inflammation could be a novel strategy in future adjunctive STEMI treatment. [ABSTRACT FROM AUTHOR]

Introduction Acute myocardial infarction (MI) leads to an intense inflammatory response with endothelial cell activation. Vascular cell adhesion protein 1 (VCAM-1), E-selectin, intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein 1 (MCP-1) promote the adherence of leucocytes especially monocytes, in the infarcted area which may increase infarct size (IS). Objective Our objective was to evaluate the kinetic of endothelial cell activation markers at the acute phase of ST-elevated MI (STEMI) and their relationship with IS and Major Adverse Cardiac Event (MACE). Method Blood sample of 182 STEMI patients were collected at admission and four hours after reperfusion. Infarct Size (IS) was assessed in all patients using cardiac Magnetic Resonance Imaging (cMRI) one month after discharge. We performed ELISA quantification of the main markers of endothelial cell activation in serum: VCAM-1, E-selectin, ICAM-1 and MCP-1. Results Patients mean age was 58 ± 11 years with 77% males. Median levels of each marker at admission reached 165.3 ng/mL interquartile range (IQR) [127.0–193.3] for VCAM-1, 140.6 ng/mL IQR [104.6–196.6] for ICAM-1, 15.3 ng/mL IQR [10.2–23.3] for E-selectin and 53.8 pg/mL IQR [34.7–90.5] for MCP-1. VCAM-1 and MCP-1 serum levels significantly increased four hours after admission (respectively +6% and +32%). E-selectin and ICAM-1 levels did not change four hours after admission compared to admission. Only VCAM-1 was significantly correlated with IS assessed by cMRI ( r = 0.26, P = 0.0004) and inversely correlated with left ventricular ejection fraction ( r = −0.16, P = 0.04). However, VCAM-1 level and other markers were not associated with MACE. Conclusion MI is associated with endothelial cell activation. VCAM-1 and MCP-1 significantly increased at the acute phase of MI whereas E-selectin and ICAM-1 levels are stable. Only VCAM-1 serum level was correlated with IS. However, none of these markers was associated with the occurrence of MACE. [ABSTRACT FROM AUTHOR]

Introduction Circadian rhythm modulates many physiological functions. Some studies suggest a circadian variation of infarct size (IS) in experimental models and in human. It is also known that inflammation is modulated according to circadian rhythm. Inflammation has a central role in post-MI remodeling and final IS. Circadian variation of IS and inflammation response after MI are unknown. Objective Our objective was to evaluate the modulation of IS according to the reperfusion time of the day and to assess if post-MI inflammation was also modulated by circadian rhythm. Method In our biobank, we selected 115 patients who presented with a ST-elevated Myocardial Infarction (STEMI). Two groups were done according to the reperfusion time of day. The morning group (MG) was reperfused between 6:01 am and 12:00 and the afternoon group (AG) was reperfused between 12:01 and 6:00 pm. Each patient had a blood sample upon admission and 4 hours after reperfusion. IS was assessed using cardiac magnetic resonance (MRI) imaging. Main inflammatory markers as interleukin (IL)-6, IL-8, IL-10 and C-reactive protein (CRP) were dosed using ELISA. Results There were 53 patients in the MG and 62 patients in the AG. Patients characteristics were similar in the two groups, especially ischemia time (median of 165 min in both groups). We observed that IS assessed by MRI was significantly reduced by 23.2% in the AG compared to the MG ( P = 0.04). Furthermore, patients reperfused the afternoon showed a less intense inflammation reaction post-MI with a 54% decrease of CRP ( P = 0.004) and 30% decrease of IL-6 ( P = 0.047) compared to the MG. IL-8 and IL-10 levels were similar in the 2 groups. Conclusion We confirmed a circadian variation of myocardial IS in STEMI reperfused patients according to the reperfusion time of the day. The largest IS was observed in the MG. CRP and IL-6 were also modulated according to circadian rhythm with a higher level the morning compared to the afternoon. [ABSTRACT FROM AUTHOR]

Background Regression of ST segment elevation after reperfusion is a strong prognostic factor in ST Elevation Myocardial Infarction (STEMI) patients. Up to 25% patients have ST segment re-elevation after the initial regression and there is little data regarding its prognostic significance. Methods Standard 12-leads electrocardiograms (ECG) were recorded in 662 anterior STEMI patients referred for Primary Percutaneous Coronary Intervention (PPCI), from the CIRCUS trial. ECGs were recorded at admission, 60–90 minutes after PPCI, and at discharge. ST segment elevation was measured on STmax, and ST segment re-elevation was defined by an increase ≥ 0.1 mV between post-PPCI and discharge ECG. Infarct size by Creatin Kinase (CK) peak, echocardiography at baseline and follow-up, and all-cause death and heart failure events were assessed at one year. Results 128 (19%) patients had ST segment re-elevation (ReST+ group). There was no difference between ReST+ patients and patients without re-elevation (ReST− group) on infarct size (CK peak: 4231 ± 2656 IU/l vs. 3993 ± 2819 IU/l, respectively, P = 0.402). There was no difference for 1-year Left Ventricular (LV) Ejection Fraction (50.7 ± 11.6% vs. 52.2 ± 10.8%, P = 0.186) or LV adverse remodeling (20.1 ± 38.9% vs. 18.3 ± 30.9%, P = 0.631). There was no difference in all-cause mortality and heart failure events at one year (22 [19.8%] vs. 106 [19.2%], P = 0.887). Conclusion In anterior STEMI patients treated by PPCI, ST segment re-elevation was present in 19% and was not associated with increased infarct size and major adverse events at one year. [ABSTRACT FROM AUTHOR]

Introduction La prise en charge des patients présentant un syndrome cardio-rénal de type 2 nécessite une collaboration cardio-néphrologique et une caractérisation des patients et de leur pronostic. Patients et méthodes Afin de mieux connaître et orienter ces patients, une filière de prise en charge des insuffisances cardiaques réfractaires avec insuffisance rénale a été mise en place entre les services de cardiologie du CHU de Lyon et le service de néphrologie de l’Hôpital Édouard Herriot à Lyon. Résultats Cinquante-trois patients ont été étudiés depuis janvier 2012. Le nombre moyen d’hospitalisations pour décompensations cardiaques l’année précédente était de 3,1. Le pourcentage de femmes était de 30,1 %, l’âge moyen de 68 ans. La répartition des cardiopathies était : 42 % ischémiques, 27 % dilatées, 11 % rythmiques, 8 % hypertrophiques, 8 % congénitales, 4 % restrictives. 32 % présentaient une FEVG > 50 %. Le DFG mesuré (clairance de l’inuline) était à 23 ± 14 mL/min/1,73 m 2 . L’albuminémie moyenne était à 36,9 g/L, la préalbumine à 0,22 g/L. L’impédancemétrie estimait la surcharge hydrosodée moyenne à +0,25 L. Selon leur profil, les patients ont été orientés vers la dialyse péritonéale (36 %), l’ultrafiltration par aquaphérèse (6 %), l’hémodialyse (24 %) et/ou une prise en charge médicale non invasive exclusive (33 %). Le projet thérapeutique était variable : optimisation en vue d’une transplantation cardiaque, amélioration du pronostic, diminution des réhospitalisations et/ou soulagement palliatif des symptômes congestifs. Parmi les patients dont le suivi date de plus de 6 mois ( n = 41), la survie à 6 mois est de 61 %. Aucun décès n’a été imputé à la mise en place d’une technique d’ultrafiltration. Discussion et conclusion Les patients présentant un syndrome cardiorénal de type 2, avec une insuffisance cardiaque étiquetée réfractaire, présentent des profils divers et nécessitent l’élaboration d’un projet individualisé et réévalué régulièrement. Leur bénéfice à recourir aux différentes modalités d’ultrafiltration doit être évalué, au mieux dans le cadre d’un essai contrôlé randomisé. Une évaluation à un stade plus précoce d’insuffisance cardiaque semble nécessaire. [ABSTRACT FROM AUTHOR]

The article discusses a study that investigated the impact of the drug cyclosporine on patients with acute myocardial infarction. Under this study, 970 patients with an acute anterior ST-segment elevation myocardial infraction (STEMI) undergoing percutaneous coronary intervention (PCI) were given either a bolus injection of cyclosporine or matching placebo. Findings on patient outcomes and adverse events such as death, worsening heart failure and adverse left ventricular remodeling are tackled.