Active clinical trials for "Shock, Cardiogenic"

Cardiogenic shock (CC) is one of the major challenges of current cardiology. Despite the difficulty of establishing a strict and consensual definition, it is accepted that the CC clinically corresponds to persistent hypotension (systolic blood pressure 90 mmHg for at least 30 minutes or need for vasopressor support) associated with signs of visceral hypoperfusion (confusion, mottling, oliguria, hyperlactatemia), and hemodynamic with a lowered heart index ( 1.8 L/min/m2) despite appropriate or high filling pressures. This definition of the European Society of Cardiology (ESC) masks however the great variability of hemodynamic tables grouped under the term of CC and severity levels, also variable.However, it was suggested that the etiology of CC influenced both its hemodynamic profile and therefore its therapeutic management but also its prognosis in the medium and long term.

The most frequent access site for veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is the common femoral artery (CFA), using either an open or percutaneous technique. Currently, percutaneous closure devices for femoral arterial access sites are approved for use only when a 10-F or smaller sheath has been used. However, the availability of the Perclose ProGlide (Abbott Laboratories, Chicago, IL) device has now made it possible to perform percutaneous vessel closure after using larger sheaths.The preclose technique using Perclose ProGlide, has been widely used in endovascular procedures. In a prospective randomized study, complication rates at the access site were similar in patients who underwent total percutaneous access (including percutaneous arteriotomy closure) than in those who underwent surgical cutdown and subsequent surgical closure. Total percutaneous closure of femoral arterial access sites increases patient comfort and decreases the rate of wound infections and lymphatic fistulas.[6,7] Furthermore, patients are mobilized and discharged earlier following the use of closure devices than with compression alone. Despite the above observations, no data have been published regarding percutaneous closure of femoral artery access sites in patients who have undergone VA-ECMO. In this study, we evaluated the safety and feasibility of a percutaneous closure technique using Perclose ProGlide to close the CFA access site after VA-ECMO.

The cardiogenic shock is characterized by an alteration of organs function following a decrease in cardiac output linked to an impairment of cardiac performance. The prognosis remains poor with mortality between 40 and 50%. Nowadays, Extracorporeal Life Support (ECLS or VA-ECMO) is the referent therapy to restore blood flow in the body when medical treatment is not sufficient. Despite a good blood flow provided by the ECLS, many patients develop a severe hypotension (so called vasoplegia) due to a loss of vascular resistance mainly explained by the inflammatory response to shock and extracorporeal circulation. The treatment of this reaction includes vasopressors (Norepinephrine in usual care) and serum surrogate perfusion to achieve a mean arterial pressure (MAP) above 65 mmHg. The purpose of this study is to describe the patients with vasoplegia among a retrospective cohort of patients treated with an ECLS in our university center, over the 4 last years, to determine major complication rate (including death, kidney failure and arrythmias) and their outcome. This study will provide consistent data useful for further trials about targets of pressure and treatments to increase blood pressure during ECLS.

The investigators are doing this study and medical record review to measure simultaneous pressure and volume of the heart called pressure volumes loops before and after ventricular assist device placement for cardiogenic shock ( a severe form of heart failure). Standard of care measurements will be the sole measure of clinical determination. The investigators are measuring these PV loops to help determine which patients heart have recovered and can have the ventricular assist device removed. The investigators are also using the PV loop to indicate/correlate with certain outcomes to predict the need for LVAD patients to require additional support in the form of a right ventricular assist device. The medical record review will be performed pre-operatively, intra-operatively, and post-operatively until the day of discharge.

Purpose of this study is to assess whether measurements obtained through speckle tracking (LV longitudinal and circumferential strain, RV longitudinal strain) can give additional information in identifying patients who develop adverse outcomes 30 days post successfully weaning from VA ECMO (liberation not for palliation). It is a prospective observational non-blinded pilot study. In order to achieve this purpose, speckle tracking analysis will be performed on the recorded images of the transoesophageal echocardiogram performed during the last VA ECMO weaning study of patients defined ready for VA ECMO liberation. VA ECMO liberation will be based according to LVOT VTI increase and clinical judgment during patients' VA ECMO weaning study. It will be assessed whether the population experiencing the outcomes of interest (death within 30 days from VA ECMO liberation, hospital admission for a new episode of cardiogenic shock or heart failure within 30 days from VA ECMO liberation, need for new mechanical circulatory support within 30 days from VA ECMO liberation) and the population not experiencing these outcomes have different values of strain (LV longitudinal and circumferential and RV longitudinal strain) during the weaning study.

Passive leg raising (PLR) is routinely used to predict preload responsiveness in critically ill patients. However, real-time measurements of cardiac output are required to assess its effects. Some authors have suggested that in fluid non-responders, central venous pressure (CVP) increased markedly. By analogy with the CVP rules proposed by Weill et al to assess a fluid challenge, it has been hypothesized that an increase in CVP ≥ 5 mmHg during PLR can predict preload unresponsiveness. Objective Investigation of whether an increase in CVP ≥ 5 mmHg during PLR predict preload unresponsiveness diagnosed by the absence of increase in velocity-time integral (VTI) of the flow in the left ventricular outflow tract by more than 10% (4). Methods Critically ill patients with a central venous catheter in place and for whom the physician decided to test preload responsiveness by PLR were prospectively included. Transthoracic echocardiography was performed to obtain VTI. The CVP and VTI were measured before and during PLR.

This pilot study is designed to investigate the effect of inhaled nitric oxide on cardiac, pulmonary artery, and systemic hemodynamics at various time points during venoarterial extracorporeal membrane oxygenation (VA-ECMO) support. Patients who have been initiated on VA-ECMO will be invited to participate. Inhaled nitric oxide (iNO) will be used early after VA-ECMO cannulation (once consent is obtained). After baseline hemodynamic, biochemical, and echocardiographic parameters are assessed, iNO will be initiated and all parameters will be reassessed after 30 minutes and 6 hours. Inhaled nitric oxide will then be discontinued and all parameters repeated. At the time of VA-ECMO weaning (timing determined by clinical team), iNO will be reinitiated with repeat assessment of hemodynamic, biochemical, and echocardiographic parameters both prior to the wean and after the wean (whether successful or not).

Cardiogenic shock (CS) is a medical emergency and a frequent cause of death. CS can be complicated and/or precipitated by mitral regurgitation (MR). The efficacy of percutaneous treatment of MR in patients with cardiogenic shock is unknown. The aims of the study will be to analyse the efficacy of MitraClip therapy on early (30 days) and midterm mortality (6 months) as well as the predictors of outcomes. Investigators will also report the rate of periprocedural complications such as minor and major bleeding, vessel injury and Acute Kidney Injury (AKI). It is a multicenter retrospective observational study on CE marked medical device (MitraClip® System). Retrospective time range: from 01/01/2012 to 01/01/2020

EPICAL 2 (Epidemiology and prognostic of the Acute Heart Failure) is an epidemiological, observational, prospective and multicenter study. This study includes at first an exhaustive recording of the cases on a geographic area at East of France, then the recorded patients are followed up in a cohort at least 3 years. This study follows the experiences of the EPICAL study led by our team. Main objective: To describe the characteristics of the patients affected by acute heart failure and to identify prognostic factors, in particular related to care. More exactly : To describe the sociodemographic, clinical, biological and therapeutic characteristics of the patients presenting an acute heart failure during hospitalisation and living at East of France ; To study the short and medium-term morbi-mortality of these patients, and identify the main factors determining the prognosis for survival ; To evaluate the prognostic impact of the intra and extra-hospital care ; To identify the evolution of the care's practices of the decompensated heart failure since the EPICAL study (15 years) and their influence on the prognosis of the disease. Secondary objective: to constitute a biological collection of serum, plasma and urine of patients' sample presenting an acute heart failure.

The classic physiopathology of cardiogenic shock is explained by a systolic ventricular failure, responsible for a decrease in cardiac output associated with high systemic vascular resistances (SVR). This theory is currently challenged in light of the data collected in the SHOCK study, which assessed outcome of early revascularization versus initial medical stabilization, in cardiogenic shock following myocardial infarction.13 A sub-study highlighted depressed SVR in the population with ischemic cardiogenic shock, related to a systemic inflammatory response syndrome.14 Furthermore, mean FEVG was 30% in the SHOCK trial,13 with a similar distribution with post myocardial infarction heart failure patients without signs of shock.15-19 Thus, alteration of myocardial contractility can be only moderate in cardiogenic shock and isn't the only cause responsible for the hemodynamic instability.20 Recent studies suggest the important roles of the peripheral vascular system and neurohormonal system in the genesis and prolongation of cardiogenic shock.12 Vasodilation caused by nitrous oxide synthase activation27 explains the absence of compensating vasoconstriction observed during the SHOCK trial13, and leads to decreased systemic and coronary perfusion, thus increasing myocardial ischemia and initial ventricular dysfunction. 28,29 Cotter et al. conducted an interesting study of hemodynamic evaluation of various cardiac conditions where they observed a significant variability in the peripheral vascular status, with systemic vascular resistances collapsed in certain patients (similar to those observed in septic shock) and rather close to normal or very high resistances in other patients.21 However these data were obtained from a selected group of patients without differentiating the etiology of cardiogenic shock. Finally, the majority of available studies were limited to cardiogenic shock whose etiology was myocardial infarction. Therapeutic management of cardiogenic shock is based in first intention on an inotropic support by Dobutamine.11,23 However, better outcomes on contractility and microcirculatory state have been observed with the use of a vasopressor support by Norepinephrine, suggesting the importance of SVR decreasing in genesis of cardiogenic shock.14,24 Recent reviews showed very few data on inotropic treatment and association with vasopressor support,22 hence the low level of recommendations in current guidelines.11,23 So far it is crucial to accurately characterize hemodynamic status and in particular the systemic vascular resistance for patients with cardiogenic shock. Important variabilities in hemodynamic profiles observed in Cooter's trial could explain the difficulty in defining an optimal therapeutic strategy. the investigators hypothesize that the hemodynamic profile, particularly SVR, of patients with cardiogenic shock is different depending on their etiology. Ischemic cardiogenic shock should be characterized by lower SVR, in relation to a major role of systemic inflammatory response syndrome. On the contrary, non-ischemic cardiogenic shock could be associated with normal or elevated SVR, and thus could explain the variability in distribution of SVR.