<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT03283995</url>
  </required_header>
  <id_info>
    <org_study_id>2017-15</org_study_id>
    <secondary_id>2017-A00563-50</secondary_id>
    <nct_id>NCT03283995</nct_id>
  </id_info>
  <brief_title>Hemodynamic Assessment in Cardiogenic Shock Regarding the Etiology</brief_title>
  <official_title>Hemodynamic Assessment in Cardiogenic Shock Regarding the Etiology</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Assistance Publique Hopitaux De Marseille</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Assistance Publique Hopitaux De Marseille</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
    <is_fda_regulated_drug>No</is_fda_regulated_drug>
    <is_fda_regulated_device>No</is_fda_regulated_device>
  </oversight_info>
  <brief_summary>
    <textblock>
      The classic physiopathology of cardiogenic shock is explained by a systolic ventricular&#xD;
      failure, responsible for a decrease in cardiac output associated with high systemic vascular&#xD;
      resistances (SVR). This theory is currently challenged in light of the data collected in the&#xD;
      SHOCK study, which assessed outcome of early revascularization versus initial medical&#xD;
      stabilization, in cardiogenic shock following myocardial infarction.13 A sub-study&#xD;
      highlighted depressed SVR in the population with ischemic cardiogenic shock, related to a&#xD;
      systemic inflammatory response syndrome.14 Furthermore, mean FEVG was 30% in the SHOCK&#xD;
      trial,13 with a similar distribution with post myocardial infarction heart failure patients&#xD;
      without signs of shock.15-19 Thus, alteration of myocardial contractility can be only&#xD;
      moderate in cardiogenic shock and isn't the only cause responsible for the hemodynamic&#xD;
      instability.20 Recent studies suggest the important roles of the peripheral vascular system&#xD;
      and neurohormonal system in the genesis and prolongation of cardiogenic shock.12 Vasodilation&#xD;
      caused by nitrous oxide synthase activation27 explains the absence of compensating&#xD;
      vasoconstriction observed during the SHOCK trial13, and leads to decreased systemic and&#xD;
      coronary perfusion, thus increasing myocardial ischemia and initial ventricular dysfunction.&#xD;
      28,29 Cotter et al. conducted an interesting study of hemodynamic evaluation of various&#xD;
      cardiac conditions where they observed a significant variability in the peripheral vascular&#xD;
      status, with systemic vascular resistances collapsed in certain patients (similar to those&#xD;
      observed in septic shock) and rather close to normal or very high resistances in other&#xD;
      patients.21 However these data were obtained from a selected group of patients without&#xD;
      differentiating the etiology of cardiogenic shock. Finally, the majority of available studies&#xD;
      were limited to cardiogenic shock whose etiology was myocardial infarction.&#xD;
&#xD;
      Therapeutic management of cardiogenic shock is based in first intention on an inotropic&#xD;
      support by Dobutamine.11,23 However, better outcomes on contractility and microcirculatory&#xD;
      state have been observed with the use of a vasopressor support by Norepinephrine, suggesting&#xD;
      the importance of SVR decreasing in genesis of cardiogenic shock.14,24 Recent reviews showed&#xD;
      very few data on inotropic treatment and association with vasopressor support,22 hence the&#xD;
      low level of recommendations in current guidelines.11,23&#xD;
&#xD;
      So far it is crucial to accurately characterize hemodynamic status and in particular the&#xD;
      systemic vascular resistance for patients with cardiogenic shock. Important variabilities in&#xD;
      hemodynamic profiles observed in Cooter's trial could explain the difficulty in defining an&#xD;
      optimal therapeutic strategy.&#xD;
&#xD;
      the investigators hypothesize that the hemodynamic profile, particularly SVR, of patients&#xD;
      with cardiogenic shock is different depending on their etiology. Ischemic cardiogenic shock&#xD;
      should be characterized by lower SVR, in relation to a major role of systemic inflammatory&#xD;
      response syndrome. On the contrary, non-ischemic cardiogenic shock could be associated with&#xD;
      normal or elevated SVR, and thus could explain the variability in distribution of SVR.&#xD;
    </textblock>
  </brief_summary>
  <overall_status>Unknown status</overall_status>
  <last_known_status>Recruiting</last_known_status>
  <start_date type="Actual">September 6, 2017</start_date>
  <completion_date type="Anticipated">March 2019</completion_date>
  <primary_completion_date type="Anticipated">September 2018</primary_completion_date>
  <study_type>Observational [Patient Registry]</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Case-Control</observational_model>
    <time_perspective>Prospective</time_perspective>
  </study_design_info>
  <target_duration>2 Days</target_duration>
  <primary_outcome>
    <measure>Monitoring by transpulmonary thermodilution (VolumeView</measure>
    <time_frame>2 days</time_frame>
  </primary_outcome>
  <number_of_groups>4</number_of_groups>
  <enrollment type="Anticipated">64</enrollment>
  <condition>Cardiogenic Shock</condition>
  <arm_group>
    <arm_group_label>cardiogenic shock without SCA</arm_group_label>
  </arm_group>
  <arm_group>
    <arm_group_label>cardiogenic shock with SCA</arm_group_label>
  </arm_group>
  <arm_group>
    <arm_group_label>SCA,</arm_group_label>
  </arm_group>
  <arm_group>
    <arm_group_label>acute left heart failure with severe alteration of LVEF</arm_group_label>
  </arm_group>
  <intervention>
    <intervention_type>Other</intervention_type>
    <intervention_name>Cardiac Volume Monitoring VolumeView</intervention_name>
    <description>hemodynamic measure</description>
    <arm_group_label>cardiogenic shock with SCA</arm_group_label>
    <arm_group_label>cardiogenic shock without SCA</arm_group_label>
  </intervention>
  <intervention>
    <intervention_type>Device</intervention_type>
    <intervention_name>echocardiography</intervention_name>
    <description>hemodynamic measure</description>
    <arm_group_label>SCA,</arm_group_label>
    <arm_group_label>acute left heart failure with severe alteration of LVEF</arm_group_label>
    <arm_group_label>cardiogenic shock with SCA</arm_group_label>
    <arm_group_label>cardiogenic shock without SCA</arm_group_label>
  </intervention>
  <eligibility>
    <study_pop>
      <textblock>
        patients with cardiogenic shock.&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Non-Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Persistent hypotension (systolic blood pressure &lt;90 mmHg for at least 30 minutes or&#xD;
             need for vasopressor support)&#xD;
&#xD;
          -  Signs of visceral hypoperfusion (confusion, marbling, oliguria, hyperlactataemia), 11&#xD;
&#xD;
          -  Lower heart rate (&lt;1.8 L / min / m2) Adap Suitable or high filling pressures12&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Pregnant or nursing women&#xD;
&#xD;
          -  Major under guardianship&#xD;
&#xD;
          -  Person staying in a health or social facility&#xD;
&#xD;
          -  Non-beneficiaries of a social security scheme&#xD;
&#xD;
          -  Persons deprived of liberty&#xD;
&#xD;
          -  No one is able to give consent.&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>jean-olivier ARNAUD</last_name>
    <role>Study Director</role>
    <affiliation>Assistance Publique Hopitaux De Marseille</affiliation>
  </overall_official>
  <overall_contact>
    <last_name>laurent BONELLO</last_name>
    <phone>0491968683</phone>
    <email>laurent.bonello@ap-hm.fr</email>
  </overall_contact>
  <overall_contact_backup>
    <last_name>alexandra GIULIANI</last_name>
    <phone>04 91 38 27 47</phone>
    <email>drci@ap-hm.fr</email>
  </overall_contact_backup>
  <location>
    <facility>
      <name>Assisatnce Publique Hopitaux de Marseille</name>
      <address>
        <city>Marseille</city>
        <country>France</country>
      </address>
    </facility>
    <status>Recruiting</status>
    <contact>
      <last_name>JEAN-OLIVIER ARNAUD</last_name>
      <email>drci@ap-hm.fr</email>
    </contact>
    <investigator>
      <last_name>LAURENT BONELLO</last_name>
      <role>Principal Investigator</role>
    </investigator>
  </location>
  <location_countries>
    <country>France</country>
  </location_countries>
  <verification_date>April 2018</verification_date>
  <study_first_submitted>September 13, 2017</study_first_submitted>
  <study_first_submitted_qc>September 13, 2017</study_first_submitted_qc>
  <study_first_posted type="Actual">September 15, 2017</study_first_posted>
  <last_update_submitted>April 10, 2018</last_update_submitted>
  <last_update_submitted_qc>April 10, 2018</last_update_submitted_qc>
  <last_update_posted type="Actual">April 11, 2018</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Shock, Cardiogenic</mesh_term>
    <mesh_term>Shock</mesh_term>
  </condition_browse>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT03283995
org study id: 2017-15
secondary id: 2017-A00563-50
nct id: NCT03283995
lead sponsor: 
has dmc: No
is fda regulated drug: No
is fda regulated device: No
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.
observational model: Case-Control
time perspective: Prospective
measure: Monitoring by transpulmonary thermodilution (VolumeView
time frame: 2 days
arm group label: cardiogenic shock without SCA
arm group label: cardiogenic shock with SCA
arm group label: SCA,
arm group label: acute left heart failure with severe alteration of LVEF
intervention type: Other
intervention name: Cardiac Volume Monitoring VolumeView
description: hemodynamic measure
arm group label: cardiogenic shock with SCA
arm group label: cardiogenic shock without SCA
intervention type: Device
intervention name: echocardiography
description: hemodynamic measure
arm group label: SCA,
arm group label: acute left heart failure with severe alteration of LVEF
arm group label: cardiogenic shock with SCA
arm group label: cardiogenic shock without SCA
study pop: 
sampling method: Non-Probability Sample
criteria: 
gender: All
minimum age: 18 Years
maximum age: N/A
healthy volunteers: No
last name: jean-olivier ARNAUD
role: Study Director
affiliation: Assistance Publique Hopitaux De Marseille
last name: laurent BONELLO
phone: 0491968683
email: laurent.bonello@ap-hm.fr
last name: alexandra GIULIANI
phone: 04 91 38 27 47
email: drci@ap-hm.fr
facility: 
status: Recruiting
contact: 
investigator: 
country: France
responsible party type: Sponsor
mesh term: Shock, Cardiogenic
mesh term: Shock