<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/NCT03761654</url>
  </required_header>
  <id_info>
    <org_study_id>CHUBX 2018/51</org_study_id>
    <nct_id>NCT03761654</nct_id>
  </id_info>
  <brief_title>Detection of Myocardial Dysfunction in Non-severe Subarachnoid Hemorrhage (WFNS 1-2) Using Speckle-tracking Echocardiography (STRAIN)</brief_title>
  <acronym>SAH-STRAIN</acronym>
  <official_title>Detection of Myocardial Dysfunction in Non-severe Subarachnoid Hemorrhage (WFNS 1-2) Using Speckle-tracking Echocardiography (STRAIN)</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>University Hospital, Bordeaux</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>University Hospital, Bordeaux</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>
      Subarachnoid hemorrhage (SAH) can cause transient myocardial dysfunction. Recently, it have&#xD;
      been reported that myocardial dysfunctions that occur in SAH are associated with poor&#xD;
      outcomes. It therefore appears essential to detect theses dysfunctions with the higher&#xD;
      sensitivity as possible. Strain measurement using speckle-tracking echocardiography may&#xD;
      detect myocardial dysfunction with great sensitivity. The main objective of this study is to&#xD;
      assess the prevalence of myocardial dysfunction in &quot;non-severe&quot; SAH (defined by a WFNS grade&#xD;
      1 or 2), using speckle-tracking echocardiography. This study also aims to analyse Strain&#xD;
      measurement with classical echocardiography and serum markers (troponin, BNP) of cardiac&#xD;
      dysfunction.&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Cardiac complication, occurring in the early phase of SAH has been well described. It seems&#xD;
      that the pathophysiological mechanism involves vegetative hyperactivity due to the acute&#xD;
      cerebral injury. It has been shown that stress cardiomyopathy is associated with delayed&#xD;
      cerebral ischemia (DCI) and poor outcomes. Manifestations of stress cardiomyopathy are&#xD;
      changes in electrocardiogram, release of cardiac biomarkers such as troponin and BNP, and&#xD;
      echography evidence of impaired left ventricle ejection fraction with the use of Simpson&#xD;
      technique and regional wall motion abnormalities. These two techniques bear intra-observer&#xD;
      variability. A new method is available to assess left ventricular contractility at the&#xD;
      bedside. Two-dimensional speckle-tracking images with echocardiography allows one to track a&#xD;
      natural myocardial marker within the myocardium by standard transthoracic echocardiography.&#xD;
      It provides unique insights into myocardial function such as tissue deformations and strain&#xD;
      rate, which is the rate of deformation. This method is more sensitive than classical&#xD;
      echographic left ventricular ejection fraction evaluation and bears very low interobserver&#xD;
      variability. The Global Longitudinal Strain (GLS) is the most studied parameter.&#xD;
&#xD;
      Early detection of cardiac dysfunction in SAH followed by appropriate monitoring and&#xD;
      management may improve outcome in SAH. This is a prospective, observational and mono-center&#xD;
      study.&#xD;
&#xD;
      Patients with &quot;non-severe&quot; SAH will benefit from an echocardiography where Left Ventricular&#xD;
      Ejection Fraction (LVEF) and GLS will be assessed on day 1, 3 and 7 following the acute&#xD;
      injury.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Completed</overall_status>
  <start_date type="Actual">January 2, 2019</start_date>
  <completion_date type="Actual">January 1, 2021</completion_date>
  <primary_completion_date type="Actual">December 25, 2020</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Case-Only</observational_model>
    <time_perspective>Prospective</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>Global Longitudinal Strain</measure>
    <time_frame>Day 1 of hospitalization</time_frame>
    <description>It is calculated using values of longitudinal strain measured in the three-,four-, and two-chamber of the left ventricle of the heart. GLS is expressed as percentage. Strain is a measure of myocardial muscle fiber shortening during contraction and is calculated as the systolic segment shortening between end-systolic (ES) segment length (L) and end-diastolic (ED) length: strain = (-LES - LED)/LED x 100 %.</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Global Longitudinal Strain</measure>
    <time_frame>Day 3 of hospitalization</time_frame>
    <description>is calculated using values of longitudinal strain measured in the three-,four-, and two-chamber of the left ventricle of the heart. GLS is expressed as percentage. Strain is a measure of myocardial muscle fiber shortening during contraction and is calculated as the systolic segment shortening between end-systolic (ES) segment length (L) and end-diastolic (ED) length: strain = (-LES - LED)/LED x 100 %.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Global Longitudinal Strain</measure>
    <time_frame>Day 7 of hospitalization</time_frame>
    <description>is calculated using values of longitudinal strain measured in the three-,four-, and two-chamber of the left ventricle of the heart. GLS is expressed as percentage. Strain is a measure of myocardial muscle fiber shortening during contraction and is calculated as the systolic segment shortening between end-systolic (ES) segment length (L) and end-diastolic (ED) length: strain = (-LES - LED)/LED x 100 %.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Change of Left Ventricular Ejection Fraction using Simpson technique</measure>
    <time_frame>Days 1, 3 and 7 of hospitalization</time_frame>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Change in serum troponin level</measure>
    <time_frame>Days 1, 3 and 7 of hospitalization</time_frame>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Change in brain natriuretic peptide (BNP) level</measure>
    <time_frame>Days 1, 3 and 7 of hospitalization</time_frame>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Electrocardiogram abnormalities</measure>
    <time_frame>Up to day 7 of hospitalization</time_frame>
    <description>Abnormalities expected:&#xD;
abnormal Q or QS wave (≥30 ms or a pathological R wave in V1 to V2)&#xD;
ST de- pression (ST depression ≥ 0.1 mV, 80 ms post-J point)&#xD;
ST elevation (ST elevation ≥ .1 mV)&#xD;
peaked upright T wave (prominent peaked T wave)&#xD;
T-wave inver- sion (pathologic T-wave inversion)&#xD;
nonspecific ST- or T-wave changes</description>
  </secondary_outcome>
  <number_of_groups>1</number_of_groups>
  <enrollment type="Actual">117</enrollment>
  <condition>Subarachnoid Hemorrhage (SAH)</condition>
  <condition>Left Ventricular Dysfunction</condition>
  <condition>Stress Cardiomyopathy</condition>
  <arm_group>
    <arm_group_label>Patients with a &quot;non-severe&quot; subarachnoid hemorrhage</arm_group_label>
  </arm_group>
  <intervention>
    <intervention_type>Diagnostic Test</intervention_type>
    <intervention_name>Global Longitudinal Strain measure</intervention_name>
    <description>Global Longitudinal Strain measure on day 1 of hospitalization</description>
    <arm_group_label>Patients with a &quot;non-severe&quot; subarachnoid hemorrhage</arm_group_label>
  </intervention>
  <eligibility>
    <study_pop>
      <textblock>
        Patient older than 18 years hospitalized in neuro-intensive care unit with a &quot;non-severe&quot;&#xD;
        subarachnoid hemorrhage (WFNS 1 or 2)&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Non-Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  patient older than 18 years&#xD;
&#xD;
          -  hospitalized in neuro-intensive care unit with a &quot;non-severe&quot; subarachnoid hemorrhage&#xD;
             (WFNS 1 or 2)&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  low echogenicity&#xD;
&#xD;
          -  history of cardiac malformation or cardiac surgery&#xD;
&#xD;
          -  severe valvular heart disease&#xD;
&#xD;
          -  dilated cardiomyopathy&#xD;
&#xD;
          -  acute coronary syndrome&#xD;
&#xD;
          -  permanent arrythmia&#xD;
&#xD;
          -  patient refusal&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <location>
    <facility>
      <name>CHU de Bordeaux</name>
      <address>
        <city>Bordeaux</city>
        <zip>33076</zip>
        <country>France</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>France</country>
  </location_countries>
  <verification_date>January 2021</verification_date>
  <study_first_submitted>November 29, 2018</study_first_submitted>
  <study_first_submitted_qc>November 30, 2018</study_first_submitted_qc>
  <study_first_posted type="Actual">December 3, 2018</study_first_posted>
  <last_update_submitted>January 5, 2021</last_update_submitted>
  <last_update_submitted_qc>January 5, 2021</last_update_submitted_qc>
  <last_update_posted type="Actual">January 6, 2021</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <keyword>Subarachnoid Hemorrhage (SAH)</keyword>
  <keyword>Left Ventricular Dysfunction</keyword>
  <keyword>Intensive Care Unit</keyword>
  <keyword>Speckle-tracking</keyword>
  <keyword>STRAIN</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Subarachnoid Hemorrhage</mesh_term>
    <mesh_term>Cardiomyopathies</mesh_term>
    <mesh_term>Ventricular Dysfunction</mesh_term>
    <mesh_term>Ventricular Dysfunction, Left</mesh_term>
    <mesh_term>Takotsubo Cardiomyopathy</mesh_term>
    <mesh_term>Hemorrhage</mesh_term>
  </condition_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
  </patient_data>
  <!-- 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/NCT03761654
org study id: CHUBX 2018/51
nct id: NCT03761654
lead sponsor: 
has dmc: No
is fda regulated drug: No
is fda regulated device: No
Subarachnoid hemorrhage (SAH) can cause transient myocardial dysfunction. Recently, it have
      been reported that myocardial dysfunctions that occur in SAH are associated with poor
      outcomes. It therefore appears essential to detect theses dysfunctions with the higher
      sensitivity as possible. Strain measurement using speckle-tracking echocardiography may
      detect myocardial dysfunction with great sensitivity. The main objective of this study is to
      assess the prevalence of myocardial dysfunction in "non-severe" SAH (defined by a WFNS grade
      1 or 2), using speckle-tracking echocardiography. This study also aims to analyse Strain
      measurement with classical echocardiography and serum markers (troponin, BNP) of cardiac
      dysfunction.
Cardiac complication, occurring in the early phase of SAH has been well described. It seems
      that the pathophysiological mechanism involves vegetative hyperactivity due to the acute
      cerebral injury. It has been shown that stress cardiomyopathy is associated with delayed
      cerebral ischemia (DCI) and poor outcomes. Manifestations of stress cardiomyopathy are
      changes in electrocardiogram, release of cardiac biomarkers such as troponin and BNP, and
      echography evidence of impaired left ventricle ejection fraction with the use of Simpson
      technique and regional wall motion abnormalities. These two techniques bear intra-observer
      variability. A new method is available to assess left ventricular contractility at the
      bedside. Two-dimensional speckle-tracking images with echocardiography allows one to track a
      natural myocardial marker within the myocardium by standard transthoracic echocardiography.
      It provides unique insights into myocardial function such as tissue deformations and strain
      rate, which is the rate of deformation. This method is more sensitive than classical
      echographic left ventricular ejection fraction evaluation and bears very low interobserver
      variability. The Global Longitudinal Strain (GLS) is the most studied parameter.

      Early detection of cardiac dysfunction in SAH followed by appropriate monitoring and
      management may improve outcome in SAH. This is a prospective, observational and mono-center
      study.

      Patients with "non-severe" SAH will benefit from an echocardiography where Left Ventricular
      Ejection Fraction (LVEF) and GLS will be assessed on day 1, 3 and 7 following the acute
      injury.
observational model: Case-Only
time perspective: Prospective
measure: Global Longitudinal Strain
time frame: Day 1 of hospitalization
description: It is calculated using values of longitudinal strain measured in the three-,four-, and two-chamber of the left ventricle of the heart. GLS is expressed as percentage. Strain is a measure of myocardial muscle fiber shortening during contraction and is calculated as the systolic segment shortening between end-systolic (ES) segment length (L) and end-diastolic (ED) length: strain = (-LES - LED)/LED x 100 %.
measure: Global Longitudinal Strain
time frame: Day 3 of hospitalization
description: is calculated using values of longitudinal strain measured in the three-,four-, and two-chamber of the left ventricle of the heart. GLS is expressed as percentage. Strain is a measure of myocardial muscle fiber shortening during contraction and is calculated as the systolic segment shortening between end-systolic (ES) segment length (L) and end-diastolic (ED) length: strain = (-LES - LED)/LED x 100 %.
measure: Global Longitudinal Strain
time frame: Day 7 of hospitalization
description: is calculated using values of longitudinal strain measured in the three-,four-, and two-chamber of the left ventricle of the heart. GLS is expressed as percentage. Strain is a measure of myocardial muscle fiber shortening during contraction and is calculated as the systolic segment shortening between end-systolic (ES) segment length (L) and end-diastolic (ED) length: strain = (-LES - LED)/LED x 100 %.
measure: Change of Left Ventricular Ejection Fraction using Simpson technique
time frame: Days 1, 3 and 7 of hospitalization
measure: Change in serum troponin level
time frame: Days 1, 3 and 7 of hospitalization
measure: Change in brain natriuretic peptide (BNP) level
time frame: Days 1, 3 and 7 of hospitalization
measure: Electrocardiogram abnormalities
time frame: Up to day 7 of hospitalization
description: Abnormalities expected:
abnormal Q or QS wave (≥30 ms or a pathological R wave in V1 to V2)
ST de- pression (ST depression ≥ 0.1 mV, 80 ms post-J point)
ST elevation (ST elevation ≥ .1 mV)
peaked upright T wave (prominent peaked T wave)
T-wave inver- sion (pathologic T-wave inversion)
nonspecific ST- or T-wave changes
arm group label: Patients with a "non-severe" subarachnoid hemorrhage
intervention type: Diagnostic Test
intervention name: Global Longitudinal Strain measure
description: Global Longitudinal Strain measure on day 1 of hospitalization
arm group label: Patients with a "non-severe" subarachnoid hemorrhage
study pop: 
sampling method: Non-Probability Sample
criteria: 
gender: All
minimum age: 18 Years
maximum age: N/A
healthy volunteers: No
facility: 
country: France
responsible party type: Sponsor
mesh term: Subarachnoid Hemorrhage
mesh term: Cardiomyopathies
mesh term: Ventricular Dysfunction
mesh term: Ventricular Dysfunction, Left
mesh term: Takotsubo Cardiomyopathy
mesh term: Hemorrhage
sharing ipd: No