Skip to main content
OpenTrials
Completed

NCT Number: NCT03761654

Detection of Myocardial Dysfunction in Non-severe Subarachnoid Hemorrhage (WFNS 1-2) Using Speckle-tracking Echocardiography (STRAIN)

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.

Completed

Looking for future studies?

Notify Me

Key information

Conditions

Subarachnoid Hemorrhage (SAH) Brain Diseases Cardiomyopathies Cardiovascular Diseases Central Nervous System Diseases Cerebrovascular Disorders Heart Diseases Hemorrhage Intracranial Hemorrhages Left Ventricular Dysfunction Nervous System Diseases Pathologic Processes Pathological Conditions, Signs and Symptoms Sprains and Strains Stress Cardiomyopathy Subarachnoid Hemorrhage Takotsubo Cardiomyopathy Vascular Diseases Ventricular Dysfunction Ventricular Dysfunction, Left Wounds and Injuries

Age range

18 year and older

Sex eligibility

All sexes

Study type

Observational

Primary location

CHU de Bordeaux

Bordeaux, 33076, France

About this study

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.

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • patient older than 18 years
  • hospitalized in neuro-intensive care unit with a "non-severe" subarachnoid hemorrhage (WFNS 1 or 2)

Exclusion criteria

  • low echogenicity
  • history of cardiac malformation or cardiac surgery
  • severe valvular heart disease
  • dilated cardiomyopathy
  • acute coronary syndrome
  • permanent arrythmia
  • patient refusal

Treatment and study plan

Global Longitudinal Strain measure

Diagnostic Test

Global Longitudinal Strain measure on day 1 of hospitalization

Primary outcomes

  1. Global Longitudinal Strain

    Time frame: Day 1 of hospitalization

    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 %.

Secondary outcomes

  1. Global Longitudinal Strain

    Time frame: Day 3 of hospitalization

    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 %.

  2. Global Longitudinal Strain

    Time frame: Day 7 of hospitalization

    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 %.

  3. Change of Left Ventricular Ejection Fraction using Simpson technique

    Time frame: Days 1, 3 and 7 of hospitalization

  4. Change in serum troponin level

    Time frame: Days 1, 3 and 7 of hospitalization

  5. Change in brain natriuretic peptide (BNP) level

    Time frame: Days 1, 3 and 7 of hospitalization

  6. Electrocardiogram abnormalities

    Time frame: Up to day 7 of hospitalization

    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

Sponsors and collaborators

Lead sponsor

University Hospital, Bordeaux

Other

Registry information

Acronym: SAH-STRAIN

Important dates

Study start
2019
Primary completion
2020
Study completion
2021
First posted
Dec 3, 2018
Registry last updated
Jan 6, 2021

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

Related clinical trials

Published trials that share one or more normalized conditions with this study.