This trial is active, not recruiting.

Conditions subarachnoid hemorrhage, myocardial stunning, takotsubo cardiomyopathy
Sponsor VU University Medical Center
Collaborator Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)
Start date May 2005
End date June 2008
Trial size 350 participants
Trial identifier NCT00123695, 04-193


There is increasing interest in myocardial abnormalities following central nervous system events, such as subarachnoid hemorrhage (SAH). These cardiac abnormalities include ECG changes, decreased cardiac output, decreased blood pressure, specific cardiac enzyme elevations, and segmental wall motion abnormalities (SWMA). Interestingly, wall motion abnormalities and ECG changes have shown to be reversible, and therefore the dysfunction has been described as neurogenic myocardial stunning.

The pathophysiology of cardiac dysfunction following SAH has not yet been fully elucidated. Many reports (mainly case reports) have been published, but so far no study has investigated the frequency of these abnormalities in a prospective manner, have correlated the occurrence of the different cardiac abnormalities, and have assessed which clinical variables can predict cardiac dysfunction. And only a limited number of studies have related neurological outcome with cardiac dysfunction.

United States No locations recruiting
Other countries No locations recruiting

Study Design

Observational model cohort
Time perspective prospective

Eligibility Criteria

Male or female participants at least 10 years old.

Inclusion Criteria: - Diagnosed with aneurysmal subarachnoid hemorrhage - Admitted within 72 hours of the bleed Exclusion Criteria: - No informed consent - Patients or patients' family unwillingness to participate

Additional Information

Official title Serial Echocardiography After Subarachnoid Hemorrhage (S.E.A.S.)
Principal investigator Frans C Visser, MD PhD
Description Objectives: Therefore, our study objectives are: 1) Assessment of the frequency of myocardial dysfunction (segmental wall motion abnormalities, cardiac-specific enzyme elevations, and ECG changes) in patients with SAH. 2) Determination of predictive clinical variables for the occurrence of myocardial dysfunction following SAH. 3) Impact of myocardial dysfunction on neurological prognosis: death, secondary cerebral ischemia, hydrocephalus and rebleeding. Methods: For this purpose serial echocardiograms and ECGs will be obtained and cardiac enzymes will be measured in 200-400 patients admitted to hospital with SAH in the four participating centers. The clinical variables that will be studied to predict cardiac dysfunction are: medical history, the CT-scan score, circulatory parameters, blood samples, medication, surgical intervention (coiling or clipping), and the neurological condition (Glasgow Coma Scale). The echocardiograms, ECGs and cardiac enzymes will be studied to determine if they have independent prognostic value for the outcome in SAH patients. Expected Results: As ECG changes and drops in blood pressure are known to occur frequently, the researchers expect to find that cardiac contractile dysfunction in patients with SAH occurs more frequently than is assumed now. Moreover, if cardiac abnormalities have neurological prognostic significance further studies are needed for early recognition and treatment of the cardiac abnormalities in SAH, a condition with a very poor prognosis.
Trial information was received from ClinicalTrials.gov and was last updated in March 2008.
Information provided to ClinicalTrials.gov by VU University Medical Center.