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Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
Published on: August 30, 2020
Right sylvian fissure subarachnoid hemorrhage has electrocardiographic consequences
Y Hirashima1, S Takashima, N Matsumura
1Department of Neurosurgery, Toyama Medical and Pharmaceutical University, Toyama, Japan. yhira@ms.toyama-mpu.ac.jp
Insights
Subarachnoid hemorrhage (SAH) can cause abnormal ECG changes, particularly with high blood pressure or bleeding in the right sylvian fissure. These findings highlight potential cardiac risks in SAH patients.
Area of Science:
- Neurology
- Cardiology
- Radiology
Background:
- Subarachnoid hemorrhage (SAH) is often associated with abnormal electrocardiogram (ECG) findings.
- The right insular cortex is implicated in sympathetic cardiovascular regulation.
Purpose of the Study:
- To investigate the laterality and location of SAH in relation to ECG, blood pressure, and heart rate changes.
- To determine if SAH location influences cardiovascular alterations.
Main Methods:
- Studied 118 SAH patients, excluding those deceased within 1 month.
- Collected blood pressure and pulse data on admission.
- Assessed ECG changes on admission and at 1 month.
- Quantified SAH in 8 cisterns/fissures using brain CT scans.
Main Results:
- 26 patients (22%) had abnormal admission ECGs.
- Higher systolic and diastolic blood pressure, and greater SAH volume in specific cisterns (e.g., right sylvian fissure) were linked to ECG changes.
- Multivariate analysis identified elevated systolic blood pressure (>160 mm Hg) and SAH in the quadrigeminal cistern and right sylvian fissure as independent predictors of abnormal ECGs.
Conclusions:
- Cardiac complications may occur in SAH patients with significant right sylvian fissure bleeding.
- Elevated systolic blood pressure (>160 mm Hg) is a key factor associated with cardiac consequences in SAH.
Background And Purpose:
Abnormal ECG changes are frequently observed in patients with subarachnoid hemorrhage (SAH). Recently, evidence has been obtained that right insular cortex mediates sympathetic cardiovascular effects. We therefore assessed the laterality and location of SAH dominance in inducing cardiovascular changes as measured by ECG, blood pressure, and heart rate.
Methods:
After exclusion of 11 SAH patients who died within 1 month after onset, we studied 118 consecutive patients. Data were obtained from records of blood pressure and pulse on admission. Abnormal ECG changes were determined from ECGs on admission and almost 1 month later. From brain CT scans performed immediately after admission, the amount of SAH in each of the 8 cisterns and fissures was measured semiquantitatively.
Results:
Twenty-six patients had abnormal changes on admission ECG, while 92 patients did not. Systolic blood pressure, diastolic blood pressure, and the amounts of blood in the left ambient cistern, left suprasellar cistern, quadrigeminal cistern, right ambient cistern, right suprasellar cistern, right sylvian fissure, and the set of all cisterns were significantly greater in the group with ECG change than in the group without ECG change. Multivariate logistic regression analysis with stepwise method indicated that systolic blood pressure >160 mm Hg (P=0.0006) and the amounts of SAH in the quadrigeminal cistern (P=0.022) and right sylvian fissure (P=0.0019) were independently associated with abnormal ECG change.
Conclusions:
Cardiac consequences are possible in patients with massive right sylvian fissure SAH or when systolic blood pressure is >160 mm Hg.
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