Intracranial hemorrhage is a condition characterized by high mortality rates and suboptimal functional outcomes. It precipitates both direct brain injury and subsequent secondary injuries, including delayed cerebral ischemia, brain edema, and hydrocephalus. Complications such as cardiac injury may also arise, categorizing them within the cerebrocardiac syndrome (CCS). The clinical spectrum of CCS encompasses acute myocardial injury, acute coronary syndrome, left ventricular systolic and diastolic dysfunction, cardiac arrhythmias, and sudden cardiac death, all of which are associated with increased mortality and deterioration in patient status. The precise pathophysiological mechanisms underlying both cerebral and cardiac injuries remain enigmatic, and the implications for diagnosis and therapeutic strategies are yet to be fully explored. In this study, we propose to enroll patients with intracranial hemorrhage who will undergo conventional treatment and comprehensive multidisciplinary evaluations. Our observational research is grounded in a multimodal omics and imaging approach, aimed at investigating both local and systemic injuries subsequent to intracranial hemorrhage. This comprehensive strategy is intended to facilitate precise diagnosis, risk stratification, and clinical decision-making, while also shedding light on the pathophysiological mechanisms involved. The primary objectives of this research are to address the following key questions: * \[Question 1\] What are the pathophysiological mechanisms underlying cardiac injury in patients with intracranial hemorrhage? * \[Question 2\] What are the pathophysiological mechanisms responsible for early and delayed brain injuries following intracranial hemorrhage?\"
Study Type
OBSERVATIONAL
Enrollment
1,000
Multi-disciplinary assessment including blood tests, CSF test, electrocardiograms, ultrasound, imaging, etc
Beijing Tiantan Hospital Affiliated to Capital Medical University
Beijing, Beijing Municipality, China
RECRUITINGShort-term cardiac events
Participants who suffer from sudden dysfunction or structural abnormalities of the heart (e.g., arrhythmias, myocardial infarct, sudden death) confirmed through: 1. Electrocardiogram (ECG); 2. Cardiac biomarkers (e.g., troponin); 3. Echocardiography; 4. Holter monitoring.
Time frame: At discharge (assessed up to 5 days)
Long-term cardiac events
Participants who suffer from sudden dysfunction or structural abnormalities of the heart (e.g., arrhythmias, myocardial infarct, sudden death) confirmed through: 1. Electrocardiogram (ECG); 2. Cardiac biomarkers (e.g., troponin); 3. Echocardiography; 4. Holter monitoring.
Time frame: 3 months post-discharge
Short-term delayed cerebral ischemia
Participants who suffer from secondary reduction in cerebral blood flow due to mechanisms such as vasospasm, microthrombosis, or hemodynamic disturbances, confirmed through: 1. Head CT/MRI; 2. Transcranial doppler sonography (TCD).
Time frame: At discharge (assessed up to 5 days)
Long-term delayed cerebral ishemia
Participants who suffer from secondary reduction in cerebral blood flow due to mechanisms such as vasospasm, microthrombosis, or hemodynamic disturbances, confirmed through: 1. Head CT/MRI; 2. Transcranial doppler sonography (TCD).
Time frame: 3 months post-discharge
Short-term brain-heart syndrome
Participants who suffer from cardiac dyafunction triggered by cerebral hemorrhage. Clinical manifestations include ECG abnormalities (ST-T changes, prolonged QT interval, arrhythmias), elevated cardiac enzymes (e.g., troponin), cardiac insufficiency (e.g., heart failure, pulmonary edema), chest pain mimicking myocardial ischemia and myocardial infarct. Some patients may develop life-threatening arrhythmias (e.g., ventricular fibrillation). Diagnostic evaluations involve: 1. Electrocardiogram (ECG); 2. Cardiac enzyme tests (e.g., troponin, CK-MB); 3. Echocardiography; 4. Brain imaging (CT/MRI); 5. Biomarkers (e.g., BNP).
Time frame: At discharge (assessed up to 5 days)
Long-term brain-heart syndrome
Participants who suffer from cardiac dyafunction triggered by cerebral hemorrhage. Clinical manifestations include ECG abnormalities (ST-T changes, prolonged QT interval, arrhythmias), elevated cardiac enzymes (e.g., troponin), cardiac insufficiency (e.g., heart failure, pulmonary edema), chest pain mimicking myocardial ischemia and myocardial infarct. Some patients may develop life-threatening arrhythmias (e.g., ventricular fibrillation). Diagnostic evaluations involve: 1. Electrocardiogram (ECG); 2. Cardiac enzyme tests (e.g., troponin, CK-MB); 3. Echocardiography; 4. Brain imaging (CT/MRI); 5. Biomarkers (e.g., BNP).
Time frame: 3 months post-discharge
Short-term modified Rankin Scale scores
The modified Rankin Scale (mRS) scores of participants evaluated by specialists. The mRS scores range form 0 to 6, with higher scores indicating worse outcomes.
Time frame: At discharge (assessed up to 5 days)
Long-term modified Rankin Scale scores
The modified Rankin Scale (mRS) scores of participants evaluated by specialists. The mRS scores range form 0 to 6, with higher scores indicating worse outcomes.
Time frame: 3 months post-discharge
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