• Animal model
• Cardiac injury
• Echocardiography
• Fingolimod
• Inflammation
• Macrophage
• Monocyte
• Subarachnoid hemorrhage
• Systolic function
• White blood cell

• Subarachnoid Hemorrhage/complications
• Subarachnoid Hemorrhage/physiopathology
• Animals
• Male
• Ventricular Dysfunction, Left/etiology
• Ventricular Dysfunction, Left/physiopathology
• Middle Aged
• Rats, Sprague-Dawley
• Humans
• Female
• Retrospective Studies
• Monocytes
• Macrophages
• Rats
• Aged
• Inflammation
• Adult
• Fingolimod Hydrochloride/pharmacology
• Fingolimod Hydrochloride/therapeutic use
• Echocardiography
• Disease Models, Animal

• brain injuries
• neuroscience
• cerebrovascular disorders

• Humans
• Subarachnoid Hemorrhage/diagnostic imaging
• Subarachnoid Hemorrhage/therapy
• Brain Ischemia/diagnostic imaging
• Brain Ischemia/therapy
• Cerebral Infarction/etiology
• Hypertension/complications
• Aneurysm

• appropriate use criteria
• echocardiography order
• high-value care
• quality control
• quality improvement

• Humans
• Subarachnoid Hemorrhage/complications
• Subarachnoid Hemorrhage/diagnostic imaging
• Insular Cortex

• 2017A07 Bai Qian Wan Talent Plan
• 2020YFC2004701 Research and Development Program of China
• 2021YFC2501101 Research and Development Program of China
• Research and Development Program of China

• Editorials
• myocardial injury
• stroke
• troponin
• women

• Humans
• Female
• Male
• Ischemic Stroke/complications
• Stroke/etiology
• Brain Ischemia/complications
• Heart

• K23 HL155506 NHLBI NIH HHS
• National Institutes of Health
• National Heart, Lung, and Blood Institute

• Humans
• Pulmonary Edema/etiology
• Subarachnoid Hemorrhage/complications
• Subarachnoid Hemorrhage/surgery

• Blood-brain barrier
• Neurogenic stress cardiomyopathy
• Neuroinflammation
• Stroke
• Stroke-heart-brain interactions
• Takotsubo cardiomyopathy

• SAB
• cardiomyopathy
• intensive care
• neuro ICU
• subarachnoid hemorrhage
• takotsubo

•

Takotsubo syndrome and myocardial infarction can present with ST segment elevation.

Previous studies comparing electrocardiogram (ECG) in Takotsubo syndrome (TS) versus ST elevation myocardial infarction (STEMI) included TS patients without ST elevation, did not consider the culprit lesion in STEMI or had groups that were unbalanced regarding sex and age. Accounting for these factors, we sought to conduct a more reliable comparison of ECG in TS with ST-elevation (STE-TS) versus STEMI. The secondary aim was to investigate if ST segment changes, T wave inversion or prolonged QT interval predicted ventricular arrhythmia or death in STE-TS and STEMI.

All STE-TS patients who presented at Sahlgrenska University Hospital between 2008 and 2019 were matched by sex and age to STEMI patients. STEMI patients were subcategorized according to whether or not the culprit lesion was located in the left anterior descending artery (LAD). Baseline characteristics, in‐hospital outcomes and admission ECGs were analyzed.

104 STE-TS patients were sex- and age-matched with 274 STEMI patients (113 LAD-STEMI, 161 non-LAD STEMI). Admission ECG in STE-TS was more similar to LAD STEMI than non-LAD STEMI. Reciprocal ST depression was less common in STE-TS (7/104, 6.7%) compared with STEMI (112/274, 41%; p= < 0.001). The sum of all ST elevations and the sum of all ST-deviations predicted life-threatening ventricular arrhythmia (LTVA) or death in LAD STEMI but not in STE-TS.

In conclusion, admission ECG in STE-TS was similar to LAD STEMI but reciprocal ST depression was less common in STE-TS compared with STEMI overall. ST segment changes predicted LTVA or death in STEMI but not in STE-TS.

• computed tomography
• heart arrest
• intracranial hemorrhage
• meta-analysis
• subarachnoid hemorrhage
• sudden cardiac arrest

• arrhythmias
• autonomic dysfunction
• cardiac injury
• stroke
• troponin

• UNCE/MED/002 Charles University
• Progres Q 38 Charles University

TroponinT levels are frequently elevated after subarachnoid hemorrhage (SAH). However, their clinical impact on long term outcomes still remains unclear. This study evaluates the association of TroponinT and functional outcomes 3 months after SAH. Data were obtained in the frame of a randomized controlled trial exploring the association of Goal-directed hemodynamic therapy and outcomes after SAH (NCT01832389). TroponinT was measured daily for the first 14 days after admission or until discharge from the ICU. Outcome was assessed using Glasgow Outcome Scale (GOS) 3 months after discharge. Logistic regression was used to explore the association between initial TroponinT values stratified by tertiles and admission as well as outcome parameters. TroponinT measurements were analyzed in 105 patients. TroponinT values at admission were associated with outcome assessed by GOS in a univariate analysis. TroponinT was not predictive of vasospasm or delayed cerebral ischemia, but an association with pulmonary and cardiac complications was observed. After adjustment for age, history of arterial hypertension and World Federation of Neurosurgical Societies (WFNS) grade, TroponinT levels at admission were not independently associated with worse outcome (GOS 1–3) or death at 3 months. In summary, TroponinT levels at admission are associated with 3 months-GOS but have limited ability to independently predict outcome after SAH.

This study was performed to identify genes and lncRNAs involved in the pathogenesis of subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysm (RIA).

Microarray GSE36791 was downloaded from Gene Expression Omnibus (GEO) database followed by the identification of significantly different expressed RNAs (DERs, including lncRNA and mRNA) between patients with SAH and healthy individuals. Then, the functional analyses of DEmRNAs were conducted and weighted gene co-expression network analysis (WGCNA) was also performed to extract the modules associated with SAH. Following, the lncRNA-mRNA co-expression network was constructed and the gene set enrichment analysis (GSEA) was performed to screen key RNA biomarkers involved in the pathogenesis of SAH from RIA. We also verified the results in a bigger dataset GSE7337.

Totally, 561 DERs, including 25 DElncRNAs and 536 DEmRNAs, were identified. Functional analysis revealed that the DEmRNAs were mainly associated with immune response-associated GO-BP terms and KEGG pathways. Moreover, there were 6 modules significantly positive-correlated with SAH. The lncRNA-mRNA co-expression network contained 2 lncRNAs (LINC00265 and LINC00937) and 169 mRNAs. The GSEA analysis showed that these two lncRNAs were associated with three pathways (cytokine-cytokine receptor interaction, neurotrophin signaling pathway, and apoptosis). Additionally, IRAK3 and NFKBIA involved in the neurotrophin signaling pathway and apoptosis while IL1R2, IL18RAP and IL18R1 was associated with cytokine-cytokine receptor interaction pathway. The expression levels of these genes have the same trend in GSE36791 and GSE7337.

LINC00265 and LINC00937 may be implicated with the pathogenesis of SAH from RIA. They were involved in three important regulatory pathways. 5 mRNAs played important roles in the three pathways.

The online version contains supplementary material available at 10.1186/s12883-021-02156-1.

Traumatic brain injury (TBI) is an acutely stressful condition. Stress and conglomeration of various factors predispose to the involvement of other organ systems. The stress response from TBI has been associated with cardiovascular complications reflecting as repolarization abnormalities on electrocardiogram (ECG) to systolic dysfunction on echocardiography. However, the perioperative cardiac functions in patients with TBI have not been evaluated.

We conducted a prospective observational study in 60 consecutive adult patients of either sex between the age of 10 and 70 years with an isolated head injury who were taken up for decompressive craniectomy as per institutional protocol. ECG and transthoracic echocardiography was carried out preoperatively and then postoperatively within 24–48 h.

The mean age of our study population was 39 + 13 years with a median Glasgow coma score of 11. A majority (73%) of our patients suffered moderate TBI. Preoperatively, ECG changes were seen in 48.33% of patients. Postoperatively, ECG changes declined and were seen only in 13.33% of the total patients. Similarly, echocardiography demonstrated preoperative systolic dysfunction in 13.33% of the total study population. Later, it was found that systolic function significantly improved in all the patients after surgery.

Cardiac dysfunction occurs frequently following TBI. Even patients with mild TBI had preoperative systolic dysfunction on echocardiography. Surgical intervention in the form of hematoma evacuation and decompression was associated with significant regression of both ECG and echocardiographic changes.

• Electrocardiography
• Transthoracic echocardiography
• Traumatic brain injury

Coronary artery vasospasm (CAV) is a reversible, transient form of vasoconstriction with clinical manifestations ranging from stable angina to acute coronary syndromes (ACS). Vasospasm of epicardial coronary arteries or associated micro-vasculature can lead to total or subtotal occlusion and has been demonstrated in nearly 50% of patients undergoing angiography for suspected ACS. The mechanism for CAV has been described in literature, but in a subgroup of patients presenting with intracranial hemorrhage, it appears to be multifactorial. These patients tend to have electrocardiographic changes, elevation of cardiac biomarkers of injury and neurogenic stress cardiomyopathy.

A 44-year-old woman presented with severe headaches and tonic-clonic seizures. She was found to have diffuse subarachnoid hemorrhage (SAH) requiring ventricular drain placement, coil embolization and induced hypertension. She subsequently developed chest pain with ST elevations in anterior precordial leads, elevated cardiac enzymes and apical ballooning with left ventricular ejection fraction of 35% on transthoracic echocardiogram. Coronary angiogram revealed severe diffuse triple vessel stenoses secondary to CAV seen distally. Subsequent cardiac MRI notable for apical non-viability and scar formation.

This case highlights a unique etiology of acute myocardial infarction in a patient with SAH leading to ST elevations, diffuse triple vessel CAV and apical scar.

• ST-elevation myocardial infarction
• Acute coronary syndrome
• Stress induced cardiomyopathy
• Coronary artery vasospasm
• Cerebral vasospasm
• Subarachnoid hemorrhage
• Case report

Ruptured intracranial aneurysm (IA)-induced subarachnoid hemorrhage (SAH) triggers a series of immune responses and inflammation in the brain and body. The present study was conducted to identify additional circulating biomarkers that may serve as potential therapeutic targets for SAH-induced inflammation. Differentially expressed (DE) long non-coding RNAs (lncRNAs; DElncRNAs) and genes (DEGs) in the peripheral blood mononuclear cells between patients with IA rupture-induced SAH and healthy controls were identified in the GSE36791 dataset. DEGs were used for weighted gene co-expression network analysis (WGCNA), and SAH-associated WGCNA modules were identified. Subsequently, an lncRNA-mRNA regulatory network was constructed using the DEGs in SAH-associated WGCNA modules. A total of 25 DElncRNAs and 1,979 DEGs were screened from patients with IA-induced SAH in the GSE36791 dataset compared with the controls. A total of 11 WGCNA modules, including four upregulated modules significantly associated with IA rupture-induced SAH were obtained. The DEGs in the SAH-associated modules were associated with Gene Ontology biological processes such as ‘regulation of programmed cell death’, ‘apoptosis’ and ‘immune response’. The subsequent lncRNA-mRNA regulatory network included seven upregulated lncRNAs [HCG27, ZNFX1 antisense RNA 1, long intergenic non-protein coding RNA (LINC)00265, murine retrovirus integration site 1 homolog-antisense RNA 1, cytochrome P450 1B1-AS1, LINC01347 and LINC02193] and 375 DEGs. Functional enrichment analysis and screening in the Comparative Toxicogenomics Database demonstrated that SAH-associated DEGs, including neutrophil cytosolic factor (NCF)2 and NCF4, were enriched in ‘chemokine signaling pathway’ (hsa04062), ‘leukocyte transendothelial migration’ (hsa04670) and ‘Fc gamma R-mediated phagocytosis’ (hsa04666). The upregulated lncRNAs and genes, including NCF2 and NCF4, in patients with IA rupture-induced SAH indicated their respective potentials as anti-inflammatory therapeutic targets.

• aneurysmal subarachnoid
• intra-aortic balloon pumps
• takotsubo cardiomyopathy
• vascular disorders

• subarachnoid hemorrhage
• troponin

• Acute respiratory distress syndrome
• Brain injury
• Brain-heart crosstalk
• Brain-lung crosstalk
• Cardiomyopathy
• Neurogenic pulmonary œdema

• K24 AG052573 NIA NIH HHS

• BNP
• NT-proBNP
• brain hemorrhage
• brain–heart axis
• cardiac troponin
• ischemic stroke
• meta-analysis
• stroke

• Biomarkers/blood
• Heart Diseases/blood
• Heart Diseases/etiology
• Humans
• Intracranial Hemorrhages/blood
• Intracranial Hemorrhages/complications
• Natriuretic Peptide, Brain/blood
• Peptide Fragments/blood
• Stroke/blood
• Stroke/complications
• Troponin I/blood

• exercise
• mobilization
• recovery
• rehabilitation
• stroke

Cardiac injury may occur after acute pathology of central nervous system (CNS) without any evidence of primary cardiac diseases. The resulting structural and/or functional changes are called cerebrocardiac syndrome (CCS). The great majority of studies have been performed in patients with subarachnoid hemorrhage (SAH), while CCS data after intracerebral hemorrhage (ICH) are rare. It may cause diagnostic and therapeutic pitfalls for the clinician due to a lack of specific clinical manifestations and diagnostic methods. Understanding the underlying pathophysiological and molecular mechanism(s) following cerebrovascular incidents will help to implement prevention and treatment strategies to improve the prognosis.

A 37-year-old man with a history of hypertension presented to our department on an emergency basis because of a sudden dizziness and left limb weakness. Cerebral computed tomography (CT) suggested ICH in the occipital and parietal lobes, and the chosen emergency treatment was hematoma evacuation. Left ventricular (LV) dysfunction occurred after the next 48 h and the electrocardiogram (ECG) showed non-ST elevation myocardial infarction. CCS was suspected first in the context of ICH due to the negative result of the coronary CT angiogram.

Misinterpretation of ischemic-like ECGs may lead to unnecessary or hazardous interventions and cause undue delay of rehabilitation after stroke. Our objective is to highlight the clinical implications of CCS and we hope the differential diagnoses will be considered in patients with acute CNS diseases.

• Stroke
• Intracerebral hemorrhage
• Cerebrocardiac syndrome
• Cardiac insufficiency
• Non-ST elevation myocardial infraction
• Case report
• Neurogenic stunned myocardium

• Neurocardiac axis
• Neurocardiology
• Neurological disorders

• Acute heart failure
• Arrhythmias
• Electrocardiography
• Swedish Coronary Angiography and Angioplasty Registry
• T-wave inversion
• Takotsubo syndrome

Cardiovascular complications in patients with subarachnoid hemorrhage are considered to be a neurally mediated process rather than a manifestation of coronary artery disease.

The aim of study is to show the incidence and type cardiac complications after traumatic and spontaneous SAH.

The study had prospective character in which included 104 patients, with diagnosed subarachnoid hemorrhage (SAH), in the period from 2014 to 2017. Two groups of patients were formed. Group I: patients with SAH caused by the rupture of a brain aneurysm. Group II: patients with SAH after traumatic brain injury.

Electrocardiogram (ECG) abnormalities was predominant after traumatic brain injury 74 %, with statistically significant difference atrial fibrillation 42.5 % (p = 0.043) and sinus bradycardia 31.4 % (p = 0.05). Hypertension are predominant in patients with spontaneous SAH with statistically significant difference (15 (27.7%) vs 36 (72%) p=0.034) and hypotension in group II (10 (18.5%) vs 2 (4%) p = 0.021 ) with traumatic SAH patients. The time in Intensive Care Unit (ICU) for traumatic SAH group was 6.1 ± 5.2 days and 3.9 ± 1.16 for spontaneous SAH group with statistical significance (p = 0.046). Respiratory support time was longer in traumatic SAH group (39.4 ± 23.44 vs. 15.66 ± 22.78) with p = 0.043.

Cardiac dysfunction in patients with subarachnoid hemorrhage are considered to be a neurally mediated process rather than a manifestation of coronary artery disease. Early treatment of cerebral injury could be reduce incidence of cardiac complications after traumatic brain injury. Cardiac dysfunction in patients with SAH is still very high, despite substantial qualitative progress in their treatment.

• brain injury
• cardiac dysfunction
• subarachnoid hemorrhage

• cardiopulmonary stress
• intensive care biomarker
• serum cortisol
• subarachnoid hemorrhage
• troponin I

• cardiomyopathy
• cardiopulmonary parameters
• critical care biomarker
• subarachnoid hemorrhage
• troponin I

• Acute cardiac complications
• Acute critical brain disease
• Acute critical brain injury
• Neurogenic stunned myocardium
• Stress cardiomyopathy

Subarachnoid hemorrhage (SAH) is a subtype of stroke with high mortality and morbidity. Impaired cerebral autoregulation following SAH has been reported owing to effects on sympathetic control, endothelial function, myogenic response, and cerebral metabolism. Impaired cerebral autoregulation is associated with early brain injury, cerebral vasospasm/delayed cerebral ischemia, and SAH prognosis. However, few drugs have been reported to improve cerebral autoregulation after SAH. Melatonin is a powerful antioxidant that is effective (easily crosses the blood brain barrier) and safe (tolerated in large doses without toxicity). Theoretically, melatonin may impact the control mechanisms of cerebral autoregulation via antioxidative effects, protection of endothelial cell integrity, suppression of sympathetic nerve activity, increase in nitric oxide bioavailability, mediation of the myogenic response, and amelioration of hypoxemia. Furthermore, melatonin may have a comprehensive effect on cerebral autoregulation. This review discusses the potential effects of melatonin on cerebral autoregulation following SAH, in terms of the association between pharmacological activities and the mechanisms of cerebral autoregulation.

• antioxidant
• cerebral autoregulation
• endothelial function
• melatonin
• subarachnoid hemorrhage
• sympathetic nerve

• acute coronary syndrome
• autonomic nervous system
• cardiomyopathy
• coronary heart disease
• electrocardiogram
• left ventricular dysfunction
• neurogenic
• stroke
• troponin

• Acute cardiac complications
• Acute critical brain disease
• Acute critical brain injury
• Neurogenic stunned myocardium
• Stress cardiomyopathy

• Cardiac abnormalities
• Cardiac biomarker elevation
• Death
• Delayed cerebral ischemia
• Echocardiographic wall motion abnormality
• Poor outcome
• Subarachnoid hemorrhage

• Biomarker
• Cardiac troponin
• Chronic disease
• Prognosis
• Release mechanism

• Acute Coronary Syndrome/blood
• Acute Coronary Syndrome/diagnosis
• Animals
• Biomarkers/blood
• Chronic Disease
• Humans
• Myocardial Infarction/blood
• Myocardial Infarction/diagnosis
• Myocardium/metabolism
• Troponin T/blood

• FS/15/13/31320 British Heart Foundation
• G1000737 Medical Research Council
• TG/15/1/31518 British Heart Foundation

• All-cause mortality
• Functional outcome
• Ischemic stroke
• NT-proBNP
• Prognosis

• aneurysmal subarachnoid hemorrhage
• brain natriuretic peptide
• cardiac troponin I
• neurocardiac injury
• noninvasive cardiac output