Subarachnoid haemorrhage‐induced reversible cardiac dysfunction: time course and potential mechanisms

• Published in: ESC Heart Failure 2024-06, Vol.11 (3), p.1625-1635
• Main Authors: Xiao, Yichao, Lai, Xin, Wang, Zhuo, Wang, Songyun, Wu, Zhihong, Liu, Qiming, Chen, Mingxian, Zhou, Shenghua
• Format: Article
• Language: English
• Subjects: Animals; Biomarkers; Biomarkers - blood; Cardiac dysfunction; Cerebrospinal fluid; Data acquisition systems; Disease Models, Animal; Echocardiography; Ejection fraction; Enzymes; Hemorrhage; Kinases; Laboratory animals; Male; Mortality; Neuropeptide Y; Neuropeptide Y - metabolism; Neuropeptides; Original; Physiology; Rats; Rats, Sprague-Dawley; Receptors, Neuropeptide Y - antagonists & inhibitors; Receptors, Neuropeptide Y - metabolism; Remodelling; Subarachnoid haemorrhage; Subarachnoid Hemorrhage - complications; Subarachnoid Hemorrhage - physiopathology; Sympathetic nervous system; Time Factors; Ventricular Remodeling - physiology
• ISSN: 2055-5822; 2055-5822
• DOI: 10.1002/ehf2.14732

Aims Cardiac dysfunction is commonly observed in patients with subarachnoid haemorrhage (SAH). However, the specific timeline of cardiac remodelling and the underlying mechanisms responsible for this effect following SAH remain unknown. This study aims to explore the impact of SAH on cardiac dysfunction and its potential mechanisms over time. Methods and results In Protocol 1, we investigated cardiac function and potential mechanisms in a Sprague‐Dawley rat model of SAH at six time points (baseline and Days 1, 3, 7, 14, and 28) while exploring the underlying mechanisms. Our assessments included the haemodynamic profile, echocardiography, and the concentrations of plasma biomarkers at various time points post‐SAH. We determined neuropeptide Y (NPY) 1–5 receptor protein expression levels through western blotting. In Protocol 2, we administered an NPY1 receptor antagonist to evaluate the effects of cardiac dysfunction induced by SAH on Day 3. In Protocol 1, SAH gradually provoked cardiac systolic dysfunction during the acute phase, reaching its peak on Day 3 without concurrent alterations in wall thickness. However, no significant changes were observed from Days 14 to 28 compared with Day 0. The changes in cardiac dysfunction were consistent with myocardial injury, inflammatory biomarkers, and NPY levels. SAH resulted in a heightened heart rate and systolic blood pressure, correlating with elevated epinephrine and norepinephrine levels. In Protocol 2, the administration of the NPY1 receptor antagonist effectively ameliorated cardiac dysfunction. Conclusions SAH induces transient cardiac dysfunction in the acute phase, and the underlying mechanisms for this response involve the NPY–NPY1 receptor pathway, otherwise known as catecholamines.