Mechanism of Corticocardiac Coupling in Sudden Cardiac Arrest

Sudden Cardiac Arrest;Corticocardiac Coupling;Coherence;Directional Connectivity;Physiology;Science;Molecular and Integrative Physiology

Tian, FangyunLee, UnCheol ;

University of Michigan

关键词: Sudden Cardiac Arrest;    Corticocardiac Coupling;    Coherence;    Directional Connectivity;    Physiology;    Science;    Molecular and Integrative Physiology;   

Others  :  https://deepblue.lib.umich.edu/bitstream/handle/2027.42/145850/fangyun_1.pdf?sequence=1&isAllowed=y

瑞士|英语

来源: The Illinois Digital Environment for Access to Learning and Scholarship

【 摘 要 】

Sudden cardiac arrest is a leading cause of death in the United States. The neurophysiological mechanism underlying sudden cardiac arrest is not well understood. Recent studies from our laboratory demonstrate that asphyxia-induced sudden cardiac arrest leads to a surge of brain-heart coupling, a novel form of neurophysiological activity measured by corticocardiac coherence (CCCoh) and directional connectivity (CCCon), prior to sudden death. In addition, surgical blockade of efferent signaling from the brain to the heart significantly delayed the death of both the heart and the brain during asphyxic cardiac arrest. We hypothesized that the stimulated brain functions to resuscitate the heart via activation of the sympathetic nervous system and that the surge of brain-heart coupling may be a potential biomarker for sudden cardiac arrest. In current thesis project, we tested our hypothesis in 3 different cardiac arrest models.In the first study, we tested the effectiveness of adrenergic blockers, phentolamine and atenolol, individually or combined, in prolonging functionality of the vital organs in asphyxic cardiac arrest model. Rats received either saline, phentolamine, atenolol, or phentolamine plus atenolol, 30 minutes before the onset of asphyxia. Electrocardiogram (ECG) and electroencephalogram (EEG) signals were simultaneously collected and investigated. We found that adrenergic blockade significantly (1) suppressed the initial decline of cardiac output, (2) prolonged electrical activities of both the brain and heart, and (3) altered CCCoh and CCCon bi-directionally and hemispherically. The protective effects of adrenergic blockers paralleled the suppression of brain and heart electrical connectivity, especially in the right hemisphere associated with central regulation of sympathetic function. In the second study, we investigated corticocardiac coupling in a patient died from cardiac arrest. Consistent with previous findings from rats, there was a marked increase of CCCoh and CCCon in the dying patient. However, different from rat model, CCCoh and CCCon in human patient showed changes unique to individual cortical channels and limited to particular frequency ranges. We also identified a surge of cardiac event-related potential at near-death in the right prefrontal and left occipital cortical region, which have been shown to play a role in autonomic control of the heart. In studies 1 and 2, we investigated corticocardiac coupling in sudden death induced by asphyxia that affects both the heart and the brain, or cardiac abnormalities. In the third project, we investigated corticocardiac coupling in forebrain ischemic stroke-induced sudden cardiac arrest rat model. EEG and ECG signals were simultaneously collected from 9 spontaneously hypertensive stroke-prone rats (SHRSP) and 8 Wistar-Kyoto (WKY) rats. Forebrain ischemic stroke resulted in 100% mortality in SHRSP rats within 14 hours, whereas no mortality was observed in control WKY rats. The functionality of both the brain and the heart were significantly altered in SHRSP compared to WKY rats after forebrain ischemia. In contrast to WKY rats, SHRSP rats exhibited intermittent surge of CCCoh, which was in parallel with elevated CCCon and reduced heart rate variability before sudden death, suggesting that an elevated brain-heart coupling is consistently associated with the disruption of the autonomic nervous system and the risk of sudden death.Results from these three studies suggest that strong corticocardiac coupling may be a shared mechanism for sudden cardiac arrest in both rat models and human patients. This study could improve our understanding on the mechanism underlying sudden cardiac arrest, and may provide important information for prevention of sudden death.