Role of Autonomic Nervous Dysfunction in Electrocardiographic Abnormalities and Cardiac Injury in Patients With Acute Subarachnoid Hemorrhage

Kawahara, Eisuke; Ikeda, Satoshi; Miyahara, Yoshiyuki; Kohno, Shigeru

doi:10.1253/circj.67.753

Cited by 96 publications

(60 citation statements)

References 16 publications

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“…In consequence, referral to neurosurgical department is delayed. Surprisingly, impairment of cardiac function and electrocardiographic (ECG) abnormalities have been demonstrated in miscellaneous neurological conditions, such as SAH [3][4][5][6][7][8] and other forms of intracerebral hemorrhage [9], acute brain injury [10,11], cerebral ischemia [12], brain tumors [13], refractory status epilepticus [14], meningitis [15], intracranial hypertension and brain death [16]. First reports of the impact of central nervous system on circulation date back to the very beginning of the 19 th century, when Cushing [17] described the physiological blood pressure reaction to intracranial hypertension.…”

Section: Introductionmentioning

confidence: 99%

Neurocardiogenic injury in subarachnoid hemorrhage: A wide spectrum of catecholamin-mediated brain-heart interactions

2014

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Section: Introductionmentioning

confidence: 99%

Neurocardiogenic injury in subarachnoid hemorrhage: A wide spectrum of catecholamin-mediated brain-heart interactions

2014

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“…The pathophysiology of these abnormalities is related to increased sympathetic nervous activity 15) and to increased circulating and local myocardial tissue catecholamines. [16][17][18][19] In this context, neurological status has been reported to be related to cardiac abnormalities.…”

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confidence: 99%

Prognostic Implications of Left Ventricular Wall Motion Abnormalities Associated With Subarachnoid Hemorrhage

et al. 2008

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SUMMARYLeft ventricular (LV) dysfunction generally occurs early in the course of subarachnoid hemorrhage (SAH). We evaluated the prognostic value of electrocardiographic (ECG) abnormalities and echocardiographic LV dysfunction evaluated shortly after SAH.We prospectively enrolled 47 SAH patients (62 ± 14 years, mean ± SD) who were admitted to the neurosurgical care unit of our institute. Neurological status was rated on the day of admission. Twelve-lead ECG and 2-dimensional echocardiography were recorded 2 ± 1 day after onset of SAH. ECG abnormalities (pathological Q-wave, ST-segment deviation, T-wave inversion, and QT prolongation) were evaluated and the incidences of global (LV ejection fraction < 50%) and segmental (regional wall motion abnormality [RWMA]) LV dysfunction were measured.During a follow-up period of 44 ± 23 days, 17 (36%) patients died. ECG abnormalities, LV ejection fraction < 50%, and RWMA were observed in 62%, 11%, and 28% of patients, respectively. Univariate Cox proportional hazards regression analysis revealed that neurological status, rate-corrected QT interval, LV ejection fraction, and RWMA were significant predictors of death. After adjustment for these significant clinical variables, and age and sex, independent predictors of mortality were neurological status and RWMA.RWMA may provide significant prognostic information in patients with SAH. (Int Heart J 2008; 49: 75-85)

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“…20,31 Along these lines, patients with acute subarachnoid hemorrhage, which is associated with a rapid increase in intracranial pressure, 32 displayed significantly increased HF power compared to controls, while LF power did not change. 33 These results suggest that in patients with TBI, parasympathetic (vagal) activity is augmented, resulting in an increased HF power and increased HF/LF ratio, and that elevated intracranial pressure may play an important role in this process. In addition to the above described association between TBI/increased intracranial pressure and heart rate variability as a measure of vagal tone in patients with TBI, a model of increased intracranial pressure demonstrated a direct link between intracranial pressure and vagal tone.…”

Section: Heart Rate Variability In Patients Withmentioning

confidence: 79%

“…Along these lines, patients in the chronic phase of subarachnoid hemorrhage demonstrated similar HF/LF ratios compared to control subjects, while HF/LF ratios were increased in the acute phase, as discussed before. 33 In the chronic phase of TBI or subarachnoid hemorrhage, patients usually do not have an increased intracranial pressure, possibly explaining the absence of increased vagal activity. Moreover, a potential explanation for decreased vagal output in the chronic phase of TBI may be damage to the brainstem and medulla oblongata resulting in impaired activity of the vagus nerve.…”

Section: Discussionmentioning

confidence: 99%

Increased vagal tone accounts for the observed immune paralysis in patients with traumatic brain injury

Kox¹,

Pompe²,

Pickkers³

et al. 2008

Neurology

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Traumatic brain injury (TBI) is a leading cause of death and disability, especially in the younger population. In the acute phase after TBI, patients are more vulnerable to infection, associated with a decreased immune response in vitro. The cause of this immune paralysis is poorly understood. Apart from other neurologic dysfunction, TBI also results in an increase in vagal activity. Recently, the vagus nerve has been demonstrated to exert an anti-inflammatory effect, termed the cholinergic anti-inflammatory pathway. The anti-inflammatory effects of the vagus nerve are mediated by the ␣7 nicotinic acetylcholine receptor present on macrophages and other cytokineproducing cells. From these observations, we hypothesize that the immune paralysis observed in patients with TBI may, at least in part, result from augmented vagal activity and subsequent sustained effects of the cholinergic anti-inflammatory pathway. This pathway may counteract systemic proinflammation caused by the release of endogenous compounds termed alarmins as a result of tissue trauma. However, sustained activity of this pathway may severely impair the body's ability to combat infection. Since the cholinergic anti-inflammatory pathway can be pharmacologically modulated in humans, it could represent a novel approach to prevent infections in patients with TBI. Neurology

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Role of Autonomic Nervous Dysfunction in Electrocardiographic Abnormalities and Cardiac Injury in Patients With Acute Subarachnoid Hemorrhage

Cited by 96 publications

References 16 publications

Neurocardiogenic injury in subarachnoid hemorrhage: A wide spectrum of catecholamin-mediated brain-heart interactions

Neurocardiogenic injury in subarachnoid hemorrhage: A wide spectrum of catecholamin-mediated brain-heart interactions

Prognostic Implications of Left Ventricular Wall Motion Abnormalities Associated With Subarachnoid Hemorrhage

Increased vagal tone accounts for the observed immune paralysis in patients with traumatic brain injury

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