The role of catecholamines in the pathogenesis of neurogenic pulmonary edema associated with subarachnoid hemorrhage

Inamasu, Joji; Sugimoto, Keiko; Yamada, Yoshihiko; Ganaha, Tsukasa; Ito, Keisuke; Watabe, Takeya; Hayashi, Takuro; Kato, Yōkō; Ozaki, Yukio; Hirose, Yuichi

doi:10.1007/s00701-012-1515-x

Cited by 42 publications

(28 citation statements)

References 24 publications

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“…The incidence of the disorder has remained stable over the past 30 years [1] with an aggregate worldwide incidence of about 10.5 per 100,000 person-years [2]. As many as 46% of SAH survivors suffer from long-term cognitive impairment with decreased functional status and quality of life [3–5]. …”

Section: Introductionmentioning

confidence: 99%

“…It has been suggested that the pathophysiology of cardiac injury after SAH is similar to apical ballooning syndrome (Takotsubo or stress cardiomyopathy) that is, in relation to catecholamine endogenous release [14]. Few human studies have shown an association between catecholamine release and cardiac dysfunction at an early stage after SAH, and to our knowledge few human studies have focused on the time course of catecholamine release and cardiac dysfunction during SAH [5,15]. …”

Section: Introductionmentioning

confidence: 99%

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Subarachnoid hemorrhage induces an early and reversible cardiac injury associated with catecholamine release: one-week follow-up study

et al. 2014

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IntroductionThe occurrence of cardiac dysfunction is common after subarachnoid hemorrhage (SAH) and was hypothesized to be related to the release of endogenous catecholamines. The aim of this prospective study was to evaluate the relationship between endogenous catecholamine and cardiac dysfunction at the onset and during the first week after SAH.MethodsForty consecutive patients admitted for acute SAH without known heart disease were included. Catecholamine plasma concentrations and transthoracic echocardiography (TTE) were documented on admission, on day 1 (D1), and day 7 (D7).ResultsAt baseline, 24 patients had a World Federation of Neurosurgical Societies score (WFNS) of one or two; the remaining 16 had a WFNS between three and five. Twenty patients showed signs of cardiac dysfunction on admission, including six with left ventricle (LV) systolodiastolic dysfunction and 14 with pure LV diastolic dysfunction. On admission, norepinephrine, epinephrine, dopamine, B-type Natriuretic Peptide (BNP) and Troponin Ic (cTnI) plasmatic levels were higher in patients with the higher WFNS score and in patients with altered cardiac function (all P <0.05). Among patients with cardiac injury, heart function was restored within one week in 13 patients, while seven showed persistent LV diastolic dysfunction (P = 0.002). Plasma BNP, cTnI, and catecholamine levels exerted a decrease towards normal values between D1 and D7.ConclusionOur findings show that cardiac dysfunction seen early after SAH was associated with both a rapid and sustained endogenous catecholamine release and WFNS score. SAH-induced cardiac dysfunction was regressive over the first week and paralleled the normalization of catecholamine concentration.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Subarachnoid hemorrhage induces an early and reversible cardiac injury associated with catecholamine release: one-week follow-up study

et al. 2014

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“…Neuropulmonary edema (NPE) is manifested by rapid onset of dyspnea, tachypnea, tachycardia, basal pulmonary crackles, respiratory failure and decreased PaO 2 /FiO 2 ratio in the event of cerebral incident, which represents a direct catecholamine--mediated insult to lungs [22]. Adrenergic response triggers severe pulmonary vasoconstriction, with the resultant rise in hydrostatic pressure and an increase in permeability of pulmonary capillaries [59]. Although cardiac gallop and RWMA exclude pure form of NPE, cardiac function is almost always impaired to certain extent, thus it is immensely difficult to differentiate between the NPE and pulmonary edema secondary to reduced cardiac output and increased LV end-diastolic pressure associated with acute heart failure.…”

Section: Catecholamine-mediated Toxicitymentioning

confidence: 99%

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

2014

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“…In contrast, published data for spontaneous subarachnoid haemorrhage suggests large increases in plasma NE with minor or no elevation of E levels. (38)(39)(40)(41)(42) The increase in E suggests a possible causative role from the motor overactivity that is part of the syndrome in PSH but not SAH. Whatever the cause, the difference in catecholamine response seen in these two conditions suggests that their underlying pathophysiology are not equivalent.…”

Section: Discussionmentioning

confidence: 95%

Catecholamines and Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury

Fernandez-OrtegaJuan¹,

BaguleyIan

GatesThomas

et al. 2017

Journal of Neurotrauma

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Paroxysmal sympathetic hyperactivity (PSH) affects a significant minority of people in the intensive care unit after severe traumatic brain injury. Systematic research has yet to elucidate or quantify the extent of the role of the catecholamines or adrenocortical and thyroid axis hormonal influences in the condition. Data were prospectively collected on 80 consecutive patients, 18 of whom developed clinical signs of PSH (22.5%). Catecholamine and hormonal data were collected sequentially at 4-h intervals or during and between episodes of PSH. Evaluated variables showed 200-300% increases in catecholamines and, to a lesser extent, adrenocortical hormones during paroxysms. The majority of PSH episodes (72%) were noted to be in response to an observable triggering event. These changes were not observed in subjects without PSH. These data go some way to explain why PSH produces adverse consequences in survivors of TBI with the condition.

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The role of catecholamines in the pathogenesis of neurogenic pulmonary edema associated with subarachnoid hemorrhage

Abstract: Elevated plasma norepinephrine may have more active role in the pathogenesis of SAH-induced NPE compared with epinephrine, although both catecholamines may be involved via multiple signaling pathways.

Cited by 42 publications

References 24 publications

Subarachnoid hemorrhage induces an early and reversible cardiac injury associated with catecholamine release: one-week follow-up study

Subarachnoid hemorrhage induces an early and reversible cardiac injury associated with catecholamine release: one-week follow-up study

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

Catecholamines and Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury

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