Association between elevated plasma norepinephrine levels and cardiac wall motion abnormality in poor-grade subarachnoid hemorrhage patients

Abstract

Patients with aneurysmal subarachnoid hemorrhage (SAH) are frequently complicated by acute cardiac dysfunctions, including cardiac wall motion abnormality (WMA). Massive release of catecholamine into the systemic circulation after aneurysmal rupture is believed to result in WMA, and poor-grade SAH seems to be the most important risk factor. However, plasma catecholamine levels have rarely been measured in SAH patients with WMA, and previous studies indicated that the elevated levels might not necessarily predict WMA. The objective of this study is (1) to evaluate relationship between WMA and plasma catecholamine levels in poor-grade SAH patients in the acute phase and (2) to clarify clinical characteristics of SAH patients with WMA. Among 142 poor-grade (World Federation of Neurosurgical Societies grades IV and V) SAH patients, 48 underwent both transthoracic ultrasound and measurement of plasma catecholamine levels within 24 h of SAH onset. They were divided into WMA+ (n = 23) and WMA- (n = 25) groups, and intergroup comparison was made on demographics, plasma catecholamine levels, and outcomes. Plasma norepinephrine levels were significantly higher in WMA+ group than in WMA- group (2,098.4 ± 1,773.4 vs. 962.9 ± 838.9 pg/mL, p = 0.02), and the former showed significantly worse outcomes 90 days after admission. There were no intergroup differences in the plasma levels of epinephrine. Plasma norepinephrine levels were inversely correlated with left ventricular ejection fraction. Multivariate logistic regression analysis revealed that increased plasma norepinephrine levels were predictive of WMA, although age, female sex, and grade V SAH were not. This retrospective study highlights the role of norepinephrine in pathogenesis of SAH-induced WMA.

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

“…In that preclinical study, catecholamine release lasted less than 2 hours and was followed by a sustained increase in biological markers of cardiac injury and alterations of myocardial function [14]. Our study shows that as reported in the literature [15,27], there is already marked and rapid catecholamine release at admission. The source of SAH-induced catecholamine release remains unknown.…”

“…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]. …”

The Harmful Effects of Subarachnoid Hemorrhage on Extracerebral Organs

“…Activation of the sympathetic nervous system, which leads to an elevated level of circulating, cerebrospinal fluid (CSF), and urine catecholamines, may be the link between the initial ictus and the genesis of some of the systemic complications after SAH [13]. Sympathetic activation was observed as an elevation of plasma norepinephrine following preclinical and clinical SAH studies [14, 15]. It has been well recognized that a high sympathetic tone combined with high circulating catecholamine concentrations may occur in humans with head injury, particularly after SAH [13, 16].…”

Catecholamines and Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury

“…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.…”