Clinical significance of plasma adrenaline and noradrenaline concentrations in patients with subarachnoid haemorrhage.

Benedict, C. R.; Loach, A. B.

doi:10.1136/jnnp.41.2.113

Cited by 69 publications

(18 citation statements)

References 9 publications

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“…l i 7 ' 8 The suggested preventive use of /3-adrenergic blocking agents [7][8] -15 therefore does not seem to be warranted by our present results.…”

Section: Discussioncontrasting

confidence: 44%

Effect of elevated plasma norepinephrine on electrocardiographic changes in subarachnoid hemorrhage.

Grad

Kiauta

Osredkar

1991

Stroke

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We compared electrocardiographic abnormalities and plasma norepinephrine concentrations in 40 patients with subarachnoid hemorrhage within the first 24 hours, at 72 hours, and after 1 week. In 20 patients with high plasma norepinephrine concentrations within the first 24 hours, sinus tachycardia (/><0.02) and negative T waves (/><0.01) were more frequent than in the 20 patients with normal plasma norepinephrine concentrations. After 72 hours, only sinus tachycardia (p<0.03) was found with increased frequency in the 26 patients with high plasma norepinephrine concentrations. Although 24 patients had high plasma norepinephrine concentrations after 1 week, we found no differences in the frequency of electrocardiographic abnormalities compared to patients with normal plasma norepinephrine. However, QT C prolongation, U waves, ST depression, and arrhythmias were found with similar frequency in patients with both high and normal plasma norepinephrine concentrations. We conclude that, with the exception of sinus tachycardia and negative T waves, electrocardiographic changes in patients with subarachnoid hemorrhage do not depend on elevated plasma norepinephrine concentrations. (Stroke 1991^2:746-749) S ubarachnoid hemorrhage (SAH) may be associated with cardiac abnormalities, including a high prevalence of arrhythmias and other electrocardiographic (ECG) changes.1 Although the appearance of changes in ECG during the acute phase of stroke -typically consisting of inversion of T wave, ST segment elevation or depression, prolongation of the corrected QT (QT C ) interval, and the presence of U waves 2 -4 -has been a wellrecognized phenomenon for four decades, 5 clinical significance of cardiac arrhythmias in patients with SAH has been recognized only recently. 6 The mechanism of ECG abnormalities remains obscure. It has been suggested that cardiac arrhythmias, myocardial necrosis, and ECG abnormalities may result from abnormally increased sympathetic activity. Address for correspondence: Anton Grad, MD, Univerzitetni kliniini center, Univerzitetna nevroloSka klinika, ZaloSka 7, YU-61105 Ljubljana, Yugoslavia.Received January 5, 1990; accepted February 8, 1991. suggested, 7 ' 8 no clinical reports confirm the dependence of ECG changes on high plasma norepinephrine levels in patients with SAH.The purpose of our study was to investigate the frequency of ECG abnormalities in the first week after SAH in patients with high plasma norepinephrine levels and to compare them to ECG changes in SAH patients with normal plasma norepinephrine levels. Subjects and MethodsWe prospectively studied 40 patients (14 men, 26 women) with SAH admitted to

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“…l i 7 ' 8 The suggested preventive use of /3-adrenergic blocking agents [7][8] -15 therefore does not seem to be warranted by our present results.…”

Section: Discussioncontrasting

confidence: 44%

Effect of elevated plasma norepinephrine on electrocardiographic changes in subarachnoid hemorrhage.

Grad

Kiauta

Osredkar

1991

Stroke

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“…Some authors have reported that an increase of plasma noradrenaline is related to symptomatic vasospasm 19 and that patients with symptomatic vasospasm frequently have hyponatremia. 5 Although the mechanism of the release of BNP after SAH still remains unknown, Berendes et al 17 speculated that BNP release may result from the stress response to surgery or intensive care as well as damage to the hypothalamic region.…”

Section: Tomida Et Al August 1998mentioning

confidence: 99%

Plasma Concentrations of Brain Natriuretic Peptide in Patients With Subarachnoid Hemorrhage

Tomida

Muraki

Uemura

et al. 1998

Stroke

112

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Background and Purpose-Hyponatremia after subarachnoid hemorrhage (SAH) is commonly associated with diuresis and natriuresis, but the causes are still controversial. We investigated whether brain natriuretic peptide (BNP) was related to such hyponatremia. Methods-Plasma BNP concentrations were measured by immunoradiometric assay in 18 patients at 0 to 2 days (period 1), 7 to 9 days (period 2), and Ͼ14 days (period 3) after SAH. Plasma concentrations of antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), and noradrenaline were also measured during period 2. Results-The 11 patients with hyponatremia (serum sodium concentration of Ͻ135 mEq/L) had much higher plasma BNP concentrations during each period than did healthy controls (PϽ0.05), whereas the 7 patients with normonatremia did not show statistically higher values. In the patients with hyponatremia, the plasma BNP concentration during period 2 was statistically higher than that during periods 1 and 3 (PϽ0.05). The plasma noradrenaline concentration during period 2 was higher in patients with hyponatremia than in those with normonatremia (PϽ0.05), whereas the plasma concentrations of ADH and ANP during period 2 were not statistically different between the hyponatremic and normonatremic patients. Key Words: hyponatremia Ⅲ natriuretic peptide, brain Ⅲ subarachnoid hemorrhage H yponatremia after SAH has been reported to have an incidence of 30% to 40%. Recent studies have demonstrated that this phenomenon is frequently associated with hypovolemia, which is caused not by the syndrome of inappropriate secretion of ADH but by CSW. Conclusions-We1,2,3 However, the cause of CSW is still controversial. Some authors have reported that ANP 4,5 and digoxinlike peptides 6 may cause the hyponatremia, while others have suggested that these agents are not involved. 7,8 BNP, which was isolated from porcine brain in 1988, 9 causes natriuresis and diuresis. It has recently become possible to measure BNP accurately by immunoradiometric assay. We investigated whether BNP was related to hyponatremia after SAH by measuring plasma BNP concentrations with use of an immunoradiometric assay in patients with acute SAH. Subjects and Methods Patients and ManagementEighteen patients (4 men and 14 women without cardiac, renal, or endocrine diseases; meanϮSD age, 62.3Ϯ10.8 years) with SAH verified by CT scan were investigated from January 1995 through December 1996. All patients underwent cerebral angiography and aneurysm clipping within 48 hours of the onset, except for 1 patient in whom angiography failed to identify the source of hemorrhage. Each patient received intravenous fluid at approximately 2500 to 3000 mL/d to maintain a central venous pressure of 4 to 12 cm H 2 O. Sodium administration ranged from 280 to 320 mEq/d in patients without hyponatremia, while sodium loss was replaced according to urinary excretion when hyponatremia occurred. When symptomatic vasospasm occurred, ozagrel sodium (Xanbon, Kissei Pharmaceutical Co Ltd) was intravenously administered at 80 mg/d in pa...

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“…66 Furthermore, patients with NSC have evidence of enhanced peripheral sympathetic activity with increased plasma catecholamine levels, which may also contribute to myocardial toxicity. 67,68 Animal models of SAH have shown a correlation between peak troponin and peak plasma catecholamine levels. 67,69 Patients with SAH and NSC exhibit abnormal cardiac sympathetic activity suggestive of functional sympathetic denervation when imaged with the use of meta-iodobenzylguanidine.…”

Section: Mechanismsmentioning

confidence: 99%

Stress-Related Cardiomyopathy Syndromes

Bybee

Prasad²

2008

Circulation

518

484

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he relationship between the heart and the brain is complex and integral in the maintenance of normal cardiovascular function. Certain pathological conditions can interfere with the normal brain-heart regulatory mechanisms and result in impaired cardiovascular function. The mechanisms through which the central and autonomic nervous systems regulate the heart and the manner in which their impairment adversely affects cardiovascular function have recently been reviewed by Samuels. 1 The purpose of this article is to provide an up-to-date review of the clinical presentation of the stress-related cardiomyopathy syndromes, discuss possible causal mechanisms, and highlight the similarities and differences between them. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] The stress-related cardiomyopathies appear similar in that they seemingly occur during times of enhanced sympathetic tone and may be precipitated in part or entirely by excessive endogenous or exogenous catecholamine stimulation of the myocardium. Although significant clinical overlap exists in those presenting with stress-associated cardiomyopathy, it is unclear whether myocardial adrenergic hyperstimulation is the only pathophysiological mechanism responsible for these syndromes (Tables 1 and 2). Transient Left Ventricular Dysfunction AfterAcute Emotional or Physical Stress (Takotsubo Cardiomyopathy, Apical Ballooning Syndrome)In the early 1990s, Japanese authors began reporting a unique, reversible cardiomyopathy that appeared to be precipitated by acute emotional stress. 2,13,16 They found that these patients were usually postmenopausal women and often developed signs and symptoms of an acute coronary syndrome (ACS) proximate to a strong emotional stressor associated with a transient apical and midventricular wall motion abnormality despite the lack of obstructive coronary artery disease (CAD) at the time of emergent coronary angiography. This syndrome was initially given the name Takotsubo cardiomyopathy (TC) and has subsequently been referred to as the apical ballooning syndrome and broken heart syndrome. It is now recognized that TC can also occur in the setting of acute medical illness and after surgery. TC has now been reported worldwide and has recently been acknowledged by the American College of Cardiology and AmericanHeart Association as a unique form of reversible cardiomyopathy. 17 Clinical PresentationThose presenting with TC are most commonly postmenopausal women. 2,4,18,19 In a systematic review, women accounted for 82% to 100% of patients with an average age of 62 to 75 years, although cases have been described in individuals aged 10 to 91 years. 4 The presentation of TC is usually similar to that of an ACS with symptoms primarily consisting of ischemia-like chest pain and ischemia-like ECG changes in most patients. As a result, both US and international guidelines have now included TC as an important differential diagnosis of ACS. 20 Collective reports have shown that severe emotional stress has preceded presentation with TC in Ϸ27%...

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Clinical significance of plasma adrenaline and noradrenaline concentrations in patients with subarachnoid haemorrhage.

Cited by 69 publications

References 9 publications

Effect of elevated plasma norepinephrine on electrocardiographic changes in subarachnoid hemorrhage.

Effect of elevated plasma norepinephrine on electrocardiographic changes in subarachnoid hemorrhage.

Plasma Concentrations of Brain Natriuretic Peptide in Patients With Subarachnoid Hemorrhage

Stress-Related Cardiomyopathy Syndromes

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