Characterization of the Cardiac Effects of Acute Subarachnoid Hemorrhage in Dogs

Elrifai, Amr; Bailes, Julian E.; Shih, Shou-Ren; Dianzumba, Sinda; Brillman, Jon

doi:10.1161/01.str.27.4.737

Cited by 87 publications

(54 citation statements)

References 20 publications

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“…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. 51 Experimental interventions such as administration of adrenergic blockers, stellate ganglion blockade, and spinal cord transection can reduce the magnitude of ECG change associated with subarachnoid bleeding and hypothalamic stimulation.…”

Section: Mechanismsmentioning

confidence: 99%

Stress-Related Cardiomyopathy Syndromes

Bybee

Prasad²

2008

Circulation

515

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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Section: Mechanismsmentioning

confidence: 99%

Stress-Related Cardiomyopathy Syndromes

Bybee

Prasad²

2008

Circulation

515

484

View full text Add to dashboard Cite

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“…16 This form of cardiac injury has been well characterized in animal models of SAH in which global myocardial dysfunction occurs in the absence of coronary artery occlusion. 17,18 Abnormal echocardiographic findings after SAH have a different distribution than that expected for vascular disease but correlate with sympathetic nerve terminals, further implying a sympathetic surge as the cause. 9 The strong associations between the extent of cTI elevation and various measures of SAH severity (eg, Hunt-Hess grade, intraventricular hemorrhage, global cerebral edema, extent of physiological derangement) also support a neurogenic mechanism of heart injury in most of our patients.…”

Section: Naidech Et Al Troponin Elevation After Subarachnoid Hemorrhamentioning

confidence: 99%

Cardiac Troponin Elevation, Cardiovascular Morbidity, and Outcome After Subarachnoid Hemorrhage

et al. 2005

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Background-Cardiac troponin I (cTI) release occurs frequently after subarachnoid hemorrhage (SAH) and has been associated with a neurogenic form of myocardial injury. The prognostic significance and clinical impact of these elevations remain poorly defined. Methods and Results-We studied 253 SAH patients who underwent serial cTI measurements for clinical or ECG signs of potential cardiac injury. These patients were drawn from an inception cohort of 441 subjects enrolled in the Columbia University SAH Outcomes Project between November 1998 and August 2002. Peak cTI levels were divided into quartiles or classified as undetectable. Adverse in-hospital events were prospectively recorded, and outcome at 3 months was assessed with the modified Rankin Scale.

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“…10) Various electrocardiography studies on rhythm disturbances have detected both minor abnormalities such as bradycardia, ST-T changes, and QTc prolongation, as well as less common but life-threatening arrhythmias such as ventricular tachycardia and ventricular fibrillation. 9,11) Cardiac muscle injury associated with SAH has been confirmed by histological findings of myofibrillar degeneration, myocytolysis, and inflammatory cell infiltration, 2,5) in addition to increased serum levels of myocardium-specific markers such as plasma phosphokinase myocardial fraction (CK-MB) 12) and troponin I. 26) Most patients also develop neurogenic pulmonary edema.…”

Section: Introductionmentioning

confidence: 97%

Clinical Significance of Elevated Natriuretic Peptide Levels and Cardiopulmonary Parameters After Subarachnoid Hemorrhage

Nakamura

Okuchi

Matsuyama

et al. 2009

Neurol. Med. Chir.(Tokyo)

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Daily changes in serum concentrations of natriuretic peptides and various cardiopulmonary parameters were measured after the onset of subarachnoid hemorrhage (SAH) to investigate the pathogenesis of the cardiac and pulmonary consequences in 15 patients with acute phase SAH, divided into the control group (n ＝ 5) with consciousness continuously preserved from SAH onset to admission, and the consciousness disturbance group (n ＝ 10). Daily changes in serum A-type and B-type natriuretic peptides (ANP and BNP, respectively) were measured for 10 days, and intrathoracic blood volume index and extravascular lung water index (EVLWI) were measured for 5 days by the single transpulmonary thermodilution method. Natriuretic peptides in the consciousness disturbance group showed significantly higher values during the 10-day period, with ANP 119.2 ± 12.4 pg/ml (mean ± standard error of the mean, p ＝ 0.005) on day 2 and BNP 354.1 ± 80.3 pg/ml (p ＝ 0.009) on day 1. EVLWI showed higher values in the consciousness disturbance group compared to the control group throughout the 5-day period. The increases in natriuretic peptide levels and increase in pulmonary extravascular water content found in SAH patients with consciousness disturbance show that load on the left ventricle or atrium as well as pulmonary capillary pressure are increased immediately after onset, supporting the contention that excessive release of catecholamines occurs at this time.

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Characterization of the Cardiac Effects of Acute Subarachnoid Hemorrhage in Dogs

Abstract: This study demonstrates the high incidence of cardiac involvement, specifically wall motion abnormalities, that occur after subarachnoid hemorrhage and suggests the importance of continuous cardiac monitoring, particularly echocardiographic measurements, in those patients.

Cited by 87 publications

References 20 publications

Stress-Related Cardiomyopathy Syndromes

Stress-Related Cardiomyopathy Syndromes

Cardiac Troponin Elevation, Cardiovascular Morbidity, and Outcome After Subarachnoid Hemorrhage

Clinical Significance of Elevated Natriuretic Peptide Levels and Cardiopulmonary Parameters After Subarachnoid Hemorrhage

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