Cardiac and central vascular functional alterations in the acute phase of aneurysmal subarachnoid hemorrhage*

Papanikolaou, John; Makris, Demosthènes; Karakitsos, Dimitrios; Saranteas, Theodosios; Karabinis, Andréas; Kostopanagiotou, Georgia; Zakynthinos, Epaminondas

doi:10.1097/ccm.0b013e31822e9fab

Cited by 33 publications

(23 citation statements)

References 41 publications

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“…Although similar results were previously described [9], others studies showed LV systolic dysfunction in 22 to 38% acute phase SAH patients [6,40]. This fact probably resulted from our exclusion criteria of patients with a major hemodynamic instability preventing intrahospital transport to the Nuclear Medicine Department.…”

Section: Discussionsupporting

confidence: 76%

Impairment of cardiac metabolism and sympathetic innervation after aneurysmal subarachnoid hemorrhage: a nuclear medicine imaging study

et al. 2014

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IntroductionAlthough aneurysmal subarachnoid hemorrhage (SAH) is often complicated by myocardial injury, whether this neurogenic cardiomyopathy is associated with the modification of cardiac metabolism is unknown. This study sought to explore, by positron emission tomography/computed tomography, the presence of altered cardiac glucose metabolism after SAH.MethodsDuring a 16-month period, 30 SAH acute phase patients underwent myocardial 18 F- fluorodesoxyglucose positron emission tomography (18F-FDGPET), 99mTc-tetrofosmin and 123I-meta-iodobenzylguanidine (123I-mIBG) scintigraphy, respectively, assessing glucose metabolism, cardiac perfusion, and sympathetic innervation. Patients with initial abnormalities were followed monthly for two months for 18F-FDG, and six months later for 123I-mIBG.ResultsIn this SAH population, acute cardiac metabolic disturbance was observed in 83% of patients (n = 25), and sympathetic innervation disturbance affected 90% (n = 27). Myocardial perfusion was normal for all patients. The topography and extent of metabolic defects and innervation abnormalities largely overlapped. Follow-up showed rapid improvement of glucose metabolism in one or two months. Normalization of sympathetic innervation was slower; only 27% of patients (n = 8) exhibited normal 123I-mIBG scintigraphy after six months. Presence of initial altered cardiac metabolism was not associated with more unfavorable cardiac or neurological outcomes.ConclusionsThese findings support the hypothesis of neurogenic myocardial stunning after SAH. In hemodynamically stable acute phase SAH patients, cardiomyopathy is characterized by diffuse and heterogeneous 18F-FDG and 123I-mIBG uptake defect.Trial registrationClinicaltrials.gov NCT01218191. Registered 6 October 2010.

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Section: Discussionsupporting

confidence: 76%

Impairment of cardiac metabolism and sympathetic innervation after aneurysmal subarachnoid hemorrhage: a nuclear medicine imaging study

et al. 2014

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“…However, in another study, throughout the 7 days after SAH, lower than normal aldosterone concentrations and normal plasma concentrations of ANP and C-type natriuretic peptides (CNP) were found [26]. B-type natriuretic peptide showed significant diagnostic efficiency for predicting delayed cerebral ischemia after SAH [27]. Rapid natriuresis occurs prior to the development of ischemic symptoms after SAH, indicating that it is a trigger for symptomatic vasospasm [28].…”

Section: Possible Mechanisms Of Nonneurologic Complications Followmentioning

confidence: 99%

“…Systolic dysfunction can be observed by echocardiography as a reduced LV ejection fraction and/or the presence of regional wall motion abnormalities of the LV. LV ejection fraction and pulse-wave velocity were related to poor outcomes following SAH [27]. A multicenter prospective cohort study found that the cardiac index was significantly lower in patients with high grade SAH (World Federation of Neurological Surgeons grades IV and V) on days 1 and 2 after the ictus [76].…”

Section: Manifestations Of Nonneurologic Complications After Sahmentioning

confidence: 99%

The Harmful Effects of Subarachnoid Hemorrhage on Extracerebral Organs

Chen

et al. 2014

BioMed Research International

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Subarachnoid hemorrhage (SAH) is a devastating neurological disorder. Patients with aneurysmal SAH develop secondary complications that are important causes of morbidity and mortality. Aside from secondary neurological injuries, SAH has been associated with nonneurologic medical complications, such as neurocardiogenic injury, neurogenic pulmonary edema, hyperglycemia, and electrolyte imbalance, of which cardiac and pulmonary complications are most common. The related mechanisms include activation of the sympathetic nervous system, release of catecholamines and other hormones, and inflammatory responses. Extracerebral complications are directly related to the severity of SAH-induced brain injury and indicate the clinical outcome in patients. This review provides an overview of the extracerebral complications after SAH. We also aim to describe the manifestations, underlying mechanisms, and the effects of those extracerebral complications on outcome following SAH.

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“…Several mechanisms for the cardiac complications that occur after SAH have been suggested. A generally accepted hypothesis is that the sympathetic stimulation induces catecholamine release in the myocardium leading to impaired systolic and diastolic function, repolarization abnormalities, and direct myocardial damage [3,7,8]. In addition, it has been reported that during the acute phase of SAH, there is an increase in aortic wall stiffness leading to higher left ventricular pressures [8].…”

Section: Discussionmentioning

confidence: 99%

Takotsubo cardiomyopathy secondary to intracranial hemorrhage

Shimada

Rose

2014

Int J Emerg Med

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Patients suffering from aneurysmal subarachnoid hemorrhage often present with electrocardiogram (ECG) abnormalities that mimic cardiac ischemia, but documented left ventricular regional wall-motion dysfunction has rarely been reported. This report is intended to raise the awareness of possible ECG changes secondary to subarachnoid hemorrhage (SAH). We cared for a 55-year-old female with an acute aneurysmal subarachnoid hemorrhage, whose evaluation was delayed and complicated by the presence of Takotsubo cardiomyopathy (TCM). Aneurysmal subarachnoid hemorrhage may induce Takotsubo cardiomyopathy that can present as an acute ST-elevation myocardial infarction. Physicians need to be aware of this possibility since it can lead to significant delays and treatment options for the patient.

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Cardiac and central vascular functional alterations in the acute phase of aneurysmal subarachnoid hemorrhage*

Cited by 33 publications

References 41 publications

Impairment of cardiac metabolism and sympathetic innervation after aneurysmal subarachnoid hemorrhage: a nuclear medicine imaging study

Impairment of cardiac metabolism and sympathetic innervation after aneurysmal subarachnoid hemorrhage: a nuclear medicine imaging study

The Harmful Effects of Subarachnoid Hemorrhage on Extracerebral Organs

Takotsubo cardiomyopathy secondary to intracranial hemorrhage

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