1997
DOI: 10.1007/bf03011941
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Concurrent subarachnoid haemorrhage and myocardial injury

Abstract: Concurrent subarachnoid haemorrhage and myocardial injuryPurpose: Subarachnoid haemonanage is frequently associated with myocardial injury and dysfunction. This report describes such a case, reviews the understanding of this phenomenon, and discusses the implications for timing of surgical clipping of intracranial aneurysm in patients with concurrent myocardial damage.Clinical Features: A 64-yr-old woman presented with syncope and congestive heart failure, A diagnosis of subarachnoid haemorrhage was made three… Show more

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Cited by 19 publications
(6 citation statements)
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“…Connor (20) described human autopsy evidence of myocytolysis and contraction-band necrosis of the heart in neurosurgical patients that were considered to be similar to those caused by catecholamines. Numerous case series have described both global myocardial dysfunction and regional wall motion abnormalities following SAH (21)(22)(23)(24)(25)(26). Patterns of myocardial dysfunction observed following SAH are not compatible with a coronary artery etiology, and angiography has not been revealing in these patients (23).…”
Section: Discussionmentioning
confidence: 96%
“…Connor (20) described human autopsy evidence of myocytolysis and contraction-band necrosis of the heart in neurosurgical patients that were considered to be similar to those caused by catecholamines. Numerous case series have described both global myocardial dysfunction and regional wall motion abnormalities following SAH (21)(22)(23)(24)(25)(26). Patterns of myocardial dysfunction observed following SAH are not compatible with a coronary artery etiology, and angiography has not been revealing in these patients (23).…”
Section: Discussionmentioning
confidence: 96%
“…Indeed, in neurosurgical models and clinical studies, 40% to 100% with SAH can have ECG changes or arrhythmias, [16][17][18][19][20] 11% to 21% can have myocardial enzyme elevation, 17,19,20 and 2% to 30% may have left ventricular dysfunction manifested by hypokinetic wall-motion abnormalities on echocardiography. [17][18][19][20] Compared with AIS, heart-brain interactions in SAH have been more widely investigated, [21][22][23][24][25][26][27][28][29][30][31][32][33][34] with literature describing reversible myocardial stunning, 35 histologic evidence of myocardial necrosis, 36 elevation of natriuretic factors, 37,38 secondary neurogenic pulmonary edema, 39 elevation of systemic plasma catecholamines, 40,41 and impairment of regional myocardial perfusion. 42,43 Additionally, in the neurosurgical literature, hemodynamic manipulations have been more rigorously evaluated, specifically for the management of cerebral vasospasm after SAH.…”
Section: Discussionmentioning
confidence: 99%
“…5,[23][24][25][26][27][28][29] Furthermore, it was reported that myocardial necrosis occurred in these patients, as evidenced by elevated serum concentrations of CK-MB, troponin T, or myosin light chain above the normal values within 2 to 3 days after the onset of SAH as well as the contraction band, myocardial fragmentation, and focal myocytolysis observed in the myocardium at autopsy. 9,30 -32 We investigated the pathogenesis of cardiopulmonary complications on the basis of the clinical observation of 717 cases in the acute phase of SAH.…”
Section: Discussionmentioning
confidence: 99%