Coronary vasospasm following subarachnoid hemorrhage as a cause of stunned myocardium

Yuki, Kiyoshi; Kodama, Yoshihiko; Onda, Jun; Emoto, Katsuya; Morimoto, Tadao; Uozumi, Tohru

doi:10.3171/jns.1991.75.2.0308

Cited by 69 publications

(34 citation statements)

References 21 publications

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“…In clinical studies, myocardial ischemia has been implicated as the cause of ECG changes in LV dysfunction. 12,15,16 However, substantial evidence from animal models suggests that excessive release of catecholamines from sympathetic nerve terminals in the myocardium is a more likely cause of cardiac injury after SAH. 2 The exact mechanism of catecholamine-mediated myocardial damage is unknown, although persistent activation of calcium channels, membrane damage, and microvascular spasm have been proposed as causes.…”

Section: Discussionmentioning

confidence: 99%

“…10 The pathophysiology of cardiac dysfunction after SAH in humans remains unknown and controversial. Although data from animal models indicates that catecholamine-mediated injury is the most likely cause of cardiac injury after SAH, 2 some authors have implicated myocardial ischemia due to coronary artery disease, 11 coronary vasospasm, 12 or hypertension and tachycardia. In clinical practice, LV dysfunction after SAH is frequently ascribed to myocardial infarction.…”

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confidence: 99%

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Regional Myocardial Perfusion After Experimental Subarachnoid Hemorrhage

Zaroff

Rordorf

Titus

et al. 2000

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Background and Purpose-The pathophysiology of cardiac injury after subarachnoid hemorrhage (SAH) remains controversial. Data from animal models suggest that catecholamine-mediated injury is the most likely cause of cardiac injury after SAH. However, researchers also have proposed myocardial ischemia to be the underlying cause, as a result of coronary artery disease, coronary artery spasm, or hypertension and tachycardia. To test the hypothesis that SAH-induced cardiac injury occurs in the absence of myocardial hypoperfusion, we developed an experimental canine model that reproduces the clinical and pathological cardiac lesions of SAH and defines the epicardial and microvascular coronary circulation. Methods-Serial ECG, hemodynamic measurements, coronary angiography, regional myocardial blood flow measurements by radiolabeled microspheres, 2D echocardiography, and myocardial contrast echocardiography were performed in 9 dogs with experimental SAH and 5 controls. Results-Regional wall motion abnormalities were identified in 8 of 9 SAH dogs and 1 of 5 controls (Fisher's Exact Test, Pϭ0.02) but no evidence was seen of coronary artery disease or spasm by coronary angiography and of significant myocardial hypoperfusion by either regional myocardial blood flow or myocardial contrast echocardiography. Conclusions-In this experimental model of SAH, a unique form of regional left ventricular dysfunction occurs in the absence of myocardial hypoperfusion. Future studies are justified to determine the cause of cardiac injury after SAH.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Regional Myocardial Perfusion After Experimental Subarachnoid Hemorrhage

Zaroff

Rordorf

Titus

et al. 2000

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“…In 9 patients, serial determinations of creatinine phosphokinase levels along with myocardial iso-enzyme fractions (CK-MB) were also examined (case nos. 4,7,9,11,13,14,19,22,23). Echocardiography was performed every 6 hours during the first 2 days and once a day until discharge in all patients.…”

Section: Clinical Materials and Methodsmentioning

confidence: 99%

Significance of ST segment elevation in electrocardiograms in patients with ruptured cerebral aneurysms

et al. 1995

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Twenty-three patients with aneurysmal subarachnoid haemorrhage (SAH), who showed an ST segment elevation in their electrocardiograms (ECG), were examined. There were 12 males and 11 females, with a mean age of 61 years. The clinical condition on admission was Hunt and Kosnik grade II in four, III in seven, IV in one, and V in 11 patients. Computerized tomography (CT) also revealed many cases of diffuse, thick SAH or intracerebral or intraventricular haematoma. Laboratory examinations including serum electrolyte, pH, and PaO2 revealed no abnormalities that might have influenced the ECG. Elevation in the levels of myocardial enzymes in serum was observed in two of the nine patients examined, although the elevation was only slight in one of them. Echocardiography, which was performed on several occasions on all patients, and cardiac catheterization, which was performed on eight patients, revealed a reduction in the motion of the left ventricular apex that was synchronous with ST segment elevation. This is the first report about these phenomena. No abnormalities were observed in the coronary artery. The elevated ST segment was normalized within one week in all patients, accompanied by normalization of the apical wall motion recorded on echocardiograms. In four patients, however, T wave inversion accompanied the improvement of the ST segment and was normalized within three months after the onset. These results suggest that ST segment elevation in the acute stage of SAH reflects transient cardiac dysfunction rather than myocardial injury. In some patients, however, the elevated serum levels of myocardial enzymes or T wave inversion suggested the presence of myocardial injury. Close follow-up seems to be necessary in such cases.

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“…Another candidate for this unknown factor is coronary vasospasm. 32 This does not rule out a mediating role of magnesium because decreasing the serum magnesium causes vasospasm. 33 Another possibility is that there is a U-shaped relation between serum magnesium and QTc interval.…”

Section: Qtc Intervalmentioning

confidence: 99%

Electrocardiographic Abnormalities and Serum Magnesium in Patients With Subarachnoid Hemorrhage

Bergh

Algra

Rinkel

2004

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Background and Purpose-ECG abnormalities and hypomagnesemia frequently occur after aneurysmal subarachnoid hemorrhage (SAH). Because hypomagnesemia is associated with several ECG abnormalities, we studied whether hypomagnesemia mediates ECG abnormalities after SAH. Methods-We prospectively studied a consecutive series of 62 patients admitted within 72 hours after aneurysmal SAH.A standard 12-lead ECG and serum magnesium measurement were routinely performed at admission. The relationship between serum magnesium and ECG abnormalities was assessed with linear regression analysis and the Mann-Whitney test in case of dichotomized ECG abnormalities. Results-Hypomagnesemia was present in 23 patients (37%), and 38 patients (61%) had a long QTc duration. Low serum magnesium was related to a long PR interval (Pϭ0.001) and a shorter QTc interval (Pϭ0.004). Adjustment for World Federation of Neurological Surgeons score, hydrocephalus, and the amount of cisternal and ventricular blood did not influence these relations. Conclusions-In patients with SAH, lower serum magnesium levels are related to less pronounced increase in the QTc interval. Although the direction of the relation was unexpected, decreased serum magnesium might be the missing link between SAH and ECG abnormalities.

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Coronary vasospasm following subarachnoid hemorrhage as a cause of stunned myocardium

Cited by 69 publications

References 21 publications

Regional Myocardial Perfusion After Experimental Subarachnoid Hemorrhage

Regional Myocardial Perfusion After Experimental Subarachnoid Hemorrhage

Significance of ST segment elevation in electrocardiograms in patients with ruptured cerebral aneurysms

Electrocardiographic Abnormalities and Serum Magnesium in Patients With Subarachnoid Hemorrhage

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