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Stroke, Vol 15, 990-993, Copyright © 1984 by American Heart Association
A Kolin and JW Norris
Autopsy findings in 58 patients with intracranial lesions were compared
with those in 50 control patients for myocardial damage, characterised by a
change from a myofibrillar to a granular staining pattern, using a
histochemical method for succinic dehydrogenase. Transmurally scattered
foci of damaged myocardial fibres were significantly more common (p less
than 0.01) in patients with intracranial lesions (62%) compared to controls
(26%). No victims of sudden violent deaths showed these cardiac lesions.
Focal myocardial damage required at least six hours to develop after onset
of the acute neurological event and was not observed after the second week.
It was associated with lesions producing a rapid increase in intracranial
pressure and was usually absent in patients with slowly enlarging or small
cerebral lesions. Similar myocardial changes were seen in patients in the
control group dying from prolonged shock or other forms of acute
circulatory or metabolic failure. The postulated mechanism of cardiac
damage in these patients is increased levels of plasma catecholamines
secondary to rapidly increasing intracranial pressure, irrespective of the
cerebral pathology.
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Myocardial damage from acute cerebral lesions
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