Electrocardiographic disturbances following acute increase of intracranial pressure

Eichbaum, F. W.; Gazetta, Ben-Hur; Pereira, Carlos Britto

doi:10.1007/bf02047048

Cited by 18 publications

(8 citation statements)

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“…They indicate, especially when associated with a focal myocardial edema, a local injury of myocardial fibers which may proceed to a complete necrosis. Necrobiosis of myocardial fibers may also occur after cranial trauma, where we found in some cases spotty fuchsinophilia and foci of nitro-blue tetrazolium-negative fibers, indicating loss of suc cinic dehydrogenase activity [9], Beside myocardial infarction and encephalogenic heart lesions result ing from acute intracranial hypertension, we can also expect to find focal edema and wavy fibers in other forms of adrenergic cardiopathy such as pheochromocytoma, thyroid storm, etc. Myocardial edema likewise oc curs in numerous other pathologic conditions ranging from avitaminoses (beriberi) to hormonal disorders (myxedema), virus infections (polio myelitis), toxi-infections (diphtheria), stress, hypokalemia, anaphylaxis, etc.…”

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“…Some 10 years ago, we investigated the incidence and histologic features of myocardial lesions in fatal cranial trauma, and observed in 65% of the cases (30 of 40 patients) a pronounced focal myocardial edema [6][7][8][9]. On reading Bouchardy and M a jn o 's papers [1,2] we reexamined the microscopic slides of these hearts, and were surprised to find in almost all positive cases -i.e., those presenting focal myocardial edema -fully developed 'wavy fibers' (1st, 2nd and 3rd degree) which formerly had escaped our observation.…”

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‘Wavy’ Myocardial Fibers in Spontaneous and Experimental Adrenergic Cardiopathies

Eichbaum¹

1975

Cardiology

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Wavy myocardial fibers, especially when associated with focal edema, are a characteristic sign of acute myocardial ischemia. ‘Waving’ might be induced by the increased hydrostatic pressure of interstitial edema, which squeezes and stretches the neighboring fibers. Beside their regular occurrence in early myocardial infarcts, wavy myocardial fibers are also frequently encountered in cases of acute adrenergic heart injury, especially in fatal cranial trauma and after injection of high doses of catecholamines in experimental animals.

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‘Wavy’ Myocardial Fibers in Spontaneous and Experimental Adrenergic Cardiopathies

Eichbaum¹

1975

Cardiology

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“…15 ' 16 Experimentally, elevation of intracranial pressure produces a surge of plasma catecholamines. 16 In both experimental and clinical observations catecholamines may produce cardiac necrosis or histochemical changes similar to those described in this series.…”

Section: Table 2 Size Of Lesion and Duration Of Stroke In 38 Patientsmentioning

confidence: 99%

Myocardial damage from acute cerebral lesions.

Kolín¹,

Norris²

1984

Stroke

179

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SUMMARY Autopsy findings in 58 patients with intracranlal 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<0.01) in patients with intracranlal 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.Stroke Vol 15, No 6, 1984ELECTROCARDIOGRAPHS (ECG) changes in patients with cerebral lesions were first described in 1938 1 and these findings were later confirmed by other workers.2 ' 3 In acute stroke patients, evidence of myocardial damage was also found, including increased serum levels of cardiac enzymes, 4 -5 the occurrence of cardiac arrhythmias 6 and high levels of plasma catecholamines.7 Focal myocytolysis was described at autopsy in 8-12% of patients dying from a variety of acute cerebral lesions.8 ' 9 Since this secondary myocardial damage may indicate more widespread and subtle reversible cardiac changes, we undertook the present study using a more sensitive histochemical method to determine the frequency and extent of myocardial injury in stroke and other forms of acute cerebral lesions. Materials and MethodsConsecutive complete autopsies supervised by the same pathologist in a general teaching hospital were performed within 36 hours of death. Death was due to an acute intracranial lesion in 58 patients and to noncerebral causes, including a variety of heart diseases, in 45 patients. In five other patients, death was instant and due to a sudden violent cause, such as suicide.The hearts were weighed, measured and transversely sliced through the ventricles. Transmural blocks of the left ventricular wall were obtained from the sites of attachment of the anterior and posterior papillary muscles and split horizontally for corresponding cryostat and paraffin blocks. If either of these sites was affected by necrosis or fibrosis, an additional transmural block was obtained from an apparently healthy segment of the ventricle. Cross-sections of the three major coronary artery trunks were collected for routine histology. Unfixed cryostat sections (8u) from each cardiac sample were stained with nitro-blue tetrazolium (NBT) to demonstrate succinic dehydroge...

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“…5 Some patients dying from stroke show myocardial lesions, 6 similar to those observed in animals infused with catecholamines 718 and in animals with increased intracranial pressure, 9 or intracranial hemorrhage. 10 " 12 Taken together, these findings suggest that raised levels of catecholamines after cerebral ischemia, likely from increased sympathetic activity, contribute to myocardial damage.…”

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Acute myocardial and plasma catecholamine changes in experimental stroke.

Hachinski¹,

Smith²,

Silver³

et al. 1986

Stroke

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SUMMARY Focal cerebral ischemia hi humans increases the Incidence of cardiac arrhythmias, and serum cardiac enzyme and plasma norepinephrine levels. In addition, systemic administration of catecholamines causes myocardial damage. This suggests that cerebral ischemia may cause myocardial damage as a consequence of elevated plasma norepinephrine levels. Therefore, experiments were done hi 23 chloralosed, paralyzed and artificially ventilated cats to investigate the effects of occluding (n = 17) or sham-occluding (n = 6) the left middle cerebral artery on the myocardium and on circulating levels of plasma catecholamines. After occlusion of the middle cerebral artery for 12-22 hr, 41% (7/17) of the hearts had either acute myocardial necrosis (3/7), focal hemorrhage (3/7), or both (177). In anlmah with acute myocardial damage the levels of plasma norepinephrine and epinephrine were significantly increased compared to pre-middle cerebral artery occlusion values ( + 46 ± 18% and +142 ± 45%, respectively). As well, meats with acute myocardial damage, changes from initial levels of plasma norepinephrine and epinephrine were significantly Increased over those of experimental cats without acute myocardial damage. In animals which did not have acute myocardial damage (10/17) the circulating plasma levels of catecholamines were not significantly different from pre-occlusion values. Similarly, sham occlusion did not alter plasma catecholamine levels. These data demonstrate that a percentage of animals subjected to middle cerebral artery occlusion have myocardial damage and an increase hi plasma concentration of norepinephrine and epinephrine. This suggests that a rise hi plasma catecholamine levels, due to Increased sympathetic activity after middle cerebral artery occlusion, may cause myocardial damage. Stroke Vol 17, No 3, 1986 PATIENTS who begin to recover neurologically after a stroke may perish unexpectedly from cardiac complications or sudden death.1 Although some of these deaths could be attributed to concomitant heart disease, stroke patients have an excess of cardiac arrhythmias, increased cardiac serum enzymes and raised plasma catecholamines when compared to similarly managed controls matched for age, sex and the presence of heart disease. "5 Some patients dying from stroke show myocardial lesions, 6 similar to those observed in animals infused with catecholamines 718 and in animals with increased intracranial pressure, 9 or intracranial hemorrhage. "12 Taken together, these findings suggest that raised levels of catecholamines after cerebral ischemia, likely from increased sympathetic activity, contribute to myocardial damage. The present study was done to determine whether focal cerebral ischemia in the cat would produce cardiac lesions and whether changes in plasma levels of catecholamines were associated with the cardiac lesions. Methods Experiments were done in 23 adult cats of either sex weighing 2.0 to 3.5 kg. To isolate the middle cerebral artery (MCA) animals were anesthetized either with sodium pentoba...

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Electrocardiographic disturbances following acute increase of intracranial pressure

Cited by 18 publications

References 9 publications

‘Wavy’ Myocardial Fibers in Spontaneous and Experimental Adrenergic Cardiopathies

‘Wavy’ Myocardial Fibers in Spontaneous and Experimental Adrenergic Cardiopathies

Myocardial damage from acute cerebral lesions.

Acute myocardial and plasma catecholamine changes in experimental stroke.

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Electrocardiographic disturbances following acute increase of intracranial pressure

Cited by 18 publications

References 9 publications

&lsquo;Wavy&rsquo; Myocardial Fibers in Spontaneous and Experimental Adrenergic Cardiopathies

&lsquo;Wavy&rsquo; Myocardial Fibers in Spontaneous and Experimental Adrenergic Cardiopathies

Myocardial damage from acute cerebral lesions.

Acute myocardial and plasma catecholamine changes in experimental stroke.

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Product

Resources

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‘Wavy’ Myocardial Fibers in Spontaneous and Experimental Adrenergic Cardiopathies

‘Wavy’ Myocardial Fibers in Spontaneous and Experimental Adrenergic Cardiopathies