Electrocardiographic Patterns in Patients with Cerebrovascular Accidents

Fentz, Vagn; Gormsen, J

doi:10.1161/01.cir.25.1.22

Cited by 119 publications

(25 citation statements)

References 7 publications

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“…However, in another investigation 7 15 of 21 cases of subarachnoid and intracerebral hemorrhage were found to have Q-T prolongation and S-T segment depression in their EKGs not explicable by other factors. Hence, one might conclude that EKG changes in this study were secondary to the intracranial hemorrhages.…”

Section: Clinical Studiesmentioning

confidence: 89%

Cardiac Abnormalities in Subarachnoid Hemorrhage: A Resumé

Weintraub

McHenry

1974

Stroke

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Abstract:Cardiac Abnormalities in Subarachnoid Hemorrhage: A Resume• There have been numerous reports demonstrating electrocardiographical changes secondary to subarachnoid hemorrhage, consisting of atrial and ventricular arrhythmias, alterations in QRS configuration, Q-T interval prolongation, T-wave abnormalities, and S-T segment elevation or depression. Abnormalities of cardiac muscle and subendocardial hemorrhage have been seen in patients dying of subarachnoid hemorrhage. Experimental work has shown that electrical impulses in the sympathetic nervous system and hypothalamus produce most of these changes, and the implication is that these changes can be prevented by sympathetic blockade. Pulmonary edema also has been shown to occur frequently after subarachnoid hemorrhage, and again the sympathetic nervous system is implicated in the pathophysiology. Studies done illustrating these points are discussed and conclusions drawn with reference to therapy.Additional Key Words myocytolysis pulmonary edema Q-T interval prolongation hypothalamus propranolol sympathetic nervous system reserpine

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Section: Clinical Studiesmentioning

confidence: 89%

Cardiac Abnormalities in Subarachnoid Hemorrhage: A Resumé

Weintraub

McHenry

1974

Stroke

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“…4 " 11 Further, despite the likelihood of underlying hypertensive or atherosclerotic cardiovascular disease, no previous studies have included detailed examinations of prior ECG's to distinguish abnormalities specifically associated with acute stroke.…”

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confidence: 99%

The electrocardiogram in stroke: relationship to pathophysiological type and comparison with prior tracings.

Goldstein¹

1979

Stroke

225

121

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SUMMARYThe author reviewed electrocardiograph^ records of ISO patients with acute stroke and 150 age-and sex-matched controls, to assess the relative frequencies of ECG abnormalities among the pathophysiologic categories of stroke, and to distinguish new abnormalities at the time of the stroke from those noted on prior tracings. Of the 150 patients with stroke, 138 (92%) showed ECG abnormalities. The most common abnormalities were also changes from prior tracings: QT prolongation (68 patients, 45%), ischemic changes (59, 35%), U waves (42, 28%), tachycardia (42, 28%), and arrhythmias (41, 27%). Patients with cerebral embolus had a significantly increased frequency of atrial fibrillation (9 patients, 47%); and with subarachnoid hemorrhage an increased frequency of QT prolongation (20, 71%) and sinus arrhythmia (5, 18%). The frequencies of QT prolongation and ischemic changes related strongly to admission systolic pressure but not to mortality. Stroke patients had an increased frequency of pathologic Q waves (30 patients, 20%) and left ventricular hypertrophy (39, 26%), but these were not new findings at the time of the stroke.The results are consistent with an interaction of underlying hypertensive or atherosclerotic cardiovascular disease, sympathetic hyperactivity, and possibly myocardial necrosis, in producing ECG changes.

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“…Cushing [1,2] [3][4][5][6][7][8][9][10][11][12], An acute episode of pulmonary hyperten sion and edema constitutes one of the most serious problems after head injury [10][11][12][13][14][15], In the past, our laboratory had carried out a series of animal experiments on the neural and hemodynamic mechanisms involved in the neurogenic pulmonary edema (NPE) [10,12,[16][17][18][19][20][21][22][23][24][25][26]. This brief review presents and dis cusses early and recent studies on the patho genesis of pulmonary edema induced by cere bral compression (CC) or ICH.…”

Section: Hemodynamic Mechanisms Of Neurogenic Pulmonary Edema Abstractmentioning

confidence: 99%

Hemodynamic Mechanisms of Neurogenic Pulmonary Edema

1995

Neurosignals

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Electrocardiographic Patterns in Patients with Cerebrovascular Accidents

Cited by 119 publications

References 7 publications

Cardiac Abnormalities in Subarachnoid Hemorrhage: A Resumé

Cardiac Abnormalities in Subarachnoid Hemorrhage: A Resumé

The electrocardiogram in stroke: relationship to pathophysiological type and comparison with prior tracings.

Hemodynamic Mechanisms of Neurogenic Pulmonary Edema

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