Digitalis cardiotoxicity revisited

Lathers, Claire M.; Roberts, Jay

doi:10.1016/0024-3205(80)90439-7

Cited by 27 publications

(5 citation statements)

References 120 publications

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“…Autonomic neural factors are also involved in sudden death (Lown and Verrier, 1978). Autonomic neural dysfunction associated with cardiac arrhythmias produced by digitalis toxicity has been reviewed in depth by Gillis and Quest (1979) and by Lathers and Roberts (1980). Autonomic dysfunction, as indicated by the development of sympathetic imbalance, has been shown to increase the incidence of cardiac arrhythmias.…”

Section: Discussionmentioning

confidence: 99%

Autonomic Dysfunction in Epilepsy: Characterization of Autonomic Cardiac Neural Discharge Associated with Pentylenetetrazol‐Induced Epileptogenic Activity

1982

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The purpose of this study was to determine if epileptogenic activity is associated with changes in autonomic cardiac neural discharge and the development of arrhythmias. Nine cats, anesthetized with alpha-chloralose, received pentylenetetrazol (PTZ), 10, 20, 50, 100, 200, and 2,000 mg/kg, intravenously at 10 min intervals. The following were monitored: neural discharge from 1 to 3 postganglionic cardiac sympathetic branches (8 cats, 17 nerves) and the vagus (7 cats, 8 nerves); the electrocorticogram; blood pressure; heart rate; and lead II electrocardiogram. Autonomic dysfunction was manifested by: the observation that autonomic cardiac nerves did not always respond in a predictable manner to changes in blood pressure; the development of a marked increase in variability in mean autonomic cardiac sympathetic and parasympathetic neural discharge; and the fact that the very large increase in the variability of the discharge rate of parasympathetic nerves was seen after PTZ, 50 mg/kg, but did not develop until 100 mg/kg in sympathetic neural discharge. This autonomic imbalance was associated with both interictal and ictal epileptogenic activity. Almost invariably, interictal discharge occurred after PTZ, 10 mg/kg; with higher doses, the duration of ictal activity increased although interictal discharges were present. The altered cardiac autonomic neural discharge was associated with minimal epileptogenic activity in the form of interictal discharges and cardiac arrhythmias which may contribute to sudden unexplained death of the epileptic.

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Section: Discussionmentioning

confidence: 99%

Autonomic Dysfunction in Epilepsy: Characterization of Autonomic Cardiac Neural Discharge Associated with Pentylenetetrazol‐Induced Epileptogenic Activity

1982

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“…digoxin, digitoxin) (Dutta et al 1977, Dutta et al 1968. Although some glycosides fail to cross the blood brain barrier, these glycosides still produce the same spectrum of arrhythmic toxicity (Lathers and Roberts 1980). This supports the contention that digitalis glycosides produce part of their toxic effects through a portion of the central nervous system outside of the blood brain barrier, probably in the area postrema (Borison 1951, Cammermeyer 1947.…”

Section: A-6mentioning

confidence: 52%

Commentary and Scientific Review of Studies on Cardiac Function and Cardiac Sensitization Models

Brock¹,

Kimmel²,

Jederberg³

2003

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“…A complication of heart failure treatment with digitalis is cardiac toxicity, the incidence of which has been reported to vary from 8-35%.311- 32 This subject has been reviewed r e~e n t l y .~' Digitalis toxicity is assumed to be a product of three components: nonuniform neural activity resulting from an action on the adrenergic nervous system; an action on the adrenal medulla; and a direct action on cardiac Factors which increase the risk of digitalis toxicity are the following: renal failure, old age, electrolyte imbalance, and acute myocardial ischemia. 26 The very narrow therapeutic index for the cardiac glycosides has encouraged the search for new analogs with reduced toxicity and a greater therapeutic index.…”

Section: Cardiac Glycosides (Fig 1)mentioning

confidence: 99%