Thyroid heart disease.

Symons, Cecil

doi:10.1136/hrt.41.3.257

Cited by 64 publications

(12 citation statements)

References 52 publications

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“…Hypokalemia can be a cause of ventricular fibrillation in Cushing's syndrome [395]. Thyroid-related heart disease is recognized [396,397], but there has been recent interest in an apparent association between chronic thyroiditis and sudden death [398][399][400]. Death due to presumed arrhythmia has been noted in association with thyrotoxicosis [39] and abuse of thyroid hormone [401].…”

Section: Central Nervous System Causes Of Sudden Deathmentioning

confidence: 99%

Sudden adult death

Langlois

2009

Forensic Sci Med Pathol

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In the investigation of sudden death in adults, channelopathies, such as long QT syndrome, have risen to the fore in the minds of forensic pathologists in recent years. Examples of these disorders are touched upon in this review as an absence of abnormal findings at postmortem examination is characteristic and the importance of considering the diagnosis lies in the heritable nature of these conditions. Typically, a diagnosis of a possible channelopathy is evoked as an explanation for a 'negative autopsy' in a case of apparent sudden natural death. However, the one potential adverse effect of this approach is that subtle causes of sudden death may be overlooked. The intention of this article is to review and discuss potential causes of sudden adult death (mostly natural) that should be considered before resorting to a diagnosis of possible channelopathy. Nonetheless, it becomes apparent that many of the potential causes of sudden death can have a genetic basis. Thus, it becomes an important consideration that there may be a genetic basis to sudden death that extends beyond the negative autopsy.

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Section: Central Nervous System Causes Of Sudden Deathmentioning

confidence: 99%

Sudden adult death

Langlois

2009

Forensic Sci Med Pathol

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“…As a result, we have not needed to perform EC so frequently in the last few years. Staffurth et al (1965) and Symons (1979) believe that thyrotoxicosis may cause permanent damage to the heart which is more likely when there is delay in treatment. Davis and Pomerance (1972) reported an apparent loss of muscle fibres in the sinoatrial node in patients dying in AF, which might well obtain in thyrotoxicosis, though there is no direct evidence in this condition.…”

Section: Resultsmentioning

confidence: 99%

Electrical cardioversion for persistent atrial fibrillation after treatment of thyrotoxicosis

Emery

Staffurth

1982

Postgraduate Medical Journal

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“…The sick sinus syndrome and AV blocks have been reported both in patients cured from thyreotoxicosis and hypothyroidism (7). It has been suggested that the bradyarrhythmias in the hypothyroid state might be caused by oedema in the heart muscle and conduction system which later become fibrotic (8).…”

Section: Discussionmentioning

confidence: 99%

Long‐term ECG Recordings in Thyroxine‐substituted Hypothyroid Subjects

Hylander

Kennebäck

Rosenqvist

et al. 1987

Journal of Internal Medicine

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ABSTRACT. Bradyarrhythmias are sometimes observed in hypothyroid patients. This phenomenon could either be due to the disease process with structural changes of the heart or to an abnormal hormone level. The purpose of the present paper was to study the prevalence of bradyarrhythimas in hypothyroid patients on long‐term substitution therapy. Nineteen subjects were studied 9–53 months after they had reached the final thyroxine substitution level. Ambulatory ECG registrations were performed during 48 hours. Ventricular ectopic beats were observed in 10 of the 19 patients, but no bradyarrhythmias were detected. The results support the notion that arrhythmias found in hypothyroid patients are at least mainly due to the low thyroid hormone level.

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Thyroid heart disease.

Cited by 64 publications

References 52 publications

Sudden adult death

Sudden adult death

Electrical cardioversion for persistent atrial fibrillation after treatment of thyrotoxicosis

Long‐term ECG Recordings in Thyroxine‐substituted Hypothyroid Subjects

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