Thyroxine and cardiac electrophysiology—a forgotten physiological duo?

Ker, James

doi:10.1186/1756-6614-5-8

Cited by 8 publications

(5 citation statements)

References 11 publications

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“…Marked anterior TWIs are usually seen only in the context of significant QTc prolongation 9 10. Conversely, a normal QTc seems to be associated with mild, less extensive TWIs 6 8 13. Our patient's case was notable for her widespread and deep TWIs in the absence of other ECG signs of hypothyroidism, except for a mild sinus bradycardia.…”

Section: Discussionmentioning

confidence: 60%

T-wave inversions on ECG as primary manifestation of Hashimoto's disease

2016

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A middle-aged Hispanic woman presented to the emergency department (ED) reporting of acute new onset pressure-like chest pain developed at rest. It was radiated to the right arm and associated with malaise. Initial ECG demonstrated T-wave inversions (TWIs) in all anterior and lateral leads. Electrolytes, serial cardiac troponin and D-dimer were all normal. Comprehensive transthoracic echocardiogram and nuclear stress test did not reveal a cardiac cause of her symptoms.Serum thyroid-stimulating hormone was markedly elevated (207 mIU/L) and free thyroxine was low (FT4 0.07 ng/dL), consistent with severe primary hypothyroidism. Thyroperoxidase (TPO) antibodies were positive. Therapy with levothyroxine was started. No other cause of the TWIs was identified. A repeat ECG obtained 8 weeks later showed partial resolution of the TWIs. Our observations indicate that Hashimoto's disease is the most likely primary cause of this patient's extensive and profound TWI, which improved after thyroid replacement therapy.

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Section: Discussionmentioning

confidence: 60%

T-wave inversions on ECG as primary manifestation of Hashimoto's disease

2016

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“…(13) Excessive thyroxine can damage the heart in a number of ways that result in arrhythmias, cardiac hypertrophy, and heart failure. (14,15) Cardiac hypertrophy is a common pathological feature of some major cardiovascular diseases, such as hypertension and myocardial infarction, and strongly associated with increased risk of heart failure and sudden cardiac death. Experimental induction of cardiac hypertrophy by L-thy is a wellestablished model to study the protective role of different anti-cardiac hypertrophy agents in animals.…”

Section: Discussionmentioning

confidence: 99%

Cyclovirobuxinum D alleviates cardiac hypertrophy in hyperthyroid rats by preventing apoptosis of cardiac cells and inhibiting the p38 mitogen-activated protein kinase signaling pathway

Zhou

Liang

et al. 2016

Chin. J. Integr. Med.

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“…Undiagnosed and/or untreated hypothyroidism may pose a threat of sudden cardiac death, which may be mirrored by myocardial ventricular late potentials in overt hypothyroidism [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Second degree AV block and severely impaired contractility in cardiac myxedema: a case report

et al. 2015

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The heart is a major target organ for thyroid hormone action. Severe overt hypothyroidism can result in diastolic hypertension, lowered cardiac output, impaired left ventricular contractility and diastolic relaxation, pericardial effusion and bradycardia. However, the function of the atrial pacemaker is usually normal and the degree by which the heart rate slows down is often modest. Here we report the case of a 20 year old male Caucasian with severe overt hypothyroidism. He presented with syncopation due to second degree atrioventricular block type Mobitz 2 and heart failure with reduced ejection fraction (38 %). Laboratory testing revealed a severe overt hypothyroidism with markedly elevated TSH (>100 mIU/L) and reduced fT3 and fT4 levels. The condition was caused by hypothyroid Graves’ disease (Graves’ disease with Hashimoto component). Although magnetic resonance imaging of the heart demonstrated decreased cardiac contractility and pericardial effusion, suggesting peri-myocarditis, plasma levels for BNP and troponin I were low. A possible infectious cause was unlikely, since testing for cardiotropic viruses was negative. The patient was treated with intravenous levothyroxine and after peripheral euthyroidism had been achieved, left ventricular ejection fraction returned to normal and pericardial effusion dissolved. Additionally, bradycardiac episodes abated, although intermittent second degree AV block was still occasionally present during the night. In conclusion, overt hypothyroidism may be associated by cardiac myxedema affecting both electrophysiology and contractility, observations that underscore the necessity of thyroid testing in different phenotypes of heart failure.Electronic supplementary materialThe online version of this article (doi:10.1186/s13044-015-0018-2) contains supplementary material, which is available to authorized users.

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Thyroxine and cardiac electrophysiology—a forgotten physiological duo?

Cited by 8 publications

References 11 publications

T-wave inversions on ECG as primary manifestation of Hashimoto's disease

T-wave inversions on ECG as primary manifestation of Hashimoto's disease

Cyclovirobuxinum D alleviates cardiac hypertrophy in hyperthyroid rats by preventing apoptosis of cardiac cells and inhibiting the p38 mitogen-activated protein kinase signaling pathway

Second degree AV block and severely impaired contractility in cardiac myxedema: a case report

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