Effects of Thyroid Hormone on Cardiac Function - The Relative Importance of Heart Rate, Loading Conditions, and Myocardial Contractility in the Regulation of Cardiac Performance in Human Hyperthyroidism

Biondi, Bernadette; Palmieri, Emiliano Antonio; Lombardi, Gaetano; Fazio, Serafino

doi:10.1210/jcem.87.3.8302

Cited by 174 publications

(77 citation statements)

References 69 publications

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“…In adults, T3 regulates bone turnover and bone mineral density [4], and normal euthyroid status is essential to maintain optimal bone strength [5,6]. In addition, alterations in THs levels have a profound effect on the cardiovascular system [7], which includes changes in myocardial contractility, heart rate, and resistance of peripheral vasculature [8][9][10]. Recently, mRNAs for TR isoforms were identified in aortic and coronary smooth muscle cells [11], suggesting that THs may play a direct role in vascular smooth muscle.…”

Section: Introductionmentioning

confidence: 99%

Thyroid Hormone Attenuates Vascular Calcification Induced by Vitamin D3 Plus Nicotine in Rats

et al. 2014

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Thyroid hormones (THs) including thyroxine (T4) and triiodothyronine (T3) play critical roles in bone remodeling. However, the role and mechanism of THs in vascular calcification (VC) have been unclear. To explore the pathophysiological roles of T3 on VC, we investigated the changes in plasma and aortas of THs concentrations and the effect of T3 on rat VC induced by vitamin D3 plus nicotine (VDN). VDN-treated rat showed decreased plasma T3 content, increased vascular calcium deposition, and alkaline phosphatase (ALP) activity. Administration of T3 (0.2 mg/kg body weight IP) for 10 days greatly reduced vascular calcium deposition and ALP activity in calcified rat aortas when compared with controls. Concurrently, the loss of smooth muscle lineage markers α-actin and SM22a was restored, and the increased bone-associated molecules, such as runt-related transcription factor2 (Runx2), Osterix, and osteopontin (OPN) levels in calcified aorta, were reduced by administration of T3. The suppression of klotho in calcified rat aorta was restored by T3. Methimazole (400 mg/L) blocked the beneficial effect of T3 on VC. These results suggested that T3 can inhibit VC development.

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Section: Introductionmentioning

confidence: 99%

Thyroid Hormone Attenuates Vascular Calcification Induced by Vitamin D3 Plus Nicotine in Rats

et al. 2014

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“…Since symptoms of hyperthyroidism are often non-specific and develop slowly, the latter may be the first clinical manifestation of thyroid dysfunction; and this arrhythmia increases the risk of blood clot formation inside the heart, with embolism and stroke if there is clot dislodgment. 17,18 The AF is usually persistent rather than paroxysmal, and is more probable in older patients ---perhaps reflecting a reduction in the threshold for this arrhythmia with age. Pulse pressure is widened, cardiac output and sympathetic tone are increased, and a hyperkinetic apex beat and a loud first heart sound are described; in addition, an accentuated pulmonic component of the second sound can be noticed frequently.…”

Section: Mechanisms Of Th Action On the Cardiovascular Systemmentioning

confidence: 99%

Effects of thyroid hormones on the heart

Vargas‐Uricoechea

Bonelo-Perdomo

Sierra‐Torres

2014

Clínica e Investigación en Arteriosclerosis

110

101

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“…In many respects, the T 3 -mediated effects on the heart and cardiovascular system are similar to the physiologic response to exercise [ 3• ]. Systolic and diastolic cardiac functions are enhanced as isovolumic ventricular relaxation improve and ejection fraction and cardiac output are increased [ 12 ].…”

Section: Cardiovascular Effects Of Thyrotoxicosismentioning

confidence: 99%

Thyrotoxic cardiac disease

Dahl

Danzi²,

Klein

2008

Curr Heart Fail Rep

108

110

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The most recognizable features of hyperthyroidism are those that result from the effects of triiodothyronine (T3) on the heart and cardiovascular system: decreased systemic vascular resistance and increased resting heart rate, left ventricular contractility, blood volume, and cardiac output. Although these measures of cardiac performance are enhanced in hyperthyroidism, the finding of clinical cardiac failure can be somewhat paradoxical. About 6% of thyrotoxic individuals develop symptoms of heart failure, but less than 1% develop dilated -cardiomyopathy with impaired left ventricular systolic function. Heart failure resulting from thyrotoxicosis is due to a tachycardia-mediated mechanism leading to an increased level of cytosolic calcium during diastole with reduced ventricular contractility and diastolic dysfunction, often with tricuspid regurgitation. Pulmonary artery hypertension in thyrotoxicosis is gaining awareness as a cause of isolated right-sided heart failure. In both cases, older individuals are more likely to be affected. Treatment needs to be directed at management of the acute cardiovascular complications, control of the heart rate, and thyroid-specific therapy to restore a euthyroid state that will lead to resolution of the signs and symptoms of heart failure.

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Effects of Thyroid Hormone on Cardiac Function - The Relative Importance of Heart Rate, Loading Conditions, and Myocardial Contractility in the Regulation of Cardiac Performance in Human Hyperthyroidism

Cited by 174 publications

References 69 publications

Thyroid Hormone Attenuates Vascular Calcification Induced by Vitamin D3 Plus Nicotine in Rats

Thyroid Hormone Attenuates Vascular Calcification Induced by Vitamin D3 Plus Nicotine in Rats

Effects of thyroid hormones on the heart

Thyrotoxic cardiac disease

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