Acute severe postischemic myocardial depression reversed by triiodothyronine

Holland, Fred W.; Brown, Paul S.; Clark, Richard E.

doi:10.1016/0003-4975(92)91389-q

Cited by 37 publications

(13 citation statements)

References 19 publications

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“…It has long been observed that administration of TH at reperfusion can improve post-ischemic left ventricular function in animal models of ischemia-reperfusion and in patients undergoing GABG [118][119][120][121][122][123][124][125] (Fig. 7).…”

Section: Th Limits Reperfusion Injurymentioning

confidence: 95%

New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?

2010

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Chronic ischemia or pressure overload decreases thyroid hormone (TH) signaling and activates the fetal gene program in the heart. While these features are of physiologic importance in the developing heart, their respective roles in the postnatal heart are debated. Administration of TH can prevent the changes of the fetal gene program and rebuild the heart after an "index event" such as ischemia. TH affects cardiac remodeling by limiting reperfusion injury, and, at later states, by inducing distinct changes in cardiac chamber geometry in a time-dependent manner. Furthermore, administration of TH can convert pathologic to physiologic hypertrophy. These effects are the result of favorable cellular remodeling. While preliminary clinical studies provide encouraging results, the potential and efficacy of TH in the treatment of heart disease still await evaluation in large clinical trials.

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Section: Th Limits Reperfusion Injurymentioning

confidence: 95%

New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?

2010

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“…Furthermore, T 3 and/or T 4 administration increased cell viability in neonatal cardiomyocytes subjected to hypoxia or to serum starvation [21,22]. A beneficial effect of thyroid hormone on reperfusion injury was also demonstrated in animal studies and recently in humans [5,[23][24][25][26][27][28][29].…”

Section: Thyroid Hormone and Ischaemia-reperfusionmentioning

confidence: 88%

Thyroid hormone and myocardial ischaemia

Pantos

Mourouzis

Xinaris

et al. 2008

The Journal of Steroid Biochemistry and Molecular Biology

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“…This effect was not related to the hypertrophy since propranolol or irbesartan, an AT1 receptor inhibitor, diminished cardiac hypertrophy, but did not abolish the increased tolerance of the hyperthyroid heart to ischemia [20,24]. Further studies showed that T3 and/or T4 administration can increase cell viability in neonatal cardiomyocytes subjected to hypoxia or to serum starvation [25,26] and thyroid hormone has a protective effect on reperfusion injury in animals and as recently shown also in humans [27][28][29][30][31][32][33].…”

Section: Cardiac Hypertrophy Induced By Thyroxinementioning

confidence: 94%

Protection of the abnormal heart

2007

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Myocardial ischemia and reperfusion injury have been extensively investigated in the laboratory mainly in healthy tissues. However, in clinical settings, ischemic heart disease coexists with certain illnesses, which could potentially influence the response of the myocardium to ischemia and reperfusion. Recent research has revealed that the abnormal heart may not be always vulnerable to ischemic injury. Furthermore, the effect of powerful means of protection, such as ischemic preconditioning, may not be in operation under certain pathological conditions. With this evidence in mind, the present review will focus on the response of the abnormal heart to ischemia and reperfusion, the possible underlying mechanisms, and potential cardioprotective strategies.

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Acute severe postischemic myocardial depression reversed by triiodothyronine

Cited by 37 publications

References 19 publications

New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?

New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?

Thyroid hormone and myocardial ischaemia

Protection of the abnormal heart

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