Cardiac dysfunction in the CABG patient

Siribaddana, Sisira

doi:10.1016/j.coph.2012.01.010

Cited by 19 publications

(12 citation statements)

References 63 publications

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“…Changes in thyroid hormone levels are evident in myocardial infarction, heart failure, and other diseases and can thus be considered a predictor of multiple prognostic indicators [ 7 , 8 , 20 ]. Furthermore, other studies [ 21 , 22 ] also suggested that the selective application of thyroid hormone in patients with myocardial infarction and extracorporeal circulation can improve the survival rates. The results of the present study suggest that NTIS might also be an important prognostic marker in patients with other diagnoses, not cardiac related, in the ICU.…”

Section: Discussionmentioning

confidence: 99%

Prognostic Value of Thyroid Hormone FT3 in General Patients Admitted to the Intensive Care Unit

Guo

Hong

Wang

et al. 2020

BioMed Research International

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Low plasma triiodothyronine (T3) concentration indicates nonthyroidal illness syndrome (NTIS), which might be associated with a poor outcome in patients in the intensive care unit (ICU). This study evaluated the relationship between NTIS and prognostic indicators in patients admitted to the ICU and examined the fT3 cut-off points that could be associated with 28-day mortality. This prospective observational study included patients admitted to the ICU of The Third Hospital of Hebei Medical University from February to November 2018. The baseline variables and the occurrence of low free T3 (FT3) were collected. The patients were divided into the NTIS (FT3<3.28) and non-NTIS groups. Among 305 patients, 118 (38.7%) were in the NTIS group. FT3 (P<0.001) and FT4 (P=0.001) were lower, while the 28-day mortality rate (P<0.001) and hospitalization expenses in ICU (P=0.001) were higher in the NTIS group. The univariable analyses identified NTIS, FT3, free thyroxine/FT3, APACHEII, sequential organ failure score, duration of mechanical ventilation, creatinine, oxygenation index, white blood cells, albumin, age, and brain natriuretic peptide as being associated with 28-day mortality (all P<0.05). The cut-off value of FT3 for 28-day mortality was 2.88 pmol/L. The 28-day mortality rate and hospitalization expenses in the ICU were higher in patients with NTIS. NTIS was independently associated with 28-day mortality.

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Section: Discussionmentioning

confidence: 99%

Prognostic Value of Thyroid Hormone FT3 in General Patients Admitted to the Intensive Care Unit

Guo

Hong

Wang

et al. 2020

BioMed Research International

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“…‘Stunning’ was defined as depressed myocardial function following an ischaemic event (Kloner & Jennings, ). Several authors have shown cardiac benefits of levothyroxine (T 4 ) or T 3 therapies in critical transient conditions of regional ischaemia–reperfusion (I/R; Heusch, ), global I/R in patients with cardiopulmonary bypass (Siribaddana, ) and I/R in brain‐dead potential organ donors (Novitzky & Cooper, ). All these conditions induce variable degrees of myocardial stunning.…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effect of hyperthyroidism on the stunned rat heart during ischaemia–reperfusion: energetics and role of mitochondria

Ragone

Bonazzola

Colareda

et al. 2015

Experimental Physiology

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New Findings r What is the central question of this study?Hyperthyroidism is a cardiac risk factor, but thyroid therapy is used on myocardial stunning. What is the consequence of hyperthyroidism for mitochondrial metabolism and Ca 2+handling of the postischaemic stunned heart? r What is the main finding and its importance?Hyperthyroidism reduced stunning and improved muscle economy of the postischaemic rat heart. The activities of the mitochondrial sodium-calcium exchanger and mitochondrial K + channel in hyperthyroid rat hearts were different from those in the euthyroid rat hearts. These findings contribute to the understanding of mitochondrial bioenergetics in pathology and support thyroid therapy in the stunning induced by ischaemia.Transient ischaemia and hyperthyroidism are cardiovascular risk factors. Nevertheless, 3,5,3 -triiodothyronine/thyroxine therapy has been used to revert myocardial stunning. We studied the influence of hyperthyroidism on the role played by mitochondria in myocardial stunning consequent to ischaemia-reperfusion. Rats were injected s.c. daily with 20 μg kg −1 triiodothyronine for 15 days (HpT group). Isolated ventricles from either HpT or euthyroid (EuT) rats were perfused in a calorimeter, and left intraventricular pressure (in millimetres of mercury) and heat release (Ht; in milliwatts per gram) were measured. Stunning was evoked by 20 min of no-flow ischaemia and 45 min reperfusion. The HpT hearts developed higher postischaemic contractile recovery (PICR) and improved total muscle economy (P/Ht) with lower diastolic contracture ( LVEDP) than EuT hearts. Release of Ca 2+ from the sarcoplasmic reticulum during reperfusion with 10 mm caffeine in low-[Na + ] Krebs solution evoked a higher contracture in EuT than in HpT hearts. Blockade of the mitochondrial sodium-calcium exchanger with clonazepam increased LVEDP and reduced P/Ht and PICR in HpT but not in EuT hearts. The clonazepam-induced dysfunction in HpT hearts was reduced by ciclosporin, suggesting a dependance on activation of the mitochondrial permeability transition pore. Blockade of the mitochondrial Ca 2+ uniporter with Ru360 reduced P/Ht and PICR to ß10% in both HpT and EuT hearts. Blockade of mitochondrial K + channels with 5-hydroxydecanoate increased LVEDP and reduced PICR and P/Ht in HpT hearts, while it only increased LVEDP in EuT hearts. The results suggest that hyperthyroidism prevents the stunning with high dependence on the mitochondrial sodium-calcium exchanger and mitochondrial K + channels. IntroductionThyroid dysfunction, either clinical or subclinical, has been related to the increase in morbidity and mortality associated with cardiovascular episodes (Klein & Danzi, 2007). In particular, hyperthyroidism predisposes to long-term cardiac conditions such as hypertrophy and cardiac remodelling. Severe and untreated hyperthyroidism induces tachycardia, high cardiac workload and a risk of atrial fibrillation related to the upregulation of β-adrenergic receptors (Nyirenda et al. 2005). Some patients suffer symptoms...

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“…These include any condition in which a period of regional or global myocardial ischemia (inadequate blood perfusion) has occurred followed by revascularization and/or reperfusion. In particular, the effect of T 3 /T 4 therapy has been studied under three conditions in which the ESS and myocardial functional depression have been documented -i) transient regional myocardial ischemia and reperfusion (Heusch 2013), ii) transient global myocardial ischemia in patients undergoing cardiac surgery on cardiopulmonary bypass (CPB) (Siribaddana 2012), and iii) transient inadequate global myocardial perfusion in brain-dead potential organ donors (Novitzky et al 1984). Under all three conditions, following administration of T 3 /T 4 , the myocardial dysfunction was rapidly reversed.…”

Section: Thyroid Hormones In the Treatment Of The Essmentioning

confidence: 99%

Thyroid hormone and the stunned myocardium

Novitzky¹,

Cooper²

2014

Journal of Endocrinology

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Acute critically ill patients experience a rapid decline in plasma free thyroid hormone levels (free triiodothyronine (FT 3 ) and free levothyroxine (FT 4 )), with a marked elevation of reverse T 3 , recognized as the euthyroid sick syndrome (ESS) or low-T 3 syndrome. The ESS is also often associated with depressed myocardial function, sometimes referred to as the 'stunned myocardium'. Its clinical effects may vary from minimal hemodynamic impairment to cardiogenic shock. Medical management may range from aspirin alone to placement of a left ventricular assist device. With adequate supportive therapy, recovery usually occurs within days or weeks. The effect of T 3 /T 4 therapy has been studied in three conditions in which the ESS and myocardial functional depression have been documented -i) transient regional myocardial ischemia and reperfusion, ii) transient global myocardial ischemia in patients undergoing cardiac surgery on cardiopulmonary bypass, and iii) transient inadequate global myocardial perfusion in brain-dead potential organ donors. Under all three conditions, myocardial ischemia leads to rapid loss of high-energy phosphates, accumulation of myocardial tissue lactate, and probably loss of homeostasis of cytosolic calcium, which may further increase cell injury. There is an inability to generate ATP through the Krebs cycle, which reduces the high-energy phosphate pool essential for all cell ATPases. Under all three conditions, following administration of T 3 /T 4 , the myocardial dysfunction was rapidly reversed. We, therefore, cautiously advocate the use of thyroid hormonal therapy to any patient with the ESS and/or a stunned myocardium.

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Cardiac dysfunction in the CABG patient

Cited by 19 publications

References 63 publications

Prognostic Value of Thyroid Hormone FT3 in General Patients Admitted to the Intensive Care Unit

Prognostic Value of Thyroid Hormone FT3 in General Patients Admitted to the Intensive Care Unit

Cardioprotective effect of hyperthyroidism on the stunned rat heart during ischaemia–reperfusion: energetics and role of mitochondria

Thyroid hormone and the stunned myocardium

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