Determination of Cardiac Output and Other Hemodynamic Data in Patients with Hyper- and Hypothyroidism, Using Dye Dilution Technique

Anthonisen, P; Holst, Elisabet; Thomsen, Aa. Chr.

doi:10.3109/00365516009065412

Cited by 45 publications

(23 citation statements)

References 23 publications

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“…One of the earliest cardiovascular responses to thyroid hormone administration in humans is a decrease in systemic vascular resistance (SVR) (1,2), and SVR is typically reduced by more than 50% in overt hyperthyroid patients (3). This is probably due to a direct effect of thyroid hormones on vascular smooth muscle cells causing relaxation (2,4), and an effect mediated by adrenergic receptors, since betaadrenergic blockade blunts the thyroid hormonemediated decrease in SVR (5).…”

Section: Introductionmentioning

confidence: 99%

Haemodynamic changes following treatment of subclinical and overt hyperthyroidism

Faber¹,

Wiinberg

Schifter

et al. 2001

European Journal of Endocrinology

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Objective: Hyperthyroidism has profound effects on the cardiovascular system, including reduced systemic vascular resistance (SVR) due to relaxation of vascular smooth muscle cells, enhanced heart rate (HR) and cardiac output (CO) due to an increase in cardiac diastolic relaxation, contractility and heart rate. Subclinical hyperthyroidism is characterised by reduced serum TSH levels despite free thyroxine (T 4 ) and tri-iodothyronine (T 3 ) estimates within the reference range, in subjects with no obvious symptoms of hyperthyroidism. We measured haemodynamic changes (using impedance cardiography) in subjects with endogenous subclinical hyperthyroidism in order to elucidate whether these patients had signs of excess thyroid hormone at the tissue level. Design: The patients were otherwise healthy women with a multinodular goitre (n 6; age 47±81 years; serum TSH 0.006±0.090 mU/l and normal free T 4 and T 3 estimates), studied before and after normalisation of TSH (0.280±1.120 mU/l) by means of radioiodine treatment, and they were compared with 9 overt hyperthyroid patients (2 with multinodular goitre and 7 with Graves' disease) in the untreated state and after euthyroidism had been obtained. Results: Treatment of the subclinical hyperthyroid women resulted in 11% reduction in HR P , 0X02Y 19% reduction in CO from (means^S.D.) 6X93^2X15 lamin to 5X58^1X94 lamin P , 0X05Y and 30% increase in SVR P , 0X02X Similar but more pronounced changes were seen in the hyperthyroid group: 17% reduction in HR, 25% reduction in CO and 46% increase in SVR (all at least P , 0X05). Taking all 15 patients together, thyroid function (as measured by free T 3 index (FT3I) or TSH) correlated signi®cantly to the haemodynamic parameters as follows: the higher the thyroid function the lower the mean arterial pressure and SVR, and the higher the CO and central aortic compliance (stroke volume/pulse pressure) P , 0X05X Plasma norepinephrine increased signi®cantly after treatment of the overt hyperthyroid patients, whereas epinephrine did not change, and no changes were seen among subclinical hyperthyroid patients. Conclusion: Treatment of endogenous subclinical hyperthyroidism resulted in signi®cant changes in several haemodynamic parameters regarding the heart and the vascular system, compatible with some degree of excess tissue exposure to thyroid hormones in the untreated state. Our data favour more aggressive treatment of these patients, and endogenous subclinical hyperthyroidism might be regarded as a mild form of hyperthyroidism.

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Section: Introductionmentioning

confidence: 99%

Haemodynamic changes following treatment of subclinical and overt hyperthyroidism

Faber¹,

Wiinberg

Schifter

et al. 2001

European Journal of Endocrinology

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“…Cortisol has a permissive influence on catecholamine effects, but both hypothyroid and thyrotoxic patients have normal plasma cortisol levels (18,19). Blood volume is increased in thyrotoxicosis and reduced in hypothyroidism (2). The effective circulating volume influences vascular tone and is partly controlled by the activities of the renin±angiotensin±aldosterone system, atrial natriuretic peptide and vasopressin.…”

Section: Introductionmentioning

confidence: 99%

“…Total peripheral vascular resistance (TPR) decreases in thyrotoxicosis and increases in hypothyroidism (1,2). The mechanism involved is incompletely understood, but is probably multifactorial: changes in heat production may contribute, along with changes in Na + /K + fluxes caused by modulation of the inward rectifying potassium channels (3).…”

Section: Introductionmentioning

confidence: 99%

Endocrine factors related to changes in total peripheral vascular resistance after treatment of thyrotoxic and hypothyroid patients

Diekman¹,

Harms²,

Endert

et al. 2001

European Journal of Endocrinology

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Objective: Total peripheral vascular resistance (TPR) decreases in thyrotoxicosis and increases in hypothyroidism. Several mechanisms may be involved, including adaptation to changes in heat production and direct non-genomic effects of tri-iodothyronine (T 3 ) on vascular smooth muscle cells. The aim of this study was to see if changes in TPR are related to changes in plasma concentrations of the endothelial hormones adrenomedullin and endothelin-1 as well as other hormones affecting vasculature. Design: A prospective study. Subjects: Eleven hypothyroid patients (pretreatment: thyroid-stimulating hormone (TSH) 68 (38±201) mU/l, T 3 0.7 (0.35±1.5) nmol/l, fT 4 3.0 (2.0±5.9) pmol/l, median (range)) and 14 with hyperthyroidism (pretreatment: TSH 0.02 (,0.01±0.06) mU/l, T 3 6.4 (2.3±13.0) nmol/l, fT 4 56.1 (22.9±70.0) pmol/l) were studied before treatment and 3 months after reaching the euthyroid state. Blood collection was carried out simultaneously with the recording of finger arterial pressure (FINAP). Cardiac output and TPR were derived from stroke volume computations by modelling flow from the FINAP signal. Results: Thyroid-function tests of hypothyroid and thyrotoxic patients did not differ after restoration of the euthyroid state. TPR, expressed in arbitrary units (AU), decreased after correction of hypothyroidism (from 1X32^0X65 to 0X96^0X36 AU, P 0X04 and increased after correction of hyperthyroidism (from 0X75^0X18 to 1X10^0X35 AU, P 0X007X Adrenomedullin concentrations did not change during the transition from the hypothyroid state 3.2(0.9±11.0) pmol/l to the euthyroid state 4.9(0.9±8.6) pmol/l, but decreased after treatment of hyperthyroidism, from 5.2(0.9±11.0) pmol/l to 2.2(0.9±5.4) pmol/l. Plasma endothelin-1 was undetectable in all samples. Changes in TPR upon treatment correlated with log DfT 4 r 20X65Y P 0X001Y log DT 3 Y r 20X57Y P 0X006Y D noradrenaline r 0X54Y P 0X02 and D ANP (atrial natriuretic peptide) r 20X59Y P 0X004X Multiple linear regression analysis indicated that only T 3 was an independent determinant of TPR. Changes in T 3 accounted for 46% of the variability in the changes in TPR. Conclusions: TPR is reduced in thyrotoxicosis and increased in hypothyroidism. Restoration of the euthyroid state normalizes TPR. Changes in TPR are not related to plasma adrenomedullin concentrations, but 46% could be explained by changes in T 3 . Altered ANP secretion and adenergic tone may contribute to the T 3 -induced changes in TPR.

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“…This effect results in a systemic vascular resistance reduction by a 50-60%. A selective increase in blood flow to certain organs such as skeletal muscles and heart, and a decrease in diastolic blood pressure with widening of the pulse pressure (9) . Lack of increase in renal blood flow cause renal perfusion pressure reduction and renin-angiotensin system activation, which cause increase inblood volume and sodium reabsorption (10) .…”

Section: Discussionmentioning

confidence: 99%

Graves Disease Induced Dilated Cardiomyopathy

Al‐Sadawi¹

2016

jmscr

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Determination of Cardiac Output and Other Hemodynamic Data in Patients with Hyper- and Hypothyroidism, Using Dye Dilution Technique

Cited by 45 publications

References 23 publications

Haemodynamic changes following treatment of subclinical and overt hyperthyroidism

Haemodynamic changes following treatment of subclinical and overt hyperthyroidism

Endocrine factors related to changes in total peripheral vascular resistance after treatment of thyrotoxic and hypothyroid patients

Graves Disease Induced Dilated Cardiomyopathy

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