Hyperthyroidism as a high cardiac output state

deGroot, William J.; Leonard, James J.

doi:10.1016/0002-8703(70)90318-2

Cited by 101 publications

(38 citation statements)

References 42 publications

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“…However, the clinical manifestations and degree of HF in hyperthyroid patients depend on a variety of factors, namely the patient's age, the cause and severity of hyperthyroidism and the underlying cardiac conditions. Many groups have assessed the association of overt hyperthyroidism with HF (47,48,49,50,51,52,53).…”

Section: Hf In Hyperthyroidismmentioning

confidence: 99%

“…Patients with severe hyperthyroidism may develop a 'high-output HF' (47). However, HF is not really the appropriate term because cardiac output is increased, although congestive circulation is present (47).…”

Section: Hf In Hyperthyroidismmentioning

confidence: 99%

“…However, HF is not really the appropriate term because cardiac output is increased, although congestive circulation is present (47). The development of high-output HF in thyrotoxicosis may be due to 'tachycardiac-mediated cardiomyopathy' (54).…”

Section: Hf In Hyperthyroidismmentioning

confidence: 99%

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MECHANISMS IN ENDOCRINOLOGY: Heart failure and thyroid dysfunction

Biondi

2012

European Journal of Endocrinology

248

187

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Context: Heart failure (HF) is a major cause of morbidity and mortality in Europe and in the United States. The aim of this review article was to assess the results of the prospective studies that evaluated the risk of HF in patients with overt and subclinical thyroid disease and discuss the mechanism of this dysfunction. Evidence Acquisition: Reports published with the following search terms were searched:, thyroid, hypothyroidism, hyperthyroidism, subclinical hyperthyroidism, subclinical hypothyroidism, levothyroxine, triiodothyronine, antithyroid drugs, radioiodine, deiodinases, clinical symptoms, heart rate, HF, systolic function, diastolic function, systemic vascular resistance, endothelial function, amiodarone and atrial fibrillation. The investigation was restricted to reports published in English. Evidence Synthesis: The outcome of this analysis suggests that patients with untreated overt thyroid dysfunction are at increased risk of HF. Moreover, persistent subclinical thyroid dysfunction is associated with the development of HF in patients with serum TSH !0.1 or O10 mU/l. Conclusions: The timely recognition and effective treatment of cardiac symptoms in patients with thyroid dysfunction is mandatory because the prognosis of HF may be improved with the appropriate treatment of thyroid dysfunction.

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Section: Hf In Hyperthyroidismmentioning

confidence: 99%

Section: Hf In Hyperthyroidismmentioning

confidence: 99%

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MECHANISMS IN ENDOCRINOLOGY: Heart failure and thyroid dysfunction

Biondi

2012

European Journal of Endocrinology

248

187

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“…Hyperthyroidism is associated with hemodynamic changes including high output state, increased heart rate and cardiac contractility, and decreased peripheral resistance (1,2), that are related both to direct cardiostimulatory effects of thyroid hormone and to increased peripheral oxygen consumption (3,4). While cardiac parameters are invariably increased, as assessed by the shortening of systolic and diastolic time-intervals, the increase of systolic and diastolic function and the reduction in the left ventricular ejection fraction (3)(4)(5)(6), regional blood flow distribution is not uniform in hyperthyroidism.…”

Section: Introductionmentioning

confidence: 99%

Thyroid vascularity and blood flow are not dependent on serum thyroid hormone levels: studies in vivo by color flow doppler sonography

Bogazzi

Bartalena

Brogioni

et al. 1999

European Journal of Endocrinology

125

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Objective: Thyroid blood flow is greatly enhanced in untreated Graves' disease, but it is not known whether it is due to thyroid hormone excess or to thyroid hyperstimulation by TSH-receptor antibody. To address this issue in vivo patients with different thyroid disorders were submitted to color flow doppler sonography (CFDS). Subjects and methods:We investigated 24 normal subjects, and 78 patients with untreated hyperthyroidism (49 with Graves' hyperthyroidism, 24 with toxic adenoma, and 5 patients with TSH-secreting pituitary adenoma (TSHoma)), 19 patients with thyrotoxicosis (7 with thyrotoxicosis factitia, and 12 with subacute thyroiditis), 37 euthyroid patients with goitrous Hashimoto's thyroiditis, and 21 untreated hypothyroid patients with Hashimoto's thyroiditis. Results: Normal subjects had CFDS pattern 0 (absent or minimal intraparenchimal spots) and mean intraparenchimal peak systolic velocity (PSV) of 4.8 Ϯ 1.2 cm/s. Patients with spontaneous hyperthyroidism due to Graves' disease, TSHoma, and toxic adenoma had significantly increased PSV (P < 0.0001, P = 0.0004, P < 0.0001 respectively vs controls) and CFDS pattern. Patients with Graves' disease had CFDS pattern II (mild increase of color flow doppler signal) in 10 (20%) and pattern III (marked increase) in 39 cases (80%). Mean PSV was 15 Ϯ 3 cm/s. Patients with toxic adenoma had CFDS pattern I (presence of parenchymal blood flow with patchy uneven distribution) in 2 (8%), pattern II in 16 (70%) and pattern III in 5 (22%). Mean PSV was 11 Ϯ 2.4 cm/s. Patients with TSHoma showed CFDS pattern I in one case (20%) and pattern II in 4 (80%). Mean PSV was 14.8 Ϯ 4.2 cm/s. Patients with thyrotoxicosis had normal PSV (4.2 Ϯ 1.1 cm/s in subacute thyroiditis, 4 Ϯ 0.8 cm/s in thyrotoxicosis factitia, P = not significant vs controls) and CFDS pattern 0. Untreated euthyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern 0, and mean PSV (4.3 Ϯ 0.9 cm/s; P = not significant vs controls). Untreated hypothyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern I in 14 cases (67%), pattern II in 4 (19%) and pattern 0 in 3 (14%) and mean PSV (5.6 Ϯ 1.4 cm/s) was higher than that of controls (P = 0.026). Conclusions: An increase in both intrathyroidal vascularity and blood velocity was observed in patients with spontaneous hyperthyroidism but not in thyrotoxicosis due to either ingestion of thyroid hormones or to a thyroidal destructive process. The slightly increased vascularity and blood velocity observed in patients with hypothyroid Hashimoto's thyroiditis suggests that thyroid stimulation by either TSH-receptor antibody or TSH is responsible for the increased thyroid blood flow.

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“…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) . The most common presentation of thyrotoxic cardiomyopathy are palpitations, irregular heartbeats, dyspnea, and chest pain.…”

Section: Discussionmentioning

confidence: 99%

Graves Disease Induced Dilated Cardiomyopathy

Al‐Sadawi¹

2016

jmscr

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Hyperthyroidism as a high cardiac output state

Cited by 101 publications

References 42 publications

MECHANISMS IN ENDOCRINOLOGY: Heart failure and thyroid dysfunction

MECHANISMS IN ENDOCRINOLOGY: Heart failure and thyroid dysfunction

Thyroid vascularity and blood flow are not dependent on serum thyroid hormone levels: studies in vivo by color flow doppler sonography

Graves Disease Induced Dilated Cardiomyopathy

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