Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

SGLT2 Inhibitors in Hypertrophic Cardiomyopathy: Emerging Evidence and Putative Mechanisms.

Biomolecules·2026
Same author

Natural history of thyroid function in ageing: an individual participant data analysis of 137 488 participants from 31 prospective cohort studies.

The lancet. Diabetes & endocrinology·2026
Same author

Multidisciplinary Delphi Consensus on management of children with moderate-severe atopic dermatitis.

Italian journal of pediatrics·2026
Same author

Cardiovascular Risk Determinants in Euthyroid Patients with Obesity: The Strange Case of TSH in Primary Prevention.

Journal of clinical medicine·2026
Same author

The use of detergents, moisturizers and the experience with therapeutic education among Italian pediatric patients with atopic dermatitis.

Italian journal of pediatrics·2026
Same author

Contemporary management of patients with native mitral regurgitation in heart valve centres.

Archives of cardiovascular diseases·2025

Related Experiment Videos

Association between increased mortality and mild thyroid dysfunction in cardiac patients.

Giorgio Iervasi1, Sabrina Molinaro, Patrizia Landi

  • 1Clinical Physiology Institute, National Council of Research, Via Moruzzi 1, 56124 Pisa, Italy. iervasi@ifc.cnr.it

Archives of Internal Medicine
|July 25, 2007
PubMed
Summary

Mild thyroid dysfunction, including subclinical hypothyroidism and subclinical hyperthyroidism, significantly increases mortality risk in cardiac patients. Early detection and management are crucial for improving outcomes in this vulnerable population.

Related Experiment Videos

Area of Science:

  • Cardiology
  • Endocrinology
  • Thyroid Research

Background:

  • Subclinical thyroid dysfunction's impact on cardiac outcomes remains unclear.
  • Cardiac patients are a high-risk group for adverse health events.

Purpose of the Study:

  • To investigate the association between mild thyroid dysfunction and mortality in cardiac patients.
  • To compare mortality rates across different thyroid status groups.

Main Methods:

  • A cohort of 3121 cardiac patients was analyzed.
  • Patients were categorized into euthyroidism, subclinical hypothyroidism (SCH), subclinical hyperthyroidism (SCT), and low triiodothyronine (low T3) groups.
  • Cardiac and overall mortality were tracked over a mean follow-up of 32 months.

Main Results:

  • SCH, SCT, and low T3 groups exhibited lower survival rates for cardiac death compared to euthyroid individuals.
  • SCH and low T3 groups showed significantly lower survival rates for overall death.
  • Adjusted analyses revealed increased hazard ratios for cardiac death in SCH, SCT, and low T3, and for overall death in SCH and low T3.

Conclusions:

  • Mildly altered thyroid status is linked to elevated mortality risk in cardiac disease patients.
  • Subclinical thyroid dysfunction warrants attention in cardiac patient management.