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Received his master degree in 1994 at Shanghai Second Medical University;

Shu Wang, MD, PhD The archiater of Department of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, China. Doctoral supervisor. Received his master degree in 1994 at Shanghai Second Medical University;

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Received his master degree in 1994 at Shanghai Second Medical University;

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  1. Shu Wang, MD, PhD The archiater of Department of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, China. Doctoral supervisor. • Received his master degree in 1994 at Shanghai Second Medical University; • Took his doctor’s degree on Endocrinology at shanghai Jiaotong University school of medicine in 2007; • From the year 2001 to 2003, He took an advanced study in Baylor College of Medicine , America. • Headman, Endocrinology and Metabolism section, Institute of Health Sciences, Shanghai Institutes for Biological Sciences since 2004. • Chief of office, Thyroid disease education project team, Ministry of Health, China since 2009; • Youth member, Endocrinology society of Chinese Medical Association in 2009. • Committee member of Chinese thyroid Association in 2010.

  2. The Cardiovascular System in Thyrotoxicosis Dept. of Endocrinology and Metabolism, Ruijin Hospital, Shanghai Jiaotong University, School of Medicine Shanghai, China Dr. Shu Wang shuw@sibs.ac.cn

  3. Thyrotoxicosishas important clinical consequencesfor the cardiovascular systems. Thyrotoxicosis can increasecardiovascular morbidity and mortality. The cause of cardiovascular signs and symptoms by thyrotoxicosis can easily be neglected. • Thyrotoxicosis is the clinical syndrome of hyperthyroidism resulting from excessive quantities of the thyroid hormones. keep “Thyrotoxicosis” in mind!

  4. Case 1 • A 63-year-old female patient • Chest distress ,palpitation behind fatigue, sweating,weight loss of 1 year • Oral glyceryl trinitrate provided no relief • PE: heart rate:120 beats per minute; arrhythmia • ECG: atrial fibrillation; ST-Tchange • Diagnosis:coronary heart disease;atrial fibrillation Is it an accurate diagnosis ?

  5. The causes of atrial fibrillation ★Thyrotoxicosis Heart Alcohol Drugs Electric shock Surgery ...... Atrial Fibrillation Neurogenic AF Pulmonary disease Infections

  6. Atrial fibrillation Angina pectoris FT3>46.08pmol/L FT4 67.5pmol/L TSH＜0.0025μU/L TRAb>40IU/L TGAb 14.51IU/L TPOAb 737.14 Sweating Weight loss heart rate increased Thyroid funtion ? thyrotoxicosis induced cardiovascular dysfunction

  7. Thyrotoxicosis induced cardiovascular dysfunction • The morbidity of thyrotoxicosis induced cardiovascular dysfunction is about 5％～10％. • Graves disease is the most common cause of thyrotoxicosis accounting for 60% to 90% of cases. • Clinical classification: • 1) Hyperthyoidism asan initial cause; • 2) Hyperthyoidism as a worsenfactor when patient has underlying cardiac disease.

  8. The patient presents Clinical manifestation Thyrotoxicosis induced cardiovascular dysfunction Hypermetabolismsyndrome: Weight loss with increased appetite Warm and sweating Coarse tremor in extremities,etc. Sweating Weight loss Cardiac symptoms in an early stage： Palptations, Exercise intolerance, Dyspnea on exertion, Tachycardia,etc. Palpitations chest distress Heart complication： Atrial fibrillation,Cardiomyopathy, Heart failure, Angina pectoris and Myocardial infarction. Atrial fibrillation Angina pectoris

  9. Thyrotoxicosis induced cardiovascular dysfunction Rarely，young patients with thyrotoxicosis may have chest pain similar in almost all respects to angina pectoris. Chinese scholars’ consensus NYHA (New York Heart Association) Along with hyperthyroidism，One having at least one item of heart abnormality can diagnosed hyperthyroidism heart disease： ①enlarged heart；②Arrhythmias；③congestive heart failure；④Angina pectoris and myocardial infarction； Meanwhile，another factors changing heart functions should be excluded ① AtrialArrhythmias, enlarged heartor ventricular failure ②Clinical manifestations and biochemical proof of Hyperthyroidism ③After specific treatment，the above-mentioned can disappear Diagnostic criteria ?

  10. Thyrotoxicosis induced cardiovascular dysfunction What type of thyrotoxicosis induced cardiovascular diseases is the patient？ Types:Arrhythmia type Heart failure type Cardiomyopathy type

  11. Arrhythmia Type Atrial fibrillation is the most common arrhythmia. The incidence is about 10%~20%hyperthyroidism patients. Heart failure Type Present in 6% of cases.It can be divided into high output failure and pump failure. Risk factors: Age＞60,long term uncontrolled hyperthyroidism,underlying heart disease and AF . Cardiomyopathy Type: (rare) Rate-related cardiomyopathy: Tachycardiainduced cardiomyopathy can cause heart failure, although LVEF usually normalizes after heart rate or rhythm control. Dilated cardiomyopathy: Associated with Graves disease might have an auto-immune origin. Thyrotoxicosis induced cardiovascular dysfunction

  12. Arch Intern Med. 2004;164:1675-1678 In patients with hyperthyroidism ：Morbidity of AF is 8.3% Male sex, increasing age, ischemic heart disease, congestive heart failure, and heart valve disease are associated with an increased risk of AF

  13. Thyrotoxicosis induced cardiovascular dysfunction Mechanisms ★The heart is main target organ of Thyroid Hormone. T3 influence cardiac action by three different routes: • T3exerts a direct effect on cardiac myocytes; 2) T3 may influence the sensitivity of the sympathetic system; 3) T3 leads to periphery hemodynamic changes.

  14. T3 effects on the cardiac myocyte Genomic nuclear effects: T3 binds to nuclear thyroid hormone receptors (TRs), combined with recruited cofactors.The complex then bind or release specific sequences of DNA , modifying the rate of transcription of specific cardiac genes. Non-genomic effects: T3 direct modulate the transport of ions (calcium, sodium andpotassium) across the plasma membrane, glucose and amino acid transport,mitochondrial function and various intracellular signalling pathways.

  15. Regulated cardiac gene as reported

  16. Interactions between THs and the sympathetic system Some T3 effects are mediated by an increased activity of the sympathetic system or an increased responsiveness and sensitivity of cardiac tissue to normal sympathomimetic stimuli. The enhanced sympathetic sensitivity of the hyperthyroid heart may be mediated by an increased number of β-adrenergic receptors.

  17. Haemodynamic changes

  18. membrane ion channels vascular relaxation SVR decreases vascular smooth muscle cells nongenomic NO T3 paracrine manner endothelial cell NO genomic T3 relaxs vascular smooth muscle cells though regulation of nitric oxide ( NO), and decreases peripheral resistance.

  19. only 50% of hyperthyroidism patients with congestive heart failure have impaired left ventricular(LV) systolic function . LVdiastolic dysfunctionmay involve in theremaining half.

  20. Thyrotoxicosis induced cardiovascular dysfunction The patient has been confirmed，and how to treat it ？

  21. Thyrotoxicosis induced cardiovascular dysfunction Management and Treatment • Principle: • ①Recover the thyroid function as soon as possible.To rapidly reduce the actions of thyroidhormone,ATDs and Radioiodine isrecommended; ②Acute treatment of cardiaccomplications； • Most patients who get immediate controlof hyperthyroidism，can self-recover cardiac disorders gradually.

  22. Therapy of atrial fibrillation • Control the thyroid function • About 50% AF in young and new onsetscanconvert to sinus rhythm after keeping euthyroid for 6~12 months. • Those AF consisting for more than 4 months after euthyroid，Drugs and Electroversion can be considered. • Anticoagulative therapy isrecommended in the absence of a specific contraindication, at least until a euthyroid state has been restoredand heart failure has been cured.(ACC/AHA)

  23. Thyrotoxicosis induced cardiovascular dysfunction Therapy of heart failure • Control the thyroid function; (The treatment of HF follows its conventional therapy.） • Expectant treatment: Sedation, oxygenuptaking, sodium limiting，etc. • β-blokers is used to stable the heart rate • Digitalis and Diuretic can effectively relieve heart burden and pulmonary congestion symptoms. However it is hard to restore totally. • Dosage of Digitalis is greater than usual loading and maintenance dosage maybe needed.

  24. what about thyroid function? laboratory analysis:FT3：20.08pmol/LFT4：44.5pmol/LTSH：0.083U/L • A 60-year-old male patient • Palpitations, fatigue, weakness, weight loss of 1 month's duration • The patient had been taking amiodarone for 2.5 years for non-sustained ventricular tachycardia episodes. amiodarone had been discontinued for six months • PE: heart rate:98 beats per minute Case 2 Is it Amiodarone-Induced Thyrotoxicosis?

  25. Amiodarone-Induced Thyrotoxicosis(AIT) • The incidence of AIT reported in different studies varies but remains within the range of 5–10% in most studies. • AIT may develop suddenly and early or after many years of treatment, the usual time period is 2–47 months; • AIT may also develop many months after drug withdrawal. • Iodine deficient individuals render more sensitive to exogenous iodine • Risk factors：female sex, complex cyanotic heart disease, previous Fontan type surgery, and a total daily dose above 200 mg

  26. Why does Amiodarone can Induce Thyrotoxicosis?

  27. Types ★ Some patients exhibit a mixed pattern

  28. The decision to stop amiodarone in the setting of thyrotoxicosis should be determined on an individual basis in consultation with a cardiologist, based on the presence or absence of effective alternative antiarrhythmic therapy. Is it need for amiodarone discontinuation?

  29. The need for amiodarone discontinuation is controversial, because : (1) This drug is frequently the only medication able to control cardiac arrhythmia, (2) The effects of this fat soluble drug may persist for many months. (3) Amiodarone may have T3-antagonistic properties and inhibit T4 to T3 conversion, withdrawal Amiodarone may aggravate cardiac manifestations of thyrotoxicosis. (4) AIT typically resolves even if amiodarone therapy is continued.

  30. Conclusion: a: Euthyroidism was reached despite continuation of amiodarone in all patients. b: Prednisone remains the preferred treatment of AIT type 2.

  31. Thyrotoxicosis and Pregnancy • Effects On Cardiovascular hemodynamics are additive • Mother: spontaneous abortion, hyperthyroidism crisis, heart failure, preeclampsia, premature delivery, etc; • Fetus:stillbirth, Growth restriction, goiter, heart failure, etc; • It is more urgent to control thyroid function and monitor heart function.

  32. Use β-blocker Cautiously in pregnancy • There is no evidence of teratogenesis following maternal exposure to beta-blockers in the first trimester. • The risk of IUGR associated with maternal use of beta- blockers exists， use the smallest effective dose (avoiding large doses) and useis limited to the third trimester. • There is also a theoretical risk of neonatal bradycardia, hypotension and hypoglycaemia if beta-blockers are used up to the time of delivery.

  33. Take Home Message • In clinics, the patient's history and thyroid function tests are important. (monitor) • The first step for treating heart complications is hyperthyroidism control. (treatment) • It is important to take risk factors into account, such as age, sex, hyperthyroidism type, underlying health problems. (prevention)

  34. Thank you!

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