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Presenter :
DR. A.B.M. KAMRUL HASAN
MD Final Part (EM)
Bangabandhu Sheikh Mujib Medical University
Irwin Klein, MD; Sara Danzi, PhD
Circulation. 2007;116:1725-1735
doi: 0.1161/CIRCULATIONAHA.106.678326
Cellular mechanisms of thyroid hormone action
Effects of thyroid hormone on cardiovascular
hemodynamics
Clinical manifestations of thyroid diseases from a
cardiovascular perspective
Changes in thyroid hormone metabolism that arise
from acute MI and chronic congestive heart failure
 Classic “feedback” loop mechanism: T4 & T3 regulate
pituitary synthesis and release of TSH
 A highly sensitive TSH assay- initial test
 Suggestion about narrowing TSH reference range
especially upper limit at which hypothyroidism may be
present
 TSH>20 mIU/L: overt hypothyroidism
 TSH 3-20 mIU/L: milder or subclinical hypothyroidism
 Suppressed TSH <0.1 mIU/L: hyperthyroidism
Diagnosis ICD-9 Code
Anemia 285.9
Atrial fibrillation 427.31
Hypertension 401.0
Hypercholesterolemia 272.0
Mixed hyperlipidemia 272.4
Diabetes mellitus 250.00
Obesity 278.00
Weight gain 783.1
Weight loss 783.21
Myopathy 359.9
 Thyroid gland secrets mainly (≈85%) T4 which is converted to T3 by
5´-monodeiodinase in various tissues
 No significant myocyte intracellular deiodinase activity- the heart
relies mainly on serum T3
 T3 binds to thyroid hormone nuclear receptors (TRs), belongs to
superfamily of steroid hormone receptors
 TRs bind to thyroid hormone response elements (TREs) in the
promoter region of positively regulated genes → mediate induction
of transcription
 TRs bind to TREs in the absence as well as in the presence of
ligand
 While bound to T3, TRs induce transcription, and in the
absence of T3 they repress the transcription
 Occur rapidly, do not involve TRE-mediated transcriptional
events
 Changes in various membrane ion channels for Na, K & Ca
 Effects on:
 Actin polymerization
 Adenine nucleotide translocator 1 in mitochondrial
membrane
 Variety of intracellular signaling pathways in heart &
vascular smooth muscle
Positively Regulated Negatively Regulated
α-Myosin heavy chain β-Myosin heavy chain
Sarcoplasmic reticulum Ca2+-ATPase Phospholamban
Na+ / K+ -ATPase Adenylyl cyclase catalytic
subunit
β1- Adrenergic receptor Thyroid hormone receptor α1
Atrial natriuretic hormone Na+ / Ca2+ exchanger
Voltage-gated potassium channels
(Kv1.5, Kv4.2, Kv4.3)
 Expression of both structural & regulatory genes in cardiac
myocyte
 ↑ T3 → cardiac hypertrophy, mainly due to ↑ hemodynamic load
 Hyperthyroidism resembles hyperadrenergic state: no evidence to
suggest ↑TH enhance cardiac sensitivity to adrenergic stimulation
 Serum catecholamines low or normal
 Several components of cardiac myocyte β adrenergic system are
regulated by thyroid hormones:
 β1 adrenergic receptors are positively regulated
 Guanine nucleotide regulatory proteins
 Adenylate cyclase
 TRα1 receptors are negatively regulated
 Pacemaker-related genes, hyperpolarization-activated cyclic
nucleotide-gated channels 2 & 4 are transcriptionally regulated by
thyroid hormones
 β-adrenergic receptor stimulation → ↑cAMP → accelerates
diastolic depolarization → ↑ HR
 Hyperthyroidism → AF; may be due to combination of genomic &
nongenomic actions on atrial ion channels plus atrial enlargement
 β-adrenergic blockade: ↓HR, enhanced diastolic performance is
not altered (indicating that T3 acts directly on the heart to increase
calcium cycling)
 BP is altered across the entire spectrum of thyroid function
 Changes are similar to physiological response to exercise
 Hyperthyroidism:
 Widened pulse pressure
 Increased arterial stiffness
 Low SVR →Isolated Systolic HTN
 Hypothyroidism:
 Endothelial dysfunction
 Impaired VSM relaxation → ↑SVR → Diastolic HTN
 High prevalence of Pulmonary HTN & AV valve regurgitation in
hyperthyroidism
 Effect of TH to ↓SVR may not occur in pulmonary vasculature
 Primary pulmonary HTN (Pulmonary Artery Pressure >25 mmHg at
rest & >30 mmHg during exercise):
• Often unknown origin
• A link to thyroid disease (both hyper- & hypothyroidism) has
been identified
• Thyroid disease should be considered in DD of Primary
pulmonary HTN
↓ Fractional
clearance of LDL
by liver:
• ↓ No. of LDL
receptors
• ↓ LDL receptor
activity
↓ Catabolism of
cholesterol into
bile
• T3 negatively
regulates liver
specific enzyme
cholesterol 7α-
hydroxylase
Overt
Hypothyroidism:
• Hypercholesterolemia
• Marked ↑ LDL &
Apolipoprotein B
• Changes are also
evident in subclinical
hypothyroidism
90% of hypothyroid patients had hypercholesterolemia
Prevalence of overt hypothyroidism in patients with hypercholesterolemia
is 1.3-2.8%
Palpitations Anginal chest pain
Exercise intolerance Atrial fibrillation
Exertional dyspnea Cardiac hypertrophy
Systolic hypertension Peripheral edema
Hyperdynamic circulation Congestive heart failure
Cardiac output increased by 50-300% of normal: combined effect of
increased resting HR, contractility, blood volume & EF with a decrease in
SVR
Cerebrovascular ischemic symptoms has been reported in young patients
with Graves’ disease
Routine TSH in cardiac & cerebral ischemic symptoms
 Prevalence: 2-20%, ↑ with age (≈15% in patients >70 yrs)
 40,628 patients in the Danish National Registry:
• 8.3% developed AF
• Male gender, ischemic or valvular heart disease or CHF
increased risk
 Subclinical hyperthyroidism carry same relative risk
 In unselected patients who present with AF, <1% were the result
of overt hyperthyroidism
 Ability to restore thyrotoxic patients to a euthyroid state & sinus
rhythm justifies TSH testing in new onset AF
 β-adrenergic blockade: by β1-selective or nonselective agent
 Rapid restoration of chemical euthyroid state: ATD or
Radioiodine
 Digitalis:
• ↑rate of digitalis clearance, ↓sensitivity of hyperthyroid heart
• Needs higher dose with less predictable response
 Calcium channel blockers: sp. parenteral, should be avoided
• Through effects on the smooth muscle cells of the resistance
arterioles, may lead to acute hypotension & CV collapse
 Risk for systemic embolization is not precisely known
 Advancing AGE rather than presence of AF was major risk factor
 Review of large series of patients failed to demonstrate a
prevalence of thromboembolic events greater than the risk
reported for major bleeding events from warfarin therapy
 In younger patients with hyperthyroidism, in absence of other
independent risk factors for embolization, the benefits of
anticoagulation may be outweighed by the risk
 Aspirin reduces risk for embolic events and safe alternative
 Majority revert to sinus rhythm within 2-3 months of successful
treatment with ATD or RI
 Older (>60 yrs) with AF of longer duration less likely to revert
• If AF persists after chemical euthyroidism is achieved,
electrical or pharmacological cardioversion should be
attempted
• Majority can be restored to sinus rhythm & will remain so for a
prolonged period of time
• Addition of Disopyramide (300mg/d) lets such patents to
maintain sinus rhythm
 Paradoxical finding- ?high-output failure, does not accurately apply
 Exaggerated sinus tachycardia or AF can produce LV dysfunction
& HF
 Preexistent ischemic or hypertensive heart disease
 Mitral valve prolapse: increased incidence, causing LA
enlargement & AF
 High prevalence of pulmonary artery HTN: some similar signs
 Exercise intolerance & Exertional dyspnea: may be due to
↓pulmonary compliance or ↓respiratory & skeletal muscle function
 Common CV signs & symptoms are:
Bradycardia
Mild hypertension (diastolic)
Narrowed pulse pressure
Cold intolerance
Fatigue
 ↓Expression of Sarcoplasmic reticulum Ca2+-ATPase
 ↑Expression of Phospholamban (inhibitor of SR Ca2+-ATPase)
 Slowing of the isovolumic relaxation phase of diastolic function
Effect
• Impaired cardiac contractility & diastolic function
• Increased systemic vascular resistance
• Decreased endothelial derived relaxation factor
• Increased serum cholesterol
• Increased C-reactive protein
• Increased homocysteine
Diastolic HTN
• Accelerated atherosclerosis
• Increased risk of CAD
• Increased risk of stroke
RESULTS
IN
• Prolongation of QT interval → Ventricular arrhythmias
• Protein rich pericardial and/or pleural effusion
 Poses some challenge
 In young healthy patients: full replacement dose of L-thyroxine of
1.6 µg/kg/d can be initiated at the outset
 In older patients: start low (25 to 50 µg/d) and go slow (increase
the dose no more rapidly than every 6 to 8 weeks)
 A predictable improvement in thyroid and CV functional measures
 Concerns that restoration of the heart to a euthyroid state might
adversely affect underlying ischemic heart disease are largely
unfounded
 Patients with atherosclerotic cardiovascular disease more often
improve, rather than worsen, with treatment
 Low or undetectable serum TSH with normal T4 & T3
 May have no clinical signs or symptoms
 Prevalence increase with age
 Low TSH is associated with increased risk for CV mortality & AF
 Treatment is controversial
 Older patients with MNG or GD: should be treated especially if
they are deemed to be at risk for cardiovascular disease
 Affects 7-10% of older women
 Frequently asymptomatic but many have symptoms of hypo
 ↑Cholesterol & CRP
 Risk of atherosclerosis, CAD & MI increased
 The benefits of the restoration of TSH levels to normal can be
considered to outweigh the risks
 The low T3 syndrome: a fall in serum T3 accompanied by
normal serum T4 and TSH levels
 Results from impaired hepatic conversion of T4 to the biologically
active hormone, T3, by 5´-monodeiodinase
 The cardiac myocyte has no appreciable deiodinase activity and
therefore relies on the plasma as the source of T3
 In experimental animals the low T3 syndrome leads to the same
changes in cardiac function and gene expression as does
primary hypothyroidism.
 Significant similarities exist between the hypothyroid phenotype
and the HF phenotype (↓cardiac contractility & cardiac output, &
an altered gene expression profile)
 ≈30% of patients with CHF have low T3 levels
 Reduction of T3 is proportional to the severity of HF
 Reduced serum T3 is a strong predictor of all-cause and CV
mortality and, in fact, is a stronger predictor than age, LV EF, or
dyslipidemia
 It has been suggested that T3 therapy might improve cardiac
function in this clinical situation
 Antiarrhythmic drug with a high iodine content (75mg iodine/200mg)
 Can cause either hypothyroidism (5% to 25% of treated patients) or
hyperthyroidism (2% to 10% of treated patients)
 Inhibits of 5´-deiodinase activity → Inhibits conversion of T4 to T3
 Iodine released from amiodarone metabolism directly inhibit thyroid
gland function, if the effect persists, lead to amiodarone-induced
hypothyroidism
 Preexistent thyroid disease and Hashimoto’s thyroiditis ↑ risk
 If hypothyroidism develop with a persistent rise in TSH: L-thyroxine
therapy started
 Type 1 hyperthyroidism:
• iodine-induced excess thyroid hormone synthesis
• underlying thyroid disorder, e.g., nodular goiter or latent GD
• in regions where iodine intake is low
 Type 2 hyperthyroidism:
• thyroiditis due to a direct cytotoxic effect of amiodarone →↑release of
thyroid hormones → transient thyrotoxicosis in a previously normal
thyroid gland
 Can overlap & difficult to distinguish, RIU is low in both types
 Point favors Type 2 hyperthyroidism: Signs of inflammation, elevated ESR
& IL-6, modest increases in thyroid gland size
 ATDs effective in type 1, ineffective in type 2 thyrotoxicosis.
 Prednisolone is beneficial in the type 2 form
 Beta blocker should be started
 A pragmatic approach is to commence combination therapy with an
ATD and glucocorticoid in patients with significant thyrotoxicosis
 A rapid response (within 1–2 weeks) usually indicates a type 2 picture
and permits withdrawal of the antithyroid therapy
 A slower response suggests a type 1 picture, when antithyroid drugs
may be continued and prednisolone withdrawn.
 Potassium perchlorate can be used to inhibit iodine trapping in thyroid
 If the cardiac state allows, amiodarone should be discontinued
 The course of the disease may last for anywhere between 1 to 3
months
 In rare cases, surgical thyroidectomy under local anesthesia has
proven to be effective
 To minimize the risk of type 1 thyrotoxicosis, thyroid function should
be measured in all patients prior to commencement of amiodarone
therapy, and amiodarone should be avoided if TSH is suppressed
 In general, patients treated with amiodarone should have thyroid
function (specifically TSH) testing periodically throughout therapy
 Thyroid dysfunction (both hypo & hyper) virtually affects the
whole spectrum of cardiovascular hemodynamics
 Thyroid functional abnormality can case a range of
cardiovascular signs-symptoms and cardiovascular
diseases are also associated with derangement of thyroid
functions
 Restoration of normal thyroid function most often reverses
the abnormal cardiovascular hemodynamics
 Prof. Md. Farid Uddin
Chairman, Department of Endocrinology, BSMMU
 Prof. M.A. Hasanat
Department of Endocrinology, BSMMU
 All the colleagues of my department
Thyroid diseade and the Heart

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Thyroid diseade and the Heart

  • 1. Presenter : DR. A.B.M. KAMRUL HASAN MD Final Part (EM) Bangabandhu Sheikh Mujib Medical University
  • 2. Irwin Klein, MD; Sara Danzi, PhD Circulation. 2007;116:1725-1735 doi: 0.1161/CIRCULATIONAHA.106.678326
  • 3. Cellular mechanisms of thyroid hormone action Effects of thyroid hormone on cardiovascular hemodynamics Clinical manifestations of thyroid diseases from a cardiovascular perspective Changes in thyroid hormone metabolism that arise from acute MI and chronic congestive heart failure
  • 4.  Classic “feedback” loop mechanism: T4 & T3 regulate pituitary synthesis and release of TSH  A highly sensitive TSH assay- initial test  Suggestion about narrowing TSH reference range especially upper limit at which hypothyroidism may be present  TSH>20 mIU/L: overt hypothyroidism  TSH 3-20 mIU/L: milder or subclinical hypothyroidism  Suppressed TSH <0.1 mIU/L: hyperthyroidism
  • 5. Diagnosis ICD-9 Code Anemia 285.9 Atrial fibrillation 427.31 Hypertension 401.0 Hypercholesterolemia 272.0 Mixed hyperlipidemia 272.4 Diabetes mellitus 250.00 Obesity 278.00 Weight gain 783.1 Weight loss 783.21 Myopathy 359.9
  • 6.  Thyroid gland secrets mainly (≈85%) T4 which is converted to T3 by 5´-monodeiodinase in various tissues  No significant myocyte intracellular deiodinase activity- the heart relies mainly on serum T3  T3 binds to thyroid hormone nuclear receptors (TRs), belongs to superfamily of steroid hormone receptors  TRs bind to thyroid hormone response elements (TREs) in the promoter region of positively regulated genes → mediate induction of transcription  TRs bind to TREs in the absence as well as in the presence of ligand  While bound to T3, TRs induce transcription, and in the absence of T3 they repress the transcription
  • 7.  Occur rapidly, do not involve TRE-mediated transcriptional events  Changes in various membrane ion channels for Na, K & Ca  Effects on:  Actin polymerization  Adenine nucleotide translocator 1 in mitochondrial membrane  Variety of intracellular signaling pathways in heart & vascular smooth muscle
  • 8. Positively Regulated Negatively Regulated α-Myosin heavy chain β-Myosin heavy chain Sarcoplasmic reticulum Ca2+-ATPase Phospholamban Na+ / K+ -ATPase Adenylyl cyclase catalytic subunit β1- Adrenergic receptor Thyroid hormone receptor α1 Atrial natriuretic hormone Na+ / Ca2+ exchanger Voltage-gated potassium channels (Kv1.5, Kv4.2, Kv4.3)
  • 9.
  • 10.
  • 11.  Expression of both structural & regulatory genes in cardiac myocyte  ↑ T3 → cardiac hypertrophy, mainly due to ↑ hemodynamic load  Hyperthyroidism resembles hyperadrenergic state: no evidence to suggest ↑TH enhance cardiac sensitivity to adrenergic stimulation  Serum catecholamines low or normal  Several components of cardiac myocyte β adrenergic system are regulated by thyroid hormones:  β1 adrenergic receptors are positively regulated  Guanine nucleotide regulatory proteins  Adenylate cyclase
  • 12.  TRα1 receptors are negatively regulated  Pacemaker-related genes, hyperpolarization-activated cyclic nucleotide-gated channels 2 & 4 are transcriptionally regulated by thyroid hormones  β-adrenergic receptor stimulation → ↑cAMP → accelerates diastolic depolarization → ↑ HR  Hyperthyroidism → AF; may be due to combination of genomic & nongenomic actions on atrial ion channels plus atrial enlargement  β-adrenergic blockade: ↓HR, enhanced diastolic performance is not altered (indicating that T3 acts directly on the heart to increase calcium cycling)
  • 13.  BP is altered across the entire spectrum of thyroid function  Changes are similar to physiological response to exercise  Hyperthyroidism:  Widened pulse pressure  Increased arterial stiffness  Low SVR →Isolated Systolic HTN  Hypothyroidism:  Endothelial dysfunction  Impaired VSM relaxation → ↑SVR → Diastolic HTN
  • 14.  High prevalence of Pulmonary HTN & AV valve regurgitation in hyperthyroidism  Effect of TH to ↓SVR may not occur in pulmonary vasculature  Primary pulmonary HTN (Pulmonary Artery Pressure >25 mmHg at rest & >30 mmHg during exercise): • Often unknown origin • A link to thyroid disease (both hyper- & hypothyroidism) has been identified • Thyroid disease should be considered in DD of Primary pulmonary HTN
  • 15. ↓ Fractional clearance of LDL by liver: • ↓ No. of LDL receptors • ↓ LDL receptor activity ↓ Catabolism of cholesterol into bile • T3 negatively regulates liver specific enzyme cholesterol 7α- hydroxylase Overt Hypothyroidism: • Hypercholesterolemia • Marked ↑ LDL & Apolipoprotein B • Changes are also evident in subclinical hypothyroidism 90% of hypothyroid patients had hypercholesterolemia Prevalence of overt hypothyroidism in patients with hypercholesterolemia is 1.3-2.8%
  • 16. Palpitations Anginal chest pain Exercise intolerance Atrial fibrillation Exertional dyspnea Cardiac hypertrophy Systolic hypertension Peripheral edema Hyperdynamic circulation Congestive heart failure Cardiac output increased by 50-300% of normal: combined effect of increased resting HR, contractility, blood volume & EF with a decrease in SVR Cerebrovascular ischemic symptoms has been reported in young patients with Graves’ disease Routine TSH in cardiac & cerebral ischemic symptoms
  • 17.  Prevalence: 2-20%, ↑ with age (≈15% in patients >70 yrs)  40,628 patients in the Danish National Registry: • 8.3% developed AF • Male gender, ischemic or valvular heart disease or CHF increased risk  Subclinical hyperthyroidism carry same relative risk  In unselected patients who present with AF, <1% were the result of overt hyperthyroidism  Ability to restore thyrotoxic patients to a euthyroid state & sinus rhythm justifies TSH testing in new onset AF
  • 18.  β-adrenergic blockade: by β1-selective or nonselective agent  Rapid restoration of chemical euthyroid state: ATD or Radioiodine  Digitalis: • ↑rate of digitalis clearance, ↓sensitivity of hyperthyroid heart • Needs higher dose with less predictable response  Calcium channel blockers: sp. parenteral, should be avoided • Through effects on the smooth muscle cells of the resistance arterioles, may lead to acute hypotension & CV collapse
  • 19.  Risk for systemic embolization is not precisely known  Advancing AGE rather than presence of AF was major risk factor  Review of large series of patients failed to demonstrate a prevalence of thromboembolic events greater than the risk reported for major bleeding events from warfarin therapy  In younger patients with hyperthyroidism, in absence of other independent risk factors for embolization, the benefits of anticoagulation may be outweighed by the risk  Aspirin reduces risk for embolic events and safe alternative
  • 20.  Majority revert to sinus rhythm within 2-3 months of successful treatment with ATD or RI  Older (>60 yrs) with AF of longer duration less likely to revert • If AF persists after chemical euthyroidism is achieved, electrical or pharmacological cardioversion should be attempted • Majority can be restored to sinus rhythm & will remain so for a prolonged period of time • Addition of Disopyramide (300mg/d) lets such patents to maintain sinus rhythm
  • 21.  Paradoxical finding- ?high-output failure, does not accurately apply  Exaggerated sinus tachycardia or AF can produce LV dysfunction & HF  Preexistent ischemic or hypertensive heart disease  Mitral valve prolapse: increased incidence, causing LA enlargement & AF  High prevalence of pulmonary artery HTN: some similar signs  Exercise intolerance & Exertional dyspnea: may be due to ↓pulmonary compliance or ↓respiratory & skeletal muscle function
  • 22.  Common CV signs & symptoms are: Bradycardia Mild hypertension (diastolic) Narrowed pulse pressure Cold intolerance Fatigue
  • 23.  ↓Expression of Sarcoplasmic reticulum Ca2+-ATPase  ↑Expression of Phospholamban (inhibitor of SR Ca2+-ATPase)  Slowing of the isovolumic relaxation phase of diastolic function
  • 24. Effect • Impaired cardiac contractility & diastolic function • Increased systemic vascular resistance • Decreased endothelial derived relaxation factor • Increased serum cholesterol • Increased C-reactive protein • Increased homocysteine Diastolic HTN • Accelerated atherosclerosis • Increased risk of CAD • Increased risk of stroke RESULTS IN • Prolongation of QT interval → Ventricular arrhythmias • Protein rich pericardial and/or pleural effusion
  • 25.  Poses some challenge  In young healthy patients: full replacement dose of L-thyroxine of 1.6 µg/kg/d can be initiated at the outset  In older patients: start low (25 to 50 µg/d) and go slow (increase the dose no more rapidly than every 6 to 8 weeks)  A predictable improvement in thyroid and CV functional measures  Concerns that restoration of the heart to a euthyroid state might adversely affect underlying ischemic heart disease are largely unfounded  Patients with atherosclerotic cardiovascular disease more often improve, rather than worsen, with treatment
  • 26.  Low or undetectable serum TSH with normal T4 & T3  May have no clinical signs or symptoms  Prevalence increase with age  Low TSH is associated with increased risk for CV mortality & AF  Treatment is controversial  Older patients with MNG or GD: should be treated especially if they are deemed to be at risk for cardiovascular disease
  • 27.  Affects 7-10% of older women  Frequently asymptomatic but many have symptoms of hypo  ↑Cholesterol & CRP  Risk of atherosclerosis, CAD & MI increased  The benefits of the restoration of TSH levels to normal can be considered to outweigh the risks
  • 28.  The low T3 syndrome: a fall in serum T3 accompanied by normal serum T4 and TSH levels  Results from impaired hepatic conversion of T4 to the biologically active hormone, T3, by 5´-monodeiodinase  The cardiac myocyte has no appreciable deiodinase activity and therefore relies on the plasma as the source of T3  In experimental animals the low T3 syndrome leads to the same changes in cardiac function and gene expression as does primary hypothyroidism.  Significant similarities exist between the hypothyroid phenotype and the HF phenotype (↓cardiac contractility & cardiac output, & an altered gene expression profile)
  • 29.  ≈30% of patients with CHF have low T3 levels  Reduction of T3 is proportional to the severity of HF  Reduced serum T3 is a strong predictor of all-cause and CV mortality and, in fact, is a stronger predictor than age, LV EF, or dyslipidemia  It has been suggested that T3 therapy might improve cardiac function in this clinical situation
  • 30.  Antiarrhythmic drug with a high iodine content (75mg iodine/200mg)  Can cause either hypothyroidism (5% to 25% of treated patients) or hyperthyroidism (2% to 10% of treated patients)  Inhibits of 5´-deiodinase activity → Inhibits conversion of T4 to T3  Iodine released from amiodarone metabolism directly inhibit thyroid gland function, if the effect persists, lead to amiodarone-induced hypothyroidism  Preexistent thyroid disease and Hashimoto’s thyroiditis ↑ risk  If hypothyroidism develop with a persistent rise in TSH: L-thyroxine therapy started
  • 31.  Type 1 hyperthyroidism: • iodine-induced excess thyroid hormone synthesis • underlying thyroid disorder, e.g., nodular goiter or latent GD • in regions where iodine intake is low  Type 2 hyperthyroidism: • thyroiditis due to a direct cytotoxic effect of amiodarone →↑release of thyroid hormones → transient thyrotoxicosis in a previously normal thyroid gland  Can overlap & difficult to distinguish, RIU is low in both types  Point favors Type 2 hyperthyroidism: Signs of inflammation, elevated ESR & IL-6, modest increases in thyroid gland size
  • 32.  ATDs effective in type 1, ineffective in type 2 thyrotoxicosis.  Prednisolone is beneficial in the type 2 form  Beta blocker should be started  A pragmatic approach is to commence combination therapy with an ATD and glucocorticoid in patients with significant thyrotoxicosis  A rapid response (within 1–2 weeks) usually indicates a type 2 picture and permits withdrawal of the antithyroid therapy  A slower response suggests a type 1 picture, when antithyroid drugs may be continued and prednisolone withdrawn.  Potassium perchlorate can be used to inhibit iodine trapping in thyroid
  • 33.  If the cardiac state allows, amiodarone should be discontinued  The course of the disease may last for anywhere between 1 to 3 months  In rare cases, surgical thyroidectomy under local anesthesia has proven to be effective  To minimize the risk of type 1 thyrotoxicosis, thyroid function should be measured in all patients prior to commencement of amiodarone therapy, and amiodarone should be avoided if TSH is suppressed  In general, patients treated with amiodarone should have thyroid function (specifically TSH) testing periodically throughout therapy
  • 34.  Thyroid dysfunction (both hypo & hyper) virtually affects the whole spectrum of cardiovascular hemodynamics  Thyroid functional abnormality can case a range of cardiovascular signs-symptoms and cardiovascular diseases are also associated with derangement of thyroid functions  Restoration of normal thyroid function most often reverses the abnormal cardiovascular hemodynamics
  • 35.  Prof. Md. Farid Uddin Chairman, Department of Endocrinology, BSMMU  Prof. M.A. Hasanat Department of Endocrinology, BSMMU  All the colleagues of my department