Thyroid disorders and heart

THYROID DISORDERS AND

CARDIOVASCULAR DISEASE

K SRINIVAS GEN MED1 February 2015

thyroid disorders and cardiovascular disease 1

INTRODUCTION

1 February 2015thyroid disorders and cardiovascular disease

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The thyroid gland and heart share a close relationship arising in

embryology.

The close physiologic relationship is affirmed by predictable changes in

cardiovascular function across entire range of thyroid disease states

Cardiovascular manifestations are some of the most common and

characteristic findings of hyperthyroidism


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HAEMODYNAMIC ALTERATION


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THYROID FUNCTION

TESTING


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The serum TSH level is the most widely used and sensitive measure for the

diagnosis of hypothyroidism and hyperthyroidism

Serum TSH levels increase(>5mIU/ml) in patients with primary

hypothyroidism

Serum TSH levels are low(<0.1 mIU/ml) in hyperthyroidism

Autoimmune thyroid disease can be diagnosed by measuring antithyroid

antibodies specifically antithyroid peroxidase (anti-TPO) or antithyroglobulin

antibodies

Thyroid hormone-catecholamine

interaction


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Early observations of the heart in hyperthyroidism proposed enhanced

sensitivity to catecholamines.

This postulate formed the basis for the test described by Emil Goetsch in

1918, in which hyperthyroidism could be diagnosed by demonstrating a

marked cardioacceleration and blood pressure in response to small

subcutaneous doses of epinephrine.


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Increased beta1-adrenergic receptors on cardiac myocytes observed in

experimental hyperthyroidism provide a mechanism for enhanced

catecholamine sensitivity.

Accompanying the increased levels of beta1-adrenergic receptors and

guanosine triphosphate–binding proteins, thyroid hormone decreases the

expression of cardiac-specific adenylyl cyclase catalytic subunit and thereby

maintains the cellular response to betaadrenergic agonists within normal

limits.


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HYPERTHYROIDISM


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Cardiovascular symptoms are often predominant clinical presentation of

pts with hyperthyroidism

Most patients experience palpitations

HR >90/min at rest and during sleep and increase during exercise is

exaggerated.

Many pts experience exertional dyspnea and exercise intolerance

caused in part by skeletal and respiratory muscle weakness.

Some patients can experience angina like chest pain

In older pts with suspected or known CAD, the increase in cardiac work

can produce myocardial ischemia


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Rarely pts,usually young women experience chest pain at rest with

ecg changes

Cardiac catheterization has demonstrated that most of these patients

have angiographically normal coronary arteries but coronary

vasospasm can occur.

Recent reports have documented cerebrovascular ischemic symptoms

in young primarily Asian women

MOYAMOYA DISEASE, characterized by anatomic occlusion of the

terminal portions of internal carotid arteries

Hyperthyroidism is associated with substantial degree of pulmonary

hypertension(Pul. Artery systolic pressure >50 mm Hg).

ATRIAL FIBRILLATION


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The most common rhythm disturbance in patients with hyperthyroidism is

sinus tachycardia.

The prevalence of atrial fibrillation and the less common forms of

supraventricular tachycardia in this disease ranges from 2% to 20%.

When compared with a control population with normal thyroid function and

a 2.3% prevalence of atrial fibrillation, the prevalence of atrial fibrillation in

overt hyperthyroidism was 13.8%.

In a study of more than 13,000 hyperthyroid patients, the prevalence for

atrial fibrillation was less than 2%,


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When that same group of patients was analyzed for age distribution,

prevalence increased stepwise in each decade, peaking at

approximately 15% in patients older than 70 years.

This study confirms that atrial fibrillation caused by hyperthyroidism is

more common with advancing age.

In a study of unselected patients presenting with atrial fibrillation, less

than 1% of cases was caused by overt hyperthyroidism.


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However, the ability to restore thyrotoxic patients to a euthyroid state and

sinus rhythm justifies TSH testing in most patients with recent onset of

otherwise unexplained atrial fibrillation or other supraventricular arrhythmias


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Treatment of atrial fibrillation in the setting of hyperthyroidism includes

beta-adrenergic blockade using a beta1 selective or nonselective agent

to control the ventricular response

This symptomatic measure can be accomplished rapidly, whereas

treatments leading to restoration of the euthyroid state requires more

time

Anticoagulation in patients with hyperthyroidism and atrial fibrillation is

controversial.


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The potential for systemic or cerebral embolization must be weighed

against the risk of bleeding and complications.

In a retrospective study of patients with hyperthyroidism, age rather than

atrial fibrillation was the main risk factor for embolization.


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In younger patients with hyperthyroidism and atrial fibrillation in the absence of

other heart disease, hypertension, or other independent risk factors for

embolization, the benefits of anticoagulation have not been proven and might be

outweighed by the risk.

Aspirin provides an alternative for lowering the risk for embolic events in younger

individuals and can be used safely.

Successful treatment of hyperthyroidism with radioiodine or antithyroid drugs and

restoration of normal serum levels of T4 and T3 are associated with reversion to

sinus rhythm in two thirds of patients within 2 to 3 months.


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In older patients or in the setting of atrial fibrillation of longer duration, the

rate of reversion to sinus rhythm is lower and electrical or pharmacologic

cardioversion should be attempted, but only after the patient has been

rendered euthyroid.

In a regimen that added disopyramide,300 mg/day, for 3 months after

successful cardioversion, patients were more likely to remain in sinus rhythm

than those not treated

HEART FAILURE IN THYROID DISEASE


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The cardiovascular alterations in hyperthyroidism include increased resting

cardiac output and enhanced cardiac contractility

A minority of patients presents with symptoms, including dyspnea on

exertion, orthopnea, and paroxysmal nocturnal dyspnea, as well as signs

peripheral edema, elevated jugular venous pressure, or an S3 indicative of

heart failure.

This complex of findings, coupled with a failure to increase the LV ejection

fraction with exercise, has suggests a hyperthyroid cardiomyopathy.


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Patients with long-standing hyperthyroidism and marked sinus

tachycardia or atrial fibrillation can develop low cardiac output, impaired

cardiac contractility with a low ejection fraction, an S3, and pulmonary

congestion, all consistent with congestive heart failure.

Review of such cases suggests that impairment in left ventricular function

results from prolonged high heart rate


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When the left ventricle becomes dilated, mitral regurgitation may also

develop

Recognition of this entity is important because treatment aimed at slowing

heart rate or controlling the ventricular response in atrial fibrillation appears

to improve left ventricular function, even before initiation of antithyroid

therapy


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Treatment can be started with lower doses of short-acting beta blockers

in conjunction with classic forms of treatment of acute congestiveheart

failure, including diuresis

It is important to recognize hyperthyroidism in older patients, because

they are at higher risk of cardiovascular and cerebral vascular events

TREATMENT. Treatment of patients with thyrotoxic cardiac disease

should include a beta-adrenergic antagonist to lower the heart rate to

10% or 15% above normal.

Definitive therapy can then be accomplished safely with iodine-131

alone or in combination with an antithyroid drug

HYPOTHYROIDISM


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The cardiovascular findings of hypothyroidism are more subtle.

Mild degrees of bradycardia, diastolic hypertension, narrow pulse

pressure and relatively quiet precordium, and decreased intensity of the

apical impulse are all characteristic.

The oxygen cost of work increases primarily as a result of the increase in

afterload.

Hypothyroidism produces increases in total and low-density lipoprotein

(LDL) cholesterol in proportion to the rise in serum TSH levels.


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The serum creatine kinase (CK) level is elevated by 50% to 10-fold in up to

30% of patients with hypothyroidism.

Pericardial effusions can occur consistent with the observation that patients

with hypothyroidism have an increase in the volume of distribution of albumin

and a decrease in lymphatic clearance function.

Although rare, tamponade with hemodynamic compromise can occur.

Echocardiography demonstrates small to moderate effusions in up to 30% of

overtly hypothyroid patients


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ECG in hypothyroidism is characterized by sinus bradycardia, low voltage,

and prolongation of the action potential duration and QT interval.

Increases in risk factors for atherosclerosis, including hypercholesterolemia,

hypertension, and elevated levels of homocysteine, may elevate the risk for

atherosclerosis in patients with hypothyroidism

One report has suggested increased cardiovascular morbidity and mortality

with untreated subclinical hypothyroidism.

In patients younger than 50 years of age with no history of heart disease, it is possible to initiate full replacement doses of l-thyroxine(100 to 150 μg/day)


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In patients older than 50yrs of age with known or suspected coronary artery

disease and coexistent hypothyroidism,three major issues need to be

addressed.

The first is whether coronary artery revascularization is required before

initiating thyroid hormone replacement.

If patients are not candidates for percutaneous intervention, CABG can be

accomplished in patients with unstable angina, left main coronary artery

disease, or three-vessel disease with impaired left ventricular function,

even in the setting of overt hypothyroidism.


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The second issue is in patients with known stable cardiac disease, in whom

cardiac revascularization is not clinically indicated.

Treatment of such patients should begin with low doses (12.5 μg) of l-

thyroxine and increased stepwise (12.5 to 25 μg) every 6 to 8 weeks until the

serum TSH level is normal.

Beta blockers are an ideal concomitant therapy to control heart rate

The third important issue involves patients who, potentially at risk for

coronary artery disease, exhibit no clinical signs or symptoms.

In this group, thyroid hormone replacement can be started at low doses, generally in the range of 25 to 50 μg/day, and increased by 25 μg every 6 to

8 weeks until the serum TSH level is normal.


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DIAGNOSIS: Hashimoto disease, post–radioiodine therapy for Graves

disease, and iodine deficiency are the leading causes of hypothyroidism

and produce diagnostic elevation in serum TSH levels.

The prevalence of hypothyroidism is estimated at 3% to 4% for overt

disease and 7% to 10% for the milder forms of disease, and increases

with advancing age.

TSH screening can therefore be advised for all adults,particularly patients

with hypertension, hypercholesterolemia, hypertriglyceridemia,coronary or

peripheral vascular disease, and unexplained pericardial or pleural

effusions and for various musculoskeletal syndromes or statin-associated

myopathy.

Myalgia

Non specific muscle symptoms.

Nocturnal cramping

Myopathy

Elevation of ck levels

Any associated disease

Usually with out elevation of ck

levels.

1 February 2015

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thyroid disorders and cardiovascular disease

Hypothyroid related Statin induced


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TREATMENT: Stepwise thyroid hormone replacement using levothyroxine

sodium incrementally decreases serum TSH, serum cholesterol,and

serum creatine kinase levels and improves left ventricular performance

In the rare condition of myxedema coma, characterized by the

development of hypothermia, altered mental status,

hypotension,bradycardia, and hypoventilation in patients with severe and

long-standing hypothyroidism

The need for thyroid hormone replacement is more emergent, and

treatment can be accomplished with 100 µg of T4 or 25 to 50 µg of T3

daily, administered intravenously.


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These patients often require intensive care unit monitoring with volume

repletion, gentle warming, and ventilatory support in the face of CO2

retention.

Administration of hydrocortisone (100 mg three times daily)should be

undertaken until results of serum cortisol testing are obtained.

When treated in this manner, hemodynamics including systemic vascular

resistance, cardiac output, and heart rate improve within 24 to 48 hours

SUBCLINICAL HYPOTHYROIDISM


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It defined as a TSH level above the upper range of the reference population

(usually >5 mIU/mL), is seen in up to 9% of unselected populations, and

prevalence increases with age

Subclinical hypothyroidism alters lipid metabolism, atherosclerosis, cardiac

contractility, and systemic vascular resistance.

A large study of women in Rotterdam has shown that atherosclerosis and

myocardial infarction increase with odds ratios of 1.7 and 2.3, respectively, in

subclinical hypothyroid women.


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Restoration of serum TSH levels to normal after thyroid hormone

replacement improves lipid levels, lowers systemic vascular resistance, and

improves cardiac contractility.

Patients with subclinical hypothyroidism have prolonged isovolumic

relaxation times, whereas systolic contractile function does not change


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It is diagnosed when the serum TSH level is low (<0.1 mIU/mL) and T4 and

T3 levels are normal.

Prevalence of atrial fibrillation after 10 years was 28% in the subclinical

hyperthyroid patient population, compared with 11% in patients with normal

thyroid function, with a relative risk of 3.1.

This population-based study of more than 1000 individuals with subclinical

hyperthyroidism not receiving l-thyroxine therapy or antithyroid medication

demonstrated that a TSH level lower than 0.5 mIU/mL associated with

twofold increased mortality, with a relative risk of 2.3 to 3.3 from all causes,

which in turn was largely accounted for by increases in cardiovascular

mortality.

SUBCLINICAL HYPERTHYROIDISM


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Therapy can be individualized with regard to three specific groups.

The first group includes patients receiving thyroid hormone replacement for

hypothyroidism, in which the low TSH level is believed to be the result of

excess medication, and reduction of the dose is indicated.

The second group includes patients with a prior diagnosis of thyroid cancer

currently receiving l-thyroxine for the purpose of TSH suppression.

In younger patients, beta blockers can reverse many cardiovascular

symptoms

In older patients, the degree of TSH suppression can be relaxed by

lowering the T4 dosage.


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The third group includes patients in whom subclinical hyperthyroidism

results from endogenous thyroid gland overactivity, including Graves

disease or nodular goiter.

Younger patients in this category appear to have little or no effects.

In patients older than 60 years of age, antithyroid therapy (methimazole,

5 to 10 mg/day) can produce improvement

In patients who respond or require long-term treatment, consideration

should be given to the use of radioiodine.

AMIODARONE AND THYROID

FUNCTION


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Amiodarone is an iodine-rich antiarrhythmic agent effective for the treatment

of ventricular and atrial tachyarrhythmias.

Its 30% by weight iodine content and its structural similarity to levothyroxine

cause abnormalities in thyroid function test results in as many as 60% of

patients

Amiodarone inhibits the 5′-monodeiodination of T4 in the liver and pituitary.

Serum TSH levels initially remain normal. With more chronic treatment and

as the total body iodide content rises, T4 synthesis and release from the

thyroid gland can be inhibited, producing a rise in TSH levels.

The overall prevalence of hypothyroidism in amiodarone treated patients is

between 15% and 30%.


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Less common, but perhaps more challenging, is the development of

amiodarone-induced thyrotoxicosis.

The onset was often sudden and could occur shortly after drug initiation,

during chronic treatment, or up to 1 year after stopping therapy.

Although the pathogenesis is multifactorial, early studies distinguished

two forms of amiodarone-induced thyrotoxicosis.


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Type I occurs primarily in patients with preexisting thyroid disease and most

commonly in iodine deficient areas.

In contrast, type II disease was identified as a form of thyroiditis presumably

mediated by a variety of proinflammatory cytokines, including IL-6.


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Changes in Thyroid Hormone Metabolism

That Accompany Cardiac Disease


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Following uncomplicated acute myocardial infarction, serum T3 levels

fall by about 20% and reach a nadir after approximately 96 hours.

Children and adults undergoing cardiac surgery with cardiopulmonary

bypass demonstrate a predictable fall in serum T3 levels in the

perioperative period.

Treatment strategies using acute administration of intravenous T3 to

adults after CABG have shown an improvement in cardiac output and a

fall in systemic vascular resistance.

Up to 30% of patients with heart failure have a low serum T3 level, which

occurs in patients treated with amiodarone and in those who are not. T3

replacement may provide benefit.


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Thyroid disorders and heart