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The Journal of Clinical Endocrinology & Metabolism 87(3):963967

Copyright 2002 by The Endocrine Society

CLINICAL REVIEW 142

Cardiac Dysrhythmias and Thyroid Dysfunction: The
Hidden Menace?
FAIZEL OSMAN, MICHAEL D. GAMMAGE, MICHAEL C. SHEPPARD,

AND

JAYNE A. FRANKLYN

Division of Medical Sciences (F.O., M.D.G., M.C.S., J.A.F.), Queen Elizabeth Hospital, University of Birmingham,
Birmingham, United Kingdom B15 2TH
Thyrotoxicosis is often perceived as a reversible disorder
without long-term consequences, perhaps because of the
availability of effective treatments, but recent evidence suggests that there may, in fact, be adverse outcomes. Long-term
follow-up studies have revealed increased mortality from cardiovascular and cerebrovascular disease in those with a past
history of overt hyperthyroidism treated with radioiodine as
well as in those with subclinical hyperthyroidism indicated by
a low serum TSH concentration. Thyroid hormones exert direct effects on the myocardium as well as the systemic vasculature predisposing to dysrhythmias, especially supraventricular. Effects of thyroid hormones on the autonomic

nervous system may also contribute to arrhythmogenesis.

Atrial fibrillation is a recognized complication of hyperthyroidism that predisposes to embolic events. Development of
atrial fibrillation, together with other supraventricular dysrhythmias (both clinically obvious and those detected only by
Holter monitoring) in those with hyperthyroidism may account for increased vascular mortality. Improved detection of
supraventricular dysrhythmias and therapeutic intervention
(e.g. anticoagulants, antiarrhythmics) may improve the longterm vascular prognosis, but their role remains to be established in large therapeutic trials. (J Clin Endocrinol Metab 87:
963967, 2002)

HYROTOXICOSIS IS A common disorder with a prevalence of 3% in females and 0.3% in males in iodinereplete areas such as the United Kingdom and the United
States (1). It is known to induce many cardiovascular effects
such as sinus tachycardia, systolic hypertension, changes in
ventricular systolic and diastolic function, and predisposition to dysrhythmias, especially atrial fibrillation (AF) (2).
The availability of effective treatments for thyrotoxicosis has
led to the widespread perception that it is a reversible disorder without long term consequences, but increasing evidence suggests that this is not the case, especially in terms of
vascular disease.
Surprisingly, there have been few population-based studies
examining the long-term influence of thyroid disease and its
treatment on morbidity and mortality. Our recent study (3) of
a cohort of 7209 subjects with thyrotoxicosis treated with radioiodine between 1950 and 1989 identified marked excess in mortality from all causes. The underlying cause of death (coded to
ICD-9) for the cohort was compared with age-specific mortality
data for England and Wales and standardized mortality ratio
(SMR) used as a measure of relative risk. The excess mortality
was largely accounted for by an excess of deaths because of
circulatory diseases, both cardiovascular (SMR 1.2, 95% confidence intervals 1.21.3, P 0.001) and cerebrovascular (SMR
1.4, 95% confidence intervals 1.21.5, P 0.001). Increases in
risk of death because of rheumatic and hypertensive heart disease were found. The observed increase in relative risk of death
because of ischemic heart disease was less striking (although
significant), and the absolute risk of death from this cause was

high, determining that many deaths in the cohort were attributed to ischemic heart disease (SMR of 1.1, 95% confidence
interval 1.0 1.1, P 0.03). Deaths secondary to dysrhythmias
and congestive cardiac failure (ICD-9 category other circulatory diseases) were also significantly increased. In addition to
our own study, excess vascular mortality has been reported in
a study of 1,762 women with thyrotoxicosis treated with radioiodine, followed for an average of 17.2 yr (4), and another study
of 10,552 hyperthyroid patients treated with radioiodine, followed for an average of 15 yr (5). Interestingly, a recent study
of patients admitted to the hospital with an acute medical problem revealed that the finding of an elevated serum-free T3
concentration was associated with a 2.6-fold greater likelihood of the presence of a coronary event (6).
Although these findings together suggest a link between
overt thyroid hormone excess and occurrence of vascular
disease, we have recently described increased mortality from
circulatory diseases (and specifically from cardiovascular
diseases) in a community-based study of subjects with subclinical hyperthyroidism (not on thyroid hormone replacement) followed over a 10-yr period (7).
It is likely that dysrhythmias contributed to the excess
mortality ascribed to cardiovascular and cerebrovascular
diseases in these cohort studies, especially in those with the
complication of AF, in whom predisposition to embolic
events is well described (8).
Arrhythmic effects of thyroid hormones on the myocardium

Overt hyperthyroidism and atrial fibrillation. In the adult population, AF is the most common cardiac rhythm disturbance
and after sinus tachycardia is the most prevalent dysrhyth-

Abbreviations: AF, Atrial fibrillation; SMR, standardized mortality

ratio; SVC, supraventricular premature complexes.

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Osman et al. Clinical Review

mia in those with hyperthyroidism. Between 10% and 15% of

hyperthyroid patients develop AF (9); this incidence increases with age irrespective of whether there is associated
heart disease. AF is well known to be an independent risk
factor for cerebrovascular events. Two studies have investigated the rate of embolism observed in thyrotoxicosis, one of
which revealed a higher embolic rate in those with AF than
those in sinus rhythm (8, 10) (Table 1).
Subclinical hyperthyroidism and atrial fibrillation

Subclinical hyperthyroidism is common in the community, with the prevalence in iodine replete areas reported to
range from 0.5% to 3.9% in adults of all ages (11) and 11.8%
in one study of the elderly (12); the prevalence may be higher
in areas of iodine deficiency. It is defined as a low-serum TSH
concentration in an asymptomatic subject with normal serum
T3 and T4 concentrations (9). The most common cause in the
general population is the ingestion of exogenous T4 as replacement or suppressive therapy. A low-serum TSH concentration is generally a sensitive marker of thyroid hormone
excess and has been reported in a large population-based
study to be associated with a 3-fold higher risk of developing
AF in the subsequent decade (9). This study followed up 2007
patients aged 60 yr or more (from the Framingham Heart
Study) for a 10-yr period. These patients did not have AF at
the start of the study and were classified according to their
serum TSH level. During the 10-yr follow-up period, 192
(10%) developed AF. The cumulative incidence of AF at 10
yr in subjects with a low TSH concentration ( 0.1 mU/liter)
was 28%, compared with 11% in those with a normal TSH
(P 0.005). The relative risk for developing AF in those with
low TSH was 3.1 (95% confidence intervals 1.7 to 5.5), compared with those with normal TSH (P 0.001). The incidences of AF in those with a slightly low TSH and a high TSH
concentration were 16% and 15%, respectively; these incidences were not significantly different when compared with
those in the normal TSH group (Fig. 1). There are no longterm follow-up mortality or morbidity data on this cohort
yet.
Whether these findings regarding risk of development of
AF in those with subclinical hyperthyroidism, together with
the study described earlier demonstrating increased vascular
mortality (7), should prompt the use of antithyroid therapy
in those with persistent suppression of TSH remains controversial (13). Some authors have advocated careful folTABLE 1. Two published studies examining embolic risk in
thyrotoxicosis

Total no. in study

Number in AF (% of total)
Number in SR (% of total)
Frequency of embolic events
In AF (%)
In SR (%)

Bar Sela et al.

(10)

Peterson and
Hansen (8)

142
30 (21%)a
112 (79%)

610
91 (15%)
519 (85%)

12 of 30 (40%)
0 of 112 (0%)

12 of 91 (13%)b
15 of 519 (3%)

SR, Sinus rhythm.

a
Mean age of AF patients significantly higher than those in SR (56
vs. 39 yr, P 0.01).
b
P 0.03 compared with those in SR.

FIG. 1. Figure demonstrating the effect of TSH on the subsequent

development of atrial fibrillation [Reproduced with permission from
C. Sawin et al.: New Engl J Med 331:1249 1252 (9)].

low-up rather than any specific therapy (14), but others have
recommended a more aggressive policy of therapy with thionamides or radioiodine in those with nodular goiter and
cardiac risk factors such as increased age or preexisting cardiac disease (13).
Other atrial arrhythmias and hyperthyroidism

Supraventricular premature complexes (SVCs) are known

to initiate AF, particularly those originating in the pulmonary veins (15), and these have been reported to be more
frequent in thyrotoxic patients than in a matched control
group (16). The number of patients with supraventricular
tachycardia (defined as 10 SVCs in a row, heart rate 130
beats/min) has been reported to decrease after antithyroid
therapy, with the prevalence of supraventricular arrhythmias being greater in older patients both before and during
therapy (16). Our own preliminary data (17) support this
view in that we found the prevalence of significant atrial
ectopic beats (defined as 240 SVCs per 24 h) to be higher
in thyrotoxic subjects at presentation to clinic, compared with
matched controls, and remained elevated 3 months after
beginning antithyroid therapy despite restoration of biochemical euthyroidism, suggesting continued arrhythmic
substrate.
Effects of thyroid hormones on the ventricles

In contrast to supraventricular arrhythmias, ventricular

arrhythmias are uncommon in thyrotoxicosis and are found
with a frequency similar to that in the normal population (16,
17). Furthermore, the prevalence of ventricular arrhythmias
in thyrotoxic subjects remains unchanged during and after
antithyroid therapy (16). Ventricular tachycardia and ventricular fibrillation are exceptional in those with thyrotoxicosis and usually occur only in those with marked heart
failure or associated cardiac disease, typically because of
ischemic heart disease (18).
Use of -adrenoceptor blocker therapy

-Adrenoceptor blockers are widely used in the management of patients with thyrotoxicosis, typically in short-term

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Osman et al. Clinical Review

management before euthyroidism is achieved. Such drugs

have a well-established role in management of symptoms,
including palpitation (19). Whether they have a specific role
in dysrhythmia prophylaxis in thyrotoxicosis has not been
evaluated formally; likewise, the role of -adrenoceptor
blockers in subclinical hyperthyroidism is unclear. Some authors have advocated use of -adrenoceptor blockers in this
condition but only in those with underlying circulatory disease (14). Prospective studies are required to define the role
of therapeutic agents including -adrenoceptor blockers, and
other antiarrhythmics, in reducing the described vascular
morbidity and mortality associated with hyperthyroidism.
Should we anticoagulate and attempt cardioversion in those
with AF?

The published data examining AF and embolic risk in

thyrotoxicosis are limited (8, 10) but considered together
suggest that the rate of embolism in thyrotoxic AF exceeds
that for nonthyrotoxic AF not associated with rheumatic
heart disease (20). Furthermore, the majority of clinically
evident emboli in thyrotoxic AF involves the central nervous
system and occurs most commonly early in the course of the
disease (20). These findings are in keeping with data demonstrating highest rates of mortality from cerebrovascular
causes within the first year following treatment for thyrotoxicosis (3).
It is generally recommended that anticoagulation be considered in those with AF and thyrotoxicosis (19); there are,
however, no published data specifically examining the use of
anticoagulants in thyrotoxic AF, so the risk/benefit ratio of
such therapy remains to be established. The decision to treat
patients who have thyrotoxicosis-induced AF with short- or
long-term anticoagulation remains one to be made on an
individual basis, taking into consideration age, associated
heart disease, and risks of such therapy. Antiplatelet and
anticoagulant agents differentially affect cardioembolic and
noncardioembolic stroke in AF (21). Aspirin has a greater
effect on noncardioembolic stroke than cardioembolic but
may offer some degree of protection against cardioembolic
stroke in AF patients, although these are more effectively
prevented by anticoagulant therapy (21).
Treatment of thyrotoxicosis has been reported to lead to
spontaneous reversion to sinus rhythm in nearly two-thirds
of those with associated AF within 8 10 wk, although beyond 3 months few revert spontaneously to sinus rhythm
(22). Cardioversion should therefore not be delayed if the
patient is rendered euthyroid and still has AF after this
period (22). Factors in addition to duration of AF should
influence the decision to attempt cardioversion, in particular
the presence or absence of concomitant heart disease.
Cellular mechanisms determining arrhythmogenesis

Cardiac myocytes constitute only one-third of the total

cells that make up the myocardium. Fibroblasts, smooth
muscle cells, endothelial cells, and other cell types constitute
the majority of cardiac cells. Thyroid hormone-responsive
proteins that have been investigated are largely of myocytic
origin, and thyroid hormone influences on nonmyocytic cardiac cells have not been investigated in detail.

J Clin Endocrinol Metab, March 2002, 87(3):963967 965

The biologically active hormone T3 mediates thyroid hormone action. Once inside the cardiac myocyte, T3 enters the
nucleus and binds to nuclear receptors that are bound to
DNA response elements of target genes. T3-responsive genes
encode both structural and regulatory proteins in the heart.
Several cardiac genes are modulated by thyroid hormone at
transcriptional and posttranscriptional levels (Table 2).
The expression of these genes is known to have important
effects on the cardiovascular system, in particular systolic
contractile function and diastolic relaxation (23, 24). Whether
any of these genes is specifically involved in predisposing the
myocardium to arrhythmogenesis is currently unknown.
The expression of genes encoding specific ion transporters in
the plasma membrane such as the sodium-potassium ATPase, sodium-calcium exchanger and, voltage-gated potassium channels (Kv1.5, Kv4.2, and Kv4.3) are also regulated
by thyroid hormone (25). Thyroid hormones also affect extranuclear sites in the cardiac myocyte independent of nuclear T3 receptor binding and increases in protein synthesis.
Extranuclear effects influence primarily the transport of
amino acids, sugars, and calcium across the cell membrane
(23). T3 can alter the performance characteristics of a number
of ion channels in the cell membrane directly (including
sodium, potassium, and calcium) to influence cardiac inotropy and chronotropy.
After commencing antithyroid therapy, biochemical euthyroidism may be achieved after 4 6 wk; the excess vascular mortality noted following treatment of thyrotoxicosis
might be related to the persistence of cellular effects, despite
the restoration of biochemical euthyroidism. There is evidence that the on-rate or induction of transcription of specific
genes by thyroid hormones differs from the off-rate of transcription (following withdrawal of the hormones) (25) with
the latter taking more time. Cellular changes could thus
persist with continuing arrhythmic consequences because of
electrical remodeling, especially of the atria.
Potential cellular differences between the atria
and ventricles

The difference between the prevalence of arrhythmias arising in the atria and ventricles may be owing to a difference
in sensitivity of the two tissues to the effects of thyroid
hormones. Golf et al. (26) found the -adrenoceptor-binding
capacity in the right atrium to be more than twice that of the
left ventricle. These findings are consistent with those of
another study demonstrating the turnover of noradrenaline
TABLE 2. Regulation by thyroid hormones of genes (at
transcriptional and posttranscriptional levels) that encode
cardiac proteins
Positive regulation

Negative regulation

-Myosin heavy chain

SR-Ca2 ATPase
1-Adrenergic receptors
GTP binding proteins
Na-K ATPase
Voltage gated K-channel
(Kv 1.5, Kv 4.2, Kv 4.3)

-Myosin heavy chain

Phospholamban
Adenylate cyclase types 5 and 6
T3 nuclear receptor -1
Na-Ca2 exchanger

SR, Sarcoplasmic-reticulum; GTP, guanine triphosphate; Na, sodium; K, potassium; Ca2, calcium.

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to be markedly higher in atrial than ventricular tissue from

laboratory animals. Furthermore, cardiac tissue is known to
contain both 1 and 2 adrenoceptors. Stiles et al. (27) found
about 26% of the receptors to be of 2 subtype in the right
atrium with about 14% in left ventricular tissue. Effects of
thyroid hormone on the expression of these receptors will
affect impulse generation and propagation and hence arrhythmogenesis. The level of expression of various voltagegated potassium channels (especially Kv1.5) has been shown
to be 30% higher in atrial, compared with ventricular, myocardium (25), which may also explain the observed
discrepancy.
Effects of thyroid status on the autonomic nervous system

Several symptoms and signs in patients with hyperthyroidism suggest an abnormality of the autonomic nervous
system. Alterations in vagal and sympathetic innervation can
influence the development of arrhythmias with areas of sympathetic supersensitivity being conducive to the development of arrhythmias. Although the effect of thyroid hormone
on the autonomic nervous system has been the subject of
study for many years, there remain doubts about the nature
of this interaction. It has been suggested that there is high
adrenergic and low vagal activity in thyrotoxicosis, but circulating concentrations of catecholamines in hyperthyroidism suggest that secretion is normal or even reduced (18). To
explain this paradox, some have suggested that thyroid hormones and catecholamines can exert similar effects because
of their structural similarity (28). Increased tissue sensitivity
to catecholamines, secondary to increased -adrenoceptors
and reduced parasympathetic activity (29), have also been
put forward as possible explanations.
Heart rate variability is a useful, noninvasive tool in the
detection of autonomic activity on the sinus node. Cacciatori et
al. (30) described patients with thyrotoxicosis who had reduced
parasympathetic activity that returned to normal following
antithyroid therapy. These findings were in keeping with the
data of Kollai and Kollai (31), who found a low state of excitability in vagal motor neurons in response to baroreceptor stimulation in hyperthyroid patients, suggesting that the reduction
in tonic vagal activity may be a consequence of secondary
baroreceptor rearrangement. In contrast, Pitzalis et al. (32)
found vagal activity (assessed by the same method) to be unaltered in patients with hyperthyroidism. Our own data suggest reduced heart rate variability (and vagal activity) in patients with hyperthyroidism that persists despite restoration of
euthyroidism (17). Studies conducted in hypothyroid patients
revealed significant reductions in normal-normal interval
variations, suggesting reduced function of the parasympathetic
nervous system, which was reversible with treatment of the
hypothyroidism (33).
Conclusion

Thyrotoxicosis exerts major effects on the cardiovascular

system, and many of these are reversible with effective antithyroid therapy. For this reason, thyrotoxicosis has been
perceived as a benign disease, but long-term follow-up of
those with both overt and subclinical thyroid hormone excess
has revealed excess vascular mortality. The role of dysrhyth-

Osman et al. Clinical Review

mias (particularly supraventricular) may be critical in accounting for some of the excess cardiovascular and cerebrovascular mortality observed. Thyroid hormones are known
to have both direct and indirect effects on the myocardium,
affect the autonomic nervous system, and predispose to a
number of arrhythmias. Routine ECG and 24-hr Holter monitoring (with heart rate variability analysis as a noninvasive
marker of autonomic function) may help identify those at
particular risk. The role of therapeutic intervention such as
antiplatelet, antithrombotic, and/or antiarrhythmic therapy
remains to be established in prospective therapeutic trials. A
multidisciplinary approach to the management of these patients appears to be very important with involvement of both
an endocrinologist and cardiologist.
Acknowledgments
We acknowledge the support of the British Heart Foundation, Endowment Fund of the former United Birmingham Hospitals, and research nurse Mrs. J. Daykin for invaluable contribution to our clinical
studies.
Received August 27, 2001. Accepted October 29, 2001.
Address all correspondence and requests for reprints to: Prof. J. A.
Franklyn, Department of Medicine, Queen Elizabeth Hospital, Birmingham B15 2TH, United Kingdom. E-mail: J.A.Franklyn@bham.ac.uk.
F.O. is supported by a British Heart Foundation Research Fellowship.

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The 15th International Symposium of the Journal of Steroid Biochemistry &

Molecular Biology
(Recent Advances in Steroid Biochemistry & Molecular Biology)
May 1720, 2002
Munich, Germany
The main topics are: Steroid receptors, structure, gene expression, and mechanism of action; non-genomic
effect of steroid hormones; steroid membrane receptors; steroids and cancer; steroids in the central and
peripheral nervous systems; steroids and the menopause; enzyme modulators; steroid hormones, phyto- and
xeno-estrogens, and the environment; steroids and sport.
For more information, contact Prof. J. R. Pasqualini, Steroid Hormone Research Unit, Institut de Pue riculture, 26 Blvd Brune, 75014 Paris, France. Telephone: 331-4539-9109; Fax: 331-4542-6121; E-mail:
Jorge.Pasqualini@wanadoo.fr.

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