3 CE Credits

Cardiovascular Effects of Thyroid Disease

Jodi K. Sangster, DVM
David L. Panciera, DVM, MS, DACVIM (Small Animal Internal Medicine)
Jonathan A. Abbott, DVM, DACVIM (Cardiology)
Virginia Tech
Blacksburg, Virginia

Abstract: Thyroid hormones have many effects on cardiovascular function, and deficiency or excess of thyroid hormones can result in
cardiac dysfunction. Abnormalities of the cardiovascular system are often identified during examination of hyperthyroid and hypothy-
roid patients. This article addresses the effects of thyroid hormones on the cardiovascular system and the clinical relevance of the
cardiovascular response to thyroid dysfunction. In addition, treatment recommendations are presented.

T
hyroid hormones have an integral role in cardiovascular ho-
meostasis, affecting myocardial function, systemic vascular
resistance, endothelial function, and response to catechol-
amines. Clinical evidence of the influence of thyroid hormones on
the cardiovascular system is most apparent in hyperthyroidism, in
which tachycardia and abnormal heart sounds are frequent findings
on physical examination. The cardiovascular effects of hypothyroid-
ism are typically more subtle, but they may be clinically important
in some situations. This review addresses the effects of thyroid
hormones on the cardiovascular system, the clinical consequences
of hyperthyroidism and hypothyroidism, and the management
of these disorders.
Cardiovascular Effects of Thyroid Hormone
Thyroid hormones alter cardiovascular function directly, through
effects on the heart, and indirectly, through effects on the peripheral
vasculature (BOX 1). Myocardial contractility and relaxation are
enhanced by the genomic actions of 3,5,3’-triiodothyronine (T3).
Specifically, T3 increases the expression of genes that encode ion
transporters, β1-adrenergic receptors, and contractile proteins. These
effects increase calcium release and reuptake from the sarcoplasmic
reticulum.1 –3 The resultant increase in cytosolic calcium increases
contractility, and the more rapid calcium reuptake enhances dia-
stolic relaxation.
Nongenomic effects of T3 on cardiac myocytes include stimu-
lation of sarco/endoplasmic reticulum calcium ATPase (SERCA)
activity, an increase in the activity of sodium-potassium pumps,
recruitment of slowly inactivating membrane sodium channels,3
and an increase in membrane permeability to sodium ions.4 In
hyperthyroidism, these effects may enhance myocardial function
but may also predispose the patient to cardiac arrhythmias.5
In addition to direct effects on cardiac function, thyroid hor-
mones induce important changes in the peripheral circulation
(BOX 1). T3 has been shown to rapidly and directly cause relaxation
of vascular smooth muscle cells,6 leading to decreased systemic
vascular resistance. Generation of nitric oxide by endothelial cells
is enhanced by thyroid hormones, contributing to arteriolar vaso-
dilation in hyperthyroidism.7 In addition, thyroid hormones increase
metabolic rate and oxygen demands of the peripheral tissues,3
resulting in locally mediated vasodilation. The renin-angiotensin-
aldosterone system (RAAS) is activated in response to the decrease
in resistance, thereby increasing plasma volume through sodium
retention.8 Thyroid hormone also stimulates erythropoietin secre-
tion,9 resulting in increased red blood cell mass.
Box 1. Effects of Thyroid Hormone on the Heart
• Increased myocardial contractility
—Increased expression of contractile proteins
—Increased numbers of β-adrenergic receptors
—Increased calcium release from sarcoplasmic reticulum
—Increased sodium-potassium pump activity
—Increased membrane permeability to sodium ions
• Enhanced myocardial relaxation via increased calcium reuptake by
sarcoplasmic reticulum
• Increased preload
—Stimulation of erythropoietin, increasing red cell mass
—Activation of the renin-angiotensin-aldosterone system, increasing
plasma volume
• Decreased afterload
—Relaxation of vascular smooth muscle
—Increased generation of nitric oxide
—Increased locally mediated vasodilation secondary to increased
metabolic rate of peripheral tissues

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 Cardiovascular Effects of Thyroid Disease

Whereas diastolic and mean arterial

blood pressures are decreased and sys-
tolic pressure is increased in people with
hyperthyroidism, systolic, diastolic, and
mean systemic arterial pressures were
all elevated in cats with experimentally
induced hyperthyroidism of 2 weeks’
duration.20 These findings suggest an
increase, rather than a decrease, in
vascular resistance, but it is unclear if
similar changes are present in cats with
naturally occurring hyperthyroidism.
Hypertension likely results from the
marked increase in cardiac output
combined with expanded plasma vol-
ume caused by activation of the RAAS
and expanded red cell mass caused
Figure 1. This electrocardiogram was recorded from a 13-year-old castrated domestic shorthaired cat with
by stimulation of erythropoietin re-
hyperthyroidism (paper speed = 50 mm/sec, sensitivity = 10 mm/mV). The heart rate is 230 bpm and the cardiac
rhythm is sinus. There is an intraventricular conduction disturbance characterized by leftward deviation of the lease.21,22 However, the role of the RAAS
mean electrical axis associated with normal QRS duration. S waves are evident in leads I, II, III, and aVF; the in cats with hypertension associated
terminal deflections of leads I and II are slurred. There are limited published data that provide pathologic validation with hyperthyroidism is unclear.23 Im-
of abnormal feline QRS configurations. However, this electrocardiogram has features of the left axis deviation, portant clinical manifestations of hyper-
sometimes described as a left anterior fascicular block, together with incomplete right bundle branch block.
thyroidism-induced cardiac dysfunc-
tion in veterinary patients include
Hyperthyroidism arrhythmias, intolerance of aggressive fluid therapy or stress,
First described in 1980, feline hyperthyroidism has become in- hypertension, and congestive heart failure (CHF).9,18
creasingly recognized and is currently the most frequently diagnosed
feline endocrinopathy, with a prevalence of 2% across cats of all Clinical Findings
ages.10,11 Because of increased awareness of hyperthyroidism and The cardiovascular effects of hyperthyroidism are responsible for
routine screening of serum thyroxine (T4) concentrations in older some of the most prevalent clinical findings in affected patients.
cats, modern clinical manifestations of feline hyperthyroidism Heart murmurs or gallop sounds are auscultated in 35% to 50% of
are often mild compared with early descriptions of the disease. In affected cats, and tachycardia is found in a slightly higher propor-
cats, hyperthyroidism is caused by adenomatous hyperplasia of tion.24 Cardiomegaly is noted radiographically in approximately
the thyroid gland or, rarely (1% to 3% of cases), by thyroid carci- 26% to 40% of hyperthyroid cats.25 –27 Hyperthyroid cats are at
noma. Hyperthyroidism in dogs is much less common and is
12
increased risk for arterial thromboembolism.28
either iatrogenic or the result of a functional thyroid follicular
13
The most common electrocardiographic (ECG) abnormality
carcinoma or adenocarcinoma.14 Only 10% to 20% of thyroid tumors in hyperthyroid cats is sinus tachycardia, detected in 34% of cases.
in dogs are functional, and unlike those affecting cats, most thyroid Other ECG abnormalities include increased R-wave amplitude
tumors of dogs are malignant.15 consistent with left ventricular enlargement (8% of patients) and
left anterior fascicle block pattern (FIGURE 1) or right bundle
Cardiovascular Effects of Hyperthyroidism branch block (6% to 10% of cases). In addition, arrhythmias—
The direct cardiac effects of excess thyroid hormone include including atrial and ventricular premature contractions and, less
enhanced contractility and diastolic function that contribute to frequently, atrioventricular block, atrial tachycardia, and ven-
an increase in stroke volume. Cardiac output is increased further tricular tachycardia—may be identified.25,29 –31 Increased R-wave
by positive chronotropic effects that result from heightened amplitude correlates poorly with echocardiographic evidence of left
responsiveness to sympathetic stimulation, conferred by an ventricular enlargement.32 While not well documented, arrhythmias
increase in the number of β1-adrenergic receptors, enhanced rate are expected to resolve after successful treatment of hyperthyroidism.
of spontaneous depolarization of sinoatrial node cells,16 and Abnormal echocardiographic findings are common, although
reduced influence of the parasympathetic nervous system.17 –19 usually mild, in hyperthyroid cats.33 The most common echocar-
The reduced systemic vascular resistance induced by peripheral diographic abnormality in hyperthyroid cats is hypertrophy of
vasodilation and increased blood flow induced by hyperthyroid- the left ventricular posterior wall, identified in approximately
ism further increase cardiac output. The resulting hemodynamic 72% of affected cats.34 Other echocardiographic abnormalities of
burden and altered myocardial dynamics can lead to cardiac hyperthyroidism include left atrial enlargement in 50% of cats,
dysfunction. increased left ventricular end-diastolic diameter in 47%, septal

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A
Figure 2. Left lateral (A) and dorsoventral (B) radiographs of a cat with
congestive heart failure. Note the cardiomegaly (vertebral heart score
9.4; normal 7.5); marked interstitial to alveolar lung pattern, particularly
in the caudal lung lobes; and pulmonary venous congestion.
hypertrophy in 40%, and increased fractional shortening in
22%.26,34 Enhanced left ventricular systolic function with normal
diastolic function has been documented using Doppler tissue
imaging in hyperthyroid cats.35 Severe ventricular dilation with
myocardial hypocontractility has also been reported.36 Eccentric
hypertrophy (an increase in myocardial mass associated with an
increase in ventricular volume) is expected secondary to the increase
in preload and decrease in systemic vascular resistance. However,
as has been reported in some human patients, concentric hyper-
trophy also occurs, possibly reflecting an increase in systolic wall
stress.37,38 The influence of concurrent disease, such as renal dys-
function or systemic hypertension, on myocardial remodeling is
unknown but could contribute to development of concentric hyper-
trophy in hyperthyroid cats.
It is unclear from investigations of hyperthyroid cats if eccentric
or concentric hypertrophy predominates. This likely reflects the
paucity of reports and the complex pathogenesis of myocardial
changes, both direct and indirect, in hyperthyroidism. There is echo-
cardiographic evidence that hyperthyroid-induced cardiac changes
resolve with treatment in many cats, but they may persist in others.33,34
However, published echocardiographic data obtained after treatment
of hyperthyroidism are limited, and factors that might affect res-
olution of cardiac changes have received little attention.
There is considerable overlap in echocardiographic findings
between cats with hyperthyroidism-related concentric hypertrophy
and those with hypertrophic cardiomyopathy.32 In addition, hyper-
tension can cause left ventricular posterior wall and/or septal
hypertrophy similar to changes induced by hyperthyroidism.39
Although the prevalence of asymmetric hypertrophy and perhaps
systolic anterior motion of the mitral valve may be greater in patients
with primary myocardial disease, echocardiography cannot reliably
differentiate these conditions; therefore, thyroid function and blood
pressure should be evaluated in middle-aged and older cats with
cardiac abnormalities.
The prevalence of CHF in hyperthyroid cats is approximately
2%.24,40 Cats in CHF show clinical signs typical of that condition,
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Cardiovascular Effects of Thyroid Disease
such as dyspnea, anorexia, cy-
anosis, and potentially weak
femoral pulses. Pleural effu-
sion secondary to CHF can
obscure the cardiac silhouette
on thoracic radiographs. Pul-
monary venous engorgement
and a patchy interstitial or al-
veolar pattern resulting from
pulmonary edema may also
be seen (FIGURE 2). As in peo-
ple, heart failure in hyperthy-
roid cats would be expected to
resolve after thyroid hormone
levels are controlled.41,42 How-
ever, the response to treat-
B ment of heart failure in
hyper­thyroid cats with con-
current primary myocardial disease is less certain.
The cardiac phenotype of hyperthyroid cats with CHF has
been incompletely described; therefore, findings in people with
hyperthyroidism may be relevant. Heart failure occurs in 6% of
people with hyperthyroidism and is usually associated with the
development of atrial fibrillation.43 Left ventricular dilation and
decreased ejection fraction are found in about 50% of hyperthyroid
humans with CHF. In people with hyperthyroidism and preserved
left ventricular ejection fraction, CHF almost always resolves after
a euthyroid state is established. Resolution of heart failure and
left ventricular dysfunction after treatment of hyperthyroidism is
less predictable in patients with reduced ejection fraction, although
indices of systolic myocardial function return to normal in most
cases.44,45
In the most detailed report of CHF in hyperthyroid cats, Jacobs
et al36 described four cases of CHF characterized by pleural effusion
in hyperthyroid cats, two of which died of CHF. The echocardio-
graphic abnormalities of these cats primarily reflected severe
ventricular dilation and myocardial hypocontractility rather
than the ventricular hyperkinesis observed in many cases of hyper-
thyroid heart disease. While the poor outcome of these cases may
be unusual, this case series demonstrates that hyperthyroidism
can contribute to, or directly cause, severe heart disease. Other, less
detailed reports of hyperthyroid cats with heart failure include
those with systolic dysfunction34 as well as normal contractility.32
Because the cases with hypocontractility were reported when dilated
cardiomyopathy (DCM) secondary to taurine deficiency was
common, it is possible that some of these cats had concurrent
hyperthyroidism and DCM. However, DCM has also been reported
in people secondary to thyrotoxicosis.46
It is likely that tachycardia and other effects of hyperthyroidism
are detrimental in patients with underlying primary cardiomy-
opathy and could cause decompensation of a previously subclinical
condition. Because 16% of apparently healthy cats were found to
have subclinical cardiomyopathy in a 2009 study,47 hyperthyroidism
and primary cardiomyopathy would be expected to coexist in a
 Cardiovascular Effects of Thyroid Disease

substantial number of feline patients. However, cardiac changes blood urea nitrogen, serum
in hyperthyroid heart disease may be similar to those resulting creatinine and T4 concen- Key Points
from primary hypertrophic cardiomyopathy, so it is unknown trations, urine specific gravi-
how frequently hyperthyroidism complicates preexisting heart ty, and blood pressure at 1, • Thyroid hormones cause vasodilation,
disease. Serial echocardiograms after resolution of hyperthyroidism 3, and 6 months after treat- increase blood volume, and enhance
myocardial contractility.
may be the most reliable method to determine if primary cardio- ment is initiated.
myopathy is present. However, diagnosis of primary cardiomy- Specific treatment for • Clinical manifestations of feline
opathy before treatment of hyperthyroidism is problematic. cardiac abnormalities is hyperthyroidism related to the
The cardiac biomarker N-terminal-pro-B-type natriuretic unnecessary in most hyper- cardiovascular system include
peptide (NT-pro-BNP) has proven useful in the diagnosis of CHF thyroid cats that do not tachycardia, heart murmur, gallop
in cats and has been shown to differentiate normal cats from have clinical signs of CHF. rhythm, and systemic arterial
those with occult cardiomyopathy.48 Hyperthyroidism induces an Treatment of hyperthy- hypertension.
increase in NT-pro-BNP in humans49 and has been shown in a roidism resolves the ab- • Hypertension may develop before or
preliminary report to result in modest elevations in hyperthyroid normal heart sounds in after treatment of hyperthyroidism,
cats.50 Cardiac troponin I, an indicator of myocardial cellular many, but not all, cats. In necessitating ongoing monitoring of
damage, was elevated in some cats with hyperthyroidism in one our experience, and as re- blood pressure after reestablishing a
study.51 Until these biomarkers are compared in cats with hyper- ported by others, persistence euthyroid state.
thyroidism and cats with primary cardiac disease, it is not clear if of a heart murmur after
• Congestive heart failure is uncommon
they will prove useful in differentiating these disorders. control of hyperthyroidism
in cats with hyperthyroidism and
Hypertension is a common complication of hyperthyroidism is not consistently associated
should be managed with antithyroid
in cats, and although the prevalence varies considerably depending with the presence of clini-
therapy in addition to treatment
on the population studied, it is likely to be 10% to 20%.52 –57 Hyper- cally significant heart dis-
deemed appropriate for the
tension has been shown to persist in at least the first 4 weeks of ease.51 Arrhythmias and left
manifestations of heart failure and
treatment with methimazole despite normalization of thyroid ventricular hypertrophy specific cardiac abnormalities.
hormone concentrations,58 and some cats that are normotensive are expected to improve or
before treatment may become hypertensive when euthyroid.52 resolve when euthyroidism • Hypothyroidism can result in
Concurrent renal disease may play a role in the latter finding; is established. However,
34 bradycardia, decreased myocardial
approximately 15% of cats become azotemic after treatment of hyperthyroid cats with se- contractility, and, rarely, clinically
hyperthyroidism57 as previously subclinical renal insufficiency is vere cardiac manifestations significant atherosclerosis and
unmasked. However, in one study,56 only 35% of cats that became need to be stabilized before myocardial failure.
hypertensive after treatment for hyperthyroidism were azotemic, surgery to minimize anes- • Hypothyroid heart disease is largely
so renal disease is likely not the sole cause of posttreatment hyper- thetic risk, or before re- reversible with levothyroxine
tension. Blood pressure should be measured at the time of diagnosis ceiving radioactive iodine supplementation.
of hyperthyroidism and after the disease has been controlled. therapy. To achieve this
The clinical findings in hyperthyroid dogs are similar to those stabilization, β-adrenergic
in cats, with presenting signs including panting, polyphagia, antagonists may be administered to reduce the detrimental effects
weight loss, and polyuria/polydipsia.13,59,60 Cardiovascular mani- of tachycardia. These agents are the mainstay of treatment of hyper-
festations of canine hyperthyroidism are also similar and include thyroid-induced heart disease, although, as discussed below, their
tachycardia, premature ventricular contractions, increased R-wave use when heart failure is present requires careful consideration.
amplitude, and hypertension.13,59 These signs, accompanied by an Propranolol (0.5 to 1.0 mg/kg PO q8h) or atenolol (1 to 2 mg/kg
elevated T4 concentration, should prompt a search for a functional PO q12h) ameliorates some of the cardiovascular complications of
thyroid tumor or oversupplementation of thyroid hormone. As in hyperthyroidism, particularly sinus tachycardia and supraventric-
cats, treatment of the hyperthyroidism resolves the cardiovascular ular arrhythmias. Propranolol has the additional potential benefit
signs. of reducing the conversion of T4 to T3 and has been demonstrated
to reduce heart rate in hyperthyroid cats.61,62 However, as a non-
Treatment selective β-blocker, propranolol may exacerbate bronchocon-
Feline hyperthyroidism can be controlled with oral antithyroid striction in cats with chronic lower airway disease. Atenolol, a
agents, a low-iodine diet, thyroidectomy, or radioactive iodine. selective β1 blocker, less likely to be associated with bronchocon-
Medical management with methimazole is recommended as the striction, so it is preferred to propranolol in cats with concurrent
initial strategy for any cat with significant cardiovascular compli- bronchial disease.63 Other potential adverse effects of β blockers
cations. Definitive treatments can be considered after heart disease include bradycardia, lethargy and/or depression, and hypotension.
has been stabilized and hyperthyroidism controlled for several The general therapeutic principles of managing heart failure in
weeks. Monitoring of cats treated for hyperthyroidism should euthyroid patients are likely valid in the setting of hyperthyroidism,
include, at minimum, evaluation of physical examination findings, although, of course, the additional need for specific treatment of

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the endocrinopathy exists. On an emergency basis, supplemental
oxygen should be provided immediately. Furosemide (0.5 to 2 mg/kg
IV or IM) is administered every 1 to 4 hours until dyspnea starts
to resolve; the dosage interval is then increased to 6 to 12 hours.
Thoracocentesis should be performed if pleural effusion is re-
sponsible for dyspnea. Diuretic doses and dosage intervals are
determined most appropriately by clinical response; the lowest
dose that relieves congestive signs is considered to be optimal.
For chronic therapy, the use of furosemide (0.5 to 2 mg/kg PO
q12–24h) and an angiotensin-converting enzyme (ACE) inhibi-
tor (enalapril at 0.25 to 0.5 mg/kg q12–24h or benazepril at 0.25
to 0.5 mg/kg q24h) is reasonable, but specific therapy might be
best guided by echocardiographic findings when available.64
The use of pimobendan in cats with primary myocardial disease
has been reported, but systematic evaluation of its efficacy in the
management of feline cardiac disease has not.65,66 Pimobendan
may be useful in feline patients with hyperthyroidism, heart failure,
and echocardiographically documented systolic myocardial dys-
function. Serial chemistry panels should be evaluated 2 weeks after
each dosage change or every 3 months to monitor renal function
and electrolytes. While there may be a role for gradual up-titration
of β-blockers in the long-term management of systolic myocardial
dysfunction, the acute hemodynamic effects of these drugs are
likely to be deleterious. Therefore, it is probably best to avoid
β-blockers in patients with clinical signs caused by congestion
unless echocardiography demonstrates hyperdynamic ventricular
performance associated with tachycardia.
The prognosis of hyperthyroid cats with CHF that do not have
concurrent primary myocardial disease is probably good. How-
ever, some cats with hyperthyroidism and CHF respond poorly
to treatment.36 It is unclear if these cats have concurrent primary
myocardial disease that has been exacerbated by hyperthyroidism
or if the hyperthyroid-induced heart disease is irreversible for
unknown reasons. Some hyperthyroid cats that have responded
poorly to treatment for CHF had impaired contractility that was
identified on echocardiography, but the significance of this is un-
clear.39 Mere cardiac structural changes, tachycardia, and arrhyth-
mias have not been shown to increase risk of death.27,67
If hypertension is of sufficient magnitude (systolic blood pressure
persistently >180 mm Hg) to carry a risk of target organ damage,
or if clinical signs or examination findings secondary to hyper-
tension (tortuous retinal vessels, retinal edema or hemorrhage,
severe proteinuria, or neurologic abnormalities) are present at
any time during management of hyperthyroidism, treatment of
hypertension should be initiated concurrently with that for hy-
perthyroidism. Because the efficacy of antihypertensive agents in
hyperthyroid cats has not been systematically evaluated, the rec-
ommended treatment is similar to that for euthyroid hypertensive
cats. The calcium channel blocker amlodipine (0.625 mg, or one-
quarter of a 2.5-mg tablet per cat PO q24h)55 is the drug of choice
for initial treatment. The dosage can be increased to 0.625 mg PO
q12h if the systolic blood pressure still exceeds 160 mm Hg after 1 to
2 weeks of treatment. An ACE inhibitor (enalapril 0.25 to 0.5 mg/kg
q12–24h or benazepril 0.25 to 0.5 mg/kg q24h) may be used in
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Cardiovascular Effects of Thyroid Disease
addition to amlodipine if hypertension persists. Administration
of atenolol to hypertensive hyperthyroid cats is insufficient to
control blood pressure in most cases, so β-blockade might be
most effective when combined with other agents.68 Evidence is
conflicting on whether hypertension affects survival in hyper-
thyroid cats,56,57 and the effects of treatment of hypertension on
survival have not been studied.
Hypothyroidism
Hypothyroidism is the most commonly diagnosed endocrinopathy
in dogs. Because thyroid hormones affect all organ systems, defi-
ciency results in a wide variety of clinical signs. Classic clinical
signs are obesity, lethargy, and alopecia. The diagnosis can be
complicated by the suppressive effects of nonthyroidal illness,
such as CHF, on thyroid function tests. Naturally occurring feline
hypothyroidism is rare,69,70 but iatrogenic hypothyroidism as a
consequence of treatment of hyperthyroidism is relatively common.
Cardiovascular Effects of Hypothyroidism
The cardiovascular manifestations of hypothyroidism tend be less
dramatic than those of hyperthyroidism, but important abnor-
malities have been seen in some patients. Hypothyroidism has
direct negative inotropic effects caused by a shift from the pre-
dominant myosin isoenzyme to the low-ATPase myosin heavy
chain β71 in some species, although this is likely of limited importance
in dogs and cats. Diastolic relaxation is prolonged and heart rate
is reduced by reductions in SERCA activity and numbers of β1-
adrenergic receptors, respectively.3 Cardiac function can be impaired
further by fibrosis and accumulation of mucopolysaccharides in the
myocardial interstitium,72,73 increasing cardiac mass and wall stiffness.
Severe, experimentally induced hypothyroidism has been shown to
result in impaired myocardial blood flow caused by a loss of arterioles
as well as progressive systolic dysfunction,74 limiting compensatory
responses for decreased myocardial mechanical work efficiency.8
Thyroid hormone deficiency increases peripheral vascular resistance,
contributing to increased cardiac afterload.75 These abnormalities
result in a decrease in cardiac output and may contribute to the
clinical abnormalities common in hypothyroid dogs.
In addition to effects on myocardial function, hypothyroidism
in humans also results in alterations of the peripheral vasculature.
Lack of adequate thyroid hormone increases peripheral vascular
resistance and arterial wall stiffness and thus contributes to increased
cardiac afterload and systemic hypertension in humans,8,75 although
this has not been documented in dogs. Reduced responsiveness to
vasodilators has been demonstrated in hypothyroid rats and likely
further contributes to increased peripheral vascular resistance.21
Impaired free water excretion, documented in hypothyroid humans
and rats,22,76 can contribute to fluid retention, hyponatremia, and
edema formation. The importance of these changes in hypothyroid
dogs and cats is unclear.
Clinical Findings
Common physical examination findings in hypothyroid dogs
include a slower than expected heart rate, weak pulses, muffled

Figure 3. A canine heart demonstrating marked atherosclerosis. The coronary
arteries are prominent and are lined with pale atherosclerotic plaques (arrows).
(Photograph courtesy of Dr. Roger Panciera)
heart sounds, and a weak apex beat.15,77 Bradycardia (<70 bpm) is
present in 5% to 22% of cases. ECG abnormalities may include
decreased amplitude of the R wave (present in up to 58% of dogs
examined),78 sinus bradycardia, and first- or, rarely, second-degree
atrioventricular block.77,79,80 Bradycardia and atrioventricular
block resolve within 9 to 19 weeks of treatment in most affected
dogs.65,66 Echocardiographic findings are indicative of decreased
left ventricular systolic function. Median fractional shortening was
26% in 10 hypothyroid dogs in one study and 29% in another
study of 11 dogs.79,80 After treatment for a mean of 9 and 19 weeks,
fractional shortening increased by 15% and 28%, respectively,
compared with pretreatment results. The thickness of the left
ventricular posterior wall and interventricular septum is decreased
in some hypothyroid dogs; this change resolves with treatment.80,81
Although the cardiovascular effects of hypothyroidism are
usually insufficient to cause clinical signs, they can cause decom-
pensation in patients with preexisting cardiac diseases, such as
DCM. It is also possible that prolonged anesthesia or aggressive
fluid therapy may compound preexisting circulatory dysfunction
and lead to congestion or edema. Myocardial failure resulting in
CHF in the apparent absence of primary cardiomyopathy has
been documented in a small number of hypothyroid dogs.82 –84
Clinical signs included lethargy, inappetence, cough, tachypnea,
and, in some dogs, ascites. Atrial fibrillation was present in most
cases. Echocardiograms revealed markedly decreased fractional
shortening and enlarged left atria and ventricles. Heart failure was
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Cardiovascular Effects of Thyroid Disease
controlled after levothyroxine supplementation with concurrent
treatment consisting of some combination of digoxin, furose-
mide, diltiazem, and an ACE inhibitor (lisinopril or benazepril).
While the atrial fibrillation persisted in all cases, myocardial
function improved substantially within 4 to 6 weeks of initiating
levothyroxine supplementation. Some of these dogs may have
had underlying, subclinical breed-related DCM made clinical by
hypothyroidism. Clinical suspicion for hypothyroidism should
be high for an obese dog with apparent DCM, particularly if
myxedema, alopecia, or hypercholesterolemia is present.
Atherosclerosis is a known complication of the hypercholes-
terolemia and lipid abnormalities induced by hypothyroidism in
people8 and has been reported to be a rare but serious complication
of hypothyroidism in dogs.84 When coronary arteries are affected
(FIGURE 3), atherosclerosis can result in myocardial ischemia and
impaired cardiac function. In people with hypothyroidism, athero-
sclerosis has been attributed to hypercholesterolemia, hypertension,
and impaired endothelial function.85 Hypothyroid dogs with athero-
sclerosis have consistently been markedly hypercholesterolemic.
Atherosclerosis predisposes dogs to thrombosis and multiorgan
disease, with clinical manifestations varying with the affected
body system. CHF has been found in some dogs with atherosclerosis
and hypothyroidism86; however, other signs, including those
compatible with thrombosis of the central nervous system, aorta,
or other organs, are more common. Treatment is palliative and
centers around levothyroxine supplementation and, if necessary,
a low-fat diet.84
Treatment
As in feline hyperthyroidism, treatment of cardiac dysfunction
associated with hypothyroidism is best accomplished by resolving
the underlying thyroid dysfunction. Only in cases with CHF or
concurrent cardiac disease is it necessary to provide cardiovascular-
specific treatment. The cardiac changes induced by hypothyroidism
are reversible; decreased fractional shortening and decreased R-wave
amplitude in hypothyroid dogs improve with supplementation
with levothyroxine.79,80,82,83 Recheck echocardiography is recom-
mended 4 to 8 weeks after initiation of levothyroxine if hypothy-
roidism is thought to be contributing to decreased contractility.
In hypothyroid dogs with CHF or significant cardiac arrhyth-
mias, the initial dose of levothyroxine should be less than the
typical dosage. This recommendation is based on the cardiac de-
compensation that sometimes follows the sudden increase in
oxygen demand in peripheral tissues and the myocardium when
the hypothyroid state is reversed rapidly in humans.87 Therefore,
levothyroxine should be initiated at 0.005 mg/kg PO q24h. The
dosage may be increased gradually by 0.005 mg/kg every 2 weeks,
with the patient being evaluated for improvement in cardiovas-
cular status and measurement of serum T4 concentration before
dosage adjustment. Hypothyroid dogs without important cardio-
vascular complications should receive levothyroxine at a starting
dose of 0.02 mg/kg PO q24h. When present, CHF should be
managed as in other dogs with heart failure caused by systolic
dysfunction. In emergent situations, supplemental oxygen should

be provided immediately and furosemide administered (2.2 to
4.4 mg/kg IV or IM q30–60min) until dyspnea starts to resolve.88
Chronic therapy for canine heart failure caused by systolic dys-
function generally consists of furosemide (1 to 2 mg/kg PO q12h;
adjusted to lowest dose that eliminates congestive signs), an ACE
inhibitor (enalapril 0.5 mg/kg PO q12h or benazepril 0.5 mg/kg
PO q12h), and pimobendan (0.25 mg/kg PO q12h).
Use of Thyroid Hormone in Primary Cardiac Disease
Cardiac disease may induce a state referred to as nonthyroidal
illness in dogs89,90 and humans,91 wherein plasma thyroid hormone
concentrations are decreased in the absence of thyroid gland dys-
function. In people, the decrease in serum T3 concentrations is
proportional to the severity of heart failure.92 Compared with many
other tissues, the myocardium is relatively deficient in deiodinases
necessary for conversion of T4 to the metabolically active T3 in
quantities sufficient to maintain a normal intracellular concen-
tration of T3 when the plasma concentration of T3 is reduced. This
finding, along with the positive inotropic, chronotropic, and lusitrop-
ic effects of thyroid hormones, has led many researchers to postulate
that supplemental administration of thyroid hormone or a thyro-
mimetic may be helpful in treating severe cardiac disease. Con-
siderable research with experimental heart failure supports potential
benefits of T3 in improving cardiac function.93 Initial studies in
humans have been promising, with improvement in left ventricular
function and neurohormonal status after supplementation with T3
or T4 in patients with DCM and CHF.94 –97 Unacceptable adverse
effects were seen in a large-scale study of administration of a thyroid
analog, but this could reflect overdosage rather than an unavoidable
effect.98 In the single published veterinary study, 19 dogs in CHF
from DCM were given a standard treatment of digoxin and furo-
semide or the standard treatment plus propranolol and levothy-
roxine. The difference in survival times between the groups was
not statistically significant,99 although because sample size was
small and variability in survival times was large, it is possible that
the study was not sufficiently powered to detect clinically relevant
differences. There is no indication for use of thyroid hormone in
euthyroid dogs with CHF until further research is conducted.
Conclusion
Thyroid hormones enhance myocardial contractility and diastolic
function. They also influence the peripheral vasculature, resulting
in abnormal heart sounds, arrhythmias, altered left ventricular
function, and hypertension in patients with hyperthyroidism.
Hypothyroidism generally results in opposing changes, including
a reduction in heart rate and myocardial contractility. Both hyper-
thyroidism and hypothyroidism can contribute to or cause CHF.
Most of the changes are reversible when the endocrinopathy is
controlled, but more severely affected animals may require specific
treatment for heart failure or hypertension.
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 Cardiovascular Effects of Thyroid Disease

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1. Which of the following is not a cardiovascular effect of 6. Which of the following is the recommended initial
thyroid hormone? treatment for severe hypertension in a hyperthyroid cat
a. increased responsiveness to sympathetic stimulation showing evidence of target organ damage?
b. increased contractility a. atenolol
c. increased myocardial oxygen consumption b. benazepril
d. arteriolar vasoconstriction c. furosemide

2. Which of the following would be a highly unlikely finding d. amlodipine

during auscultation of a hyperthyroid cat?
7. ___________ is not a potential cardiovascular effect of
a. atrial fibrillation hypothyroidism.
b. gallop rhythm a. Myocardial fibrosis
c. tachycardia
b. Decreased myocardial contractility
d. heart murmur
c. Enhanced diastolic ventricular function
3. Which is the most common echocardiographic change in d. Increased peripheral vascular resistance
hyperthyroid cats?
8. A(n) ___________ is the most common ECG change in
a. decreased fractional shortening
hypothyroid dogs.
b. left ventricular posterior wall hypertrophy
a. prolonged Q-T interval
c. right atrial enlargement
b. increased T-wave amplitude
d. septal hypertrophy
c. decreased R-wave amplitude
4. How should the initial dose of levothyroxine be adjusted
d. absent P wave
for a hypothyroid dog in congestive heart failure (CHF)?
a. No dose adjustment is necessary. 9. Which of the following would be the most reasonable
b. Approximately double the standard initial dose of palliative treatment for atherosclerosis in a hypothyroid
levothyroxine should be administered. dog?
c. Approximately 25% of a standard initial dose of a. levothyroxine supplementation and a low-fat diet
levothyroxine should be administered as an initial dose. b. furosemide and an angiotensin-converting enzyme inhibitor
d. A dog in CHF should never receive supplemental c. amlodipine and a β blocker
levothyroxine.
d. levothyroxine supplementation and a novel-protein diet
5. Which of the following would be the most appropriate
therapy for ameliorating excessive tachycardia secondary 10. In dogs, CHF secondary to hypothyroidism is consistently
to hyperthyroidism before anesthesia for thyroidectomy? associated with __________________.

a. atenolol a. atrioventricular block.

b. benazepril b. atrial fibrillation.
c. furosemide c. systemic arterial hypertension.
d. amlodipine d. jugular venous distention.

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