|
Sick sinus syndrome (SSS) is a primary conduction abnormality
resulting from sinoatrial node disease (1,2).
The syndrome has been described by many terms, including ‘sluggish sinus
syndrome,' ‘lazy sinus syndrome,' ‘bradycardia-tachycardia syndrome,' and
‘sinoatrial syncope' (3),
illustrating the variability of electrocardiographic (ECG) presentations.
The pathophysiological basis of the syndrome has yet to be fully
elucidated, with most cases being deemed idiopathic (4).
Many dogs and people with SSS also appear to have coexisting
dysfunction of the atrioventricular (AV) nodal and intraventricular
subsidiary pacemakers, resulting in a failure to generate appropriate
escape rhythms (1,3,5).
The syndrome so far has been reported in humans and dogs. Canine cases
are mostly described in older female miniature schnauzers, dachshunds,
cocker spaniels, west highland white terriers and pugs (2,5).
The inability of the animal to maintain an adequate heart rate, when
there is pathological change affecting all pacemakers, contributes to the
generation of clinical signs, such as weakness, stumbling, confusion, and
syncope (6,7).
This report describes SSS in a bull terrier that was considered to have
concurrent mitral valve endocardiosis and hypothyroidism.
A 6.5-year-old, desexed, female bull terrier was investigated for an
arrhythmia detected during a routine examination. Two years previously,
she had been diagnosed with hypothyroidism on the basis of a low free
thyroxine (fT4) level of 6 pmol/L (reference range 8 to 25 pmol/L).
Thyroxine supplementation was given at 36 μg/kg body weight (BW),
q24h, PO. A year later, she was evaluated for hyperactivity, and an
arrhythmia was auscultated. Results from a blood analysis at this time
indicated thyrotoxicosis with an fT4 concentration of 35 pmol/L;
subsequently, the thyroxine supplementation was reduced to 22 μg/kg
BW, q24h. Results from a repeat analysis done 6 wks later showed that
circulating levels of fT4 were still high (fT4 = 29 pmol/L), so the dose
was further reduced to 15 μg/kg BW, q24h. Another repeat analysis of
fT4 8 wks later (14 wks after the initial presentation) showed a normal
concentration of 20 pmol/L; however, the arrhythmia was still present.
The arrhythmia was characterized as an irregularly irregular bradycardia;
heart rate (HR) was 45 beats/min (bpm). Peripheral pulse was consistent
with the heart rate and no murmur was detected. Radiographs of the thorax
showed mild generalized cardiomegaly with no evidence of pulmonary venous
congestion or edema. The pulmonary parenchyma appeared normal.
Resting ECG (Figure
1) tracings revealed bradycardia (40 to 60 bpm), sinus pauses of
typically 2 to 4s, atrial premature contractions (APCs), and junctional
escape beats. Provocative cardiac testing was carried out. The dog was
exercised by running for 2 min, after which another tracing was recorded.
There were no significant changes from the resting trace. Vagal maneuvers
(including applying ocular pressure and carotid sinus massage) were
performed while the heart was being auscultated, but they failed to
elicit a response. Atropine was then administered at 0.04 mg/kg BW, IM,
and tracings were taken 20 mins later (Figure
2). A normal HR of approximately 135 bpm, with loss of the sinus
pauses, resulted. The post atropine ECG showed QRS complex grouping, with
more frequent APCs, where coupling of systole consists of 2 beats in
rapid succession (11),
as every sinus beat is coupled with an APC in a fixed interval.
Echocardiographic measurements showed mild, eccentric hypertrophy of
the left ventricle and dilation of the left atrium and auricle.
Subjectively, the right atrium also appeared to be enlarged. The mitral
valve was thickened and mildly nodular. No abnormality was detected in
contractility with fractional shortening of ventricular muscle fibers
measured as 31%.
The patient was discharged without any further investigation or
therapy, due to the lack of definable clinical signs.
Four months later, an episode of syncope lasting 45 s occurred after
exercise. On being questioned, the owners recalled times when the dog had
been seen shaking, was depressed, and was a little inappetent. On
auscultation, there was more variation in the HR, ranging from 45 to 80 bpm,
with the higher count being attributable to the presence of extra
systoles. The apex beat and the pulse were strong, and, clinically, in
hospital the dog appeared normal.
The history strongly suggested episodic weakness and a syncopal
episode, so the tests performed 3 mo earlier were repeated, with the
addition of a color Doppler echocardiogram. The results of the tests were
very similar to those of the initial presentation. The color Doppler
echocardiograph showed increased velocity of diastolic blood flow through
the mitral valve and evidence of mild turbulence, and although no
regurgitant jets could be identified, it was considered supporting
evidence for the presence of mild mitral valve regurgitation. The dog
still had no detectable cardiac murmur.
Due to the mild clinical signs, conservative treatment consisting of
exercise restriction was recommended. No further clinical signs were
reported at a 2-month follow-up consultation.
A specific cause for the arrhythmia could not be determined. Many
cases are idiopathic (4),
although extracardiac causes, such as autoimmune, metabolic, endocrine,
and neurological disturbances, must be considered, especially in sinus
dominated bradycardia (2,7).
A transient SSS due to thyrotoxicosis has been recorded in humans (7,8),
which raises the possibility that the concurrent thyrotoxicosis may have
played some role in the generation of this condition; however, the
abnormality persisted after the dog was euthyroid. To the author's
knowledge, the association of sinoatrial node dysfunction and
thyrotoxicosis in dogs has not been reported.
Causal associations for SSS in humans include anatomic changes, and a
variety of illnesses and drug effects (9).
There are clinical associations with digitalis toxicity, surgical
manipulation resulting in high vagal tone in people, and certain breed
associations are noted in dogs (4,10,11).
Clinical signs of the disease are variable with dogs being aclinical
or showing syncope, seizures, and episodic weakness (6,12).
Syncope is reported as the chief complaint, resulting from asystolic
episodes of greater than 4 to 6 s or tachycardic episodes resulting in
ineffective ventricular filling (3).
The ECG characteristics were consistent with some of those described
for SSS (4)
and additional diagnostics showed that neither the sympathetic nor the
parasympathetic nervous systems had a strong influence on the arrhythmia.
Vagal maneuvers did not result in significant sinus pauses, and atropine
response was normal in rate but not rhythm, implying a conduction
disturbance rather than excessive parasympathetic tone.
The systolic beats seen on the resting ECG trace may result from a
supraventricular ectopic focus, which is characterized by negative P
waves (11).
The atria in this dog were enlarged, although a cause was not determined.
The APCs seen during the ECG trace are part either of the SSS; atrial
distension from bradycardia-induced volume overload or mitral
regurgitation, resultant of ectopic foci; or a combination of the above.
Treatment for those cases that are aclinical or showing minimal
clinical signs is not usually implemented (1).
It may be argued in this case that the evidence underlying cardiac
disease as mild cardiomegaly and mitral valve regurgitation was an
indication for treatment. In cases of SSS where treatment is indicated by
the presence of clinical signs, it is possible to divide patients into 2
subsets: those having primary bradycardia and sinus arrest (as in this
case) and those showing the bradycardic-tachycardic form. Cases with
primary bradycardia that respond to the atropine response test, resulting
in an improved baseline HR or tachycardia, can be trialed on oral
anticholinergics (5,13).
This would have been a treatment option for this case, although
documented responses are inconsistent and syncopal episodes may persist
after treatment (2,13).
Anticholinergics may cause undesirable side effects of constipation,
pupillary dilation, and eye and mucous membrane dryness. Pacemaker
implantation is the treatment of choice for most SSS (1,5).
If the pacemaker option is not feasible, treatment should be aimed at the
dominant arrhythmia (in this case the bradycardia), although caution has
to be exercised in that treatment of one arrhythmia may aggravate others
(1).
This is well illustrated by this case in that treating the
bradyarrhythmia with atropine improved the sinus rate but increased the
frequency of APCs.
The prognosis associated with SSS is guarded if treated medically, as
responses are typically poor. This dog was not treated medically due to
the mild nature of her clinical signs, although it is likely that in the
long term, treatment will be necessary. CVJ
|
