CARDIOVASCULAR JOURNAL OF AFRICA • Vol 21, No 4, July/August 2010
228
AFRICA
inappropriate discharge will easily lead to the release of endog-
enous catecholamines, causing a potentially fatal sympathetic
electrical storm. For such patients, cardiac sympathectomy can
be beneficial.
6
Of course, the effectiveness of cardiac sympathec-
tomy still needs to be verified, and this treatment may be consid-
ered in patients who experience recurrent ICD discharges despite
a loading dose of beta-blocker therapy.
Some studies have shown that SSRIs can reduce the morbid-
ity and mortality of patients with depression after acute coro-
nary syndrome.
2
Autonomic regulation of cardiac function is
usually expressed by non-invasive measurements of heart rate
variability (HRV), which is a powerful independent predictor of
mortality within the first year after myocardial infarction (MI).
It was reported that HRV was significantly lower in coronary
disease patients with depression compared with non-depressed
patients.
7,8
A study showed that SSRIs facilitated the recovery of
HRV after MI.
9
With depression, chronic depletion of neurotransmitters such
as serotonin in the central synaptic clefts could lead to interrup-
tion of inhibitory inputs to central sympathetic centres, thereby
increasing sympathetic neural discharge. There is increased
sympathetic activity in patients with depression. It has been
shown that stimulation of central 5-HT receptors can also lead to
sympatho-excitation.
9
In this case, it was found that the patient no longer had ICD
discharges after an SSRI was added, possibly indicating that
SSRIs may reduce sympathetic activity and have a beneficial
therapeutic effect in CPVT. This may provide us with a novel tool
to deal with CPVT and improve the quality of patients’ lives.
8
It was reported that SSRIs had no impact on the release of
adrenaline in the hearts of patients with anxiety disorder and
panic attacks, but cardiac and whole-body norepinephrine spill-
over was significantly reduced in those subjects who initially had
elevated sympathetic activity.
10
It was also demonstrated that in
such patients with anxiety disorder and near-normal cardiac nore-
pinephrine levels, QT variability was not correlated with cardiac
norepinephrine spillover, and SSRI treatment was ineffective.
The findings of Hildreth
et al
., however, suggested that
abnormal serotonergic control of vagal input to the heart might
contribute to increased cardiovascular risk.
11
The mechanism of
anxiety or depression as the trigger(s) for arrhythmias or shock
remains unclear.
We suggest that the possible beneficial therapeutic role of
serotonin re-uptake inhibitors in the treatment of patients with
polymorphic ventricular tachycardia merits further study.
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Fig. 4. ICD discharges.
