CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 2, March 2012
AFRICA
e11
Case Report
The perils of pharmacological treatment for obesity:
a case of sibutramine-associated cardiomyopathy
and malignant arrhythmias
COLIN L SCHAMROTH
Abstract
A 58-year-old woman presented with severe left ventricular
dysfunction and malignant arrhythmias after taking combi-
nation drug treatment for weight loss. The combination
treatment included sibutramine, liothyronine, hydrochloro-
thiazide diuretic, metformin and fucus. The effect of these
drugs individually and in combination is discussed, with
particular reference to it being a malignant combination. The
patient showed reversability of the left ventricular dysfunc-
tion and negative ventricular stimulation studies after cessa-
tion of the drug concoction.
Keywords:
sibutramine, cardiomyopathy, ventricular fibrillation
Submitted 3/11/10, accepted 16/2/11
Cardiovasc J Afr
2012;
23
: e11–e12
DOI: 10.5830/CVJA-2011-003
Case report
A 58-year-old woman presented to the emergency department
complaining of shortness of breath and generalised fluid reten-
tion. Although her illness was acute, she had had major fatigue
and weakness for the past three to four months. She had never
been in hospital before and there was no history of hypertension,
hypercholesterolaemia, ischaemic heart disease, or any chronic
illness. She was a smoker of 20 cigarettes per day for many
years. She denied taking any medication. Her systolic blood
pressure was just over 100 mmHg and she was in overt conges-
tive cardiac failure with peripheral oedema, pulmonary crackles
and abdominal ascites.
A chest X-ray showed a moderate-sized left pleural effusion
and underlying features of pulmonary congestion. The ECG
taken on arrival showed only a sinus tachycardia. However, soon
after arrival she developed atrial fibrillation at a rate of just
under 200 beats per minute. She was immediately admitted to
the intensive care unit. A bedside echocardiographic evaluation
showed a mildly dilated but globally myopathic left ventricle
with an ejection fraction of 15%. Significant mitral and tricuspid
valve regurgitation was present.
She was placed on intravenous infusions of amiodarone,
dobutamine and furosemide. Laboratory investigations showed
a normal full blood count, renal function, glucose levels, mildly
deranged liver functions compatible with hepatic congestion,
and a suppressed thyroid stimulating hormone (TSH) level of
<
0.01
µ
IU/ml, with normal T3 and T4 levels. The lipogram was
normal. The pro-BNP level was elevated at 5 969 pg/ml. The
d-dimer, troponin-T test and cardiac enzymes were all normal.
Coxsackie viral titres were not elevated and a vasculitis work up
was negative.
By the following morning she was back in sinus rhythm
but was still hypotensive. She was started on oral low doses of
vasodilating beta-blockers (carvedilol) and an ACE inhibitor
(perindopril). She diuresed almost 5 l in the first two days. Renal
function remained normal, and potassium levels were maintained
at above 4 mmol/l.
Coronary angiography undertaken on the third hospital day
showed normal coronary arteries. The ejection fraction was 16%
with global hypokinesis. On the morning of the fourth day she
was haemodynamically stable and discharged to the general
ward. Later on that afternoon she had a ‘funny turn’. She was
non-responsive for about one or two minutes and became cold
and clammy. She was neurologically intact.
An ECG done immediately following this event showed her
to be in sinus rhythm. It was suspected that she may have had
an arrhythmia and was taken back to the ICU for monitoring.
Shortly after arrival she developed ventricular fibrillation. She
was immediately electrically cardioverted and the amiodarone
infusion re-commenced. Serum potassium measurements were
again normal. Over the course of the next 90 minutes she had
three bouts of ventricular fibrillation, each requiring urgent
cardioversion. Intravenous magnesium sulphate and calcium
were given and she seemed to settle down, with evidence of high-
grade ventricular ectopy.
In view of the persistent hypotension, with trepidation, a low
dose of oral sotalol (40 mg) was given orally, while the other
beta-blockers were stopped. She did not have any further major
arrhythmias but persisted in a low cardiac output state with
hypotension despite intravenous inotropic support. Diuresis was
dependent on a furosemide infusion.
In view of her not being in respiratory distress and maintain-
ing normal oxygen saturations, it was decided against intubation
and ventilation. She was considered for implantation of a left
ventricular assist device (LVAD), and it was decided that this
would be done should there be any further deterioration. She was
Milpark Hospital, Johannesburg, South Africa
COLIN L SCHAMROTH, MB BCh (Wits), FCP (SA), MMed (Wits),
