CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 3, April 2012
e14
AFRICA
Heart failure and cardiogenic shock associated with the
TB-immune reconstitution inflammatory syndrome
CHRIS KENYON, NESHAAD SCHRUEDER, MPIKO NTSEKHE, GRAEME MEINTJES
Abstract
Heart failure has not been described in the setting of
TB-immune reconstitution inflammatory syndrome (IRIS).
We describe a case of cardiogenic shock in the setting of
TB-IRIS four weeks after commencement of antiretroviral
therapy. Possible aetiologies and pathophysiology as well
as suggested diagnostic and therapeutic approaches to this
problem are discussed.
Keywords:
TB-IRIS, heart failure, HIV, antiretroviral
Submitted 4/6/11, accepted 11/9/11
Cardiovasc J Afr
2012;
23
: e14–e17
DOI: 10.5830/CVJA-2011-062
Case report
A 34-year-old man was diagnosed with pulmonary tuberculosis
(TB).
Mycobacterium tuberculosis
(susceptible to rifampicin
and isoniazid) was cultured from his sputum. After commencing
the intensive phase of TB treatment (rifampicin, isoniazid,
pyrazinamide and ethambutol) his TB symptoms improved.
He tested HIV seropositive and his CD
4
count was 34 cells/ml.
He commenced antiretroviral therapy (ART) with stavudine,
lamivudine and efavirenz two weeks after starting TB treatment.
Four days after ART initiation he developed a dry cough,
worsening shortness of breath, central cramping abdominal
pains, and recurrence of drenching night sweats.
He was admitted to another hospital and was treated with
high-dose cotrimoxazole and prednisone 80 mg daily for a
presumptive diagnosis of
Pneumocystis jiroveci
pneumonia
(which in our opinion was an incorrect diagnosis). ART was
temporarily interrupted then restarted. He initially responded
to this therapy, but symptoms worsened five days after he had
completed a 14-day course of prednisone. Over the next few
days, he developed progressively worsening shortness of breath
as well as orthopnoea, paroxysmal nocturnal dyspnoea and pedal
oedema. He was then referred to our facility, four weeks after the
initiation of ART.
On admission, he was in severe cardiogenic shock. His
peripheries were cold and radial pulses were not palpable. His
systolic blood pressure, detectable only on palpation, was 60
mmHg. He had a regular heart rate of 130 beats/min. His apex
beat was laterally displaced, diffuse and hypokinetic, his jugular
venous pressure was elevated 10 cm and there was a third heart
sound. On chest auscultation there were extensive bilateral
coarse crepitations. He had tender hepatomegaly.
A chest radiograph showed worsening of the right mid-zone
infiltrate that had been present prior to ART and was related
to his pulmonary TB, as well as a marked increase in the
cardiothoracic ratio (Fig. 1). Echocardiography confirmed a
globally dilated heart with a fractional shortening of 13%. The
ECG on presentation showed sinus tachycardia with a heart rate
of 122 beats/min (Fig. 2). The QRS axis was –30 degrees, there
was evidence of both left atrial and left ventricular hypertrophy
by Cornell criteria,
1
the QTc interval was prolonged at 453 ms,
and there were widespread non-specific T-wave abnormalities.
No other QRS or ST-segment abnormalities were noted.
A cardiac magnetic resonance image (MRI), performed
after the patient was stabilised, showed no evidence of focal
inflammation in the myocardium. The left ventricular ejection
fraction was 15% on the MRI. Renal function was normal,
haemoglobin was 10.6 g/dl, white cell count was 2.3
×
10
9
/l,
platelet count was 163
×
10
9
/l and thyroid stimulating hormone
level was 3.16 mU/l (normal range
=
0.49–5.66). There was
no history of significant ethanol abuse to suggest alcoholic
cardiomyopathy.
Two diagnoses were made. Firstly, we made a diagnosis of
paradoxical TB-associated immune reconstitution inflammatory
syndrome (TB-IRIS). This was supported by his initial diagnosis
of drug-susceptible pulmonary TB, his response to TB treatment
Department of Medicine, GF Jooste Hospital, Cape Town,
South Africa
CHRIS KENYON, MB ChB, PhD,
NESHAAD SCHRUEDER, MB ChB
GRAEME MEINTJES, MB ChB
Division of Infectious Diseases and HIV Medicine,
Department of Medicine, University of Cape Town,
South Africa
CHRIS KENYON, MB ChB, PhD
GRAEME MEINTJES, MB ChB
Department of Medicine, University of Cape Town,
South Africa
NESHAAD SCHRUEDER, MB ChB
Division of Cardiology, Department of Medicine, University
of Cape Town, South Africa
MPIKO NTSEKHE, MB ChB
Institute of Infectious Diseases and Molecular Medicine,
University of Cape Town, South Africa
GRAEME MEINTJES, MB ChB
Imperial College London, UK
GRAEME MEINTJES, MB ChB
Case Report
