CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 7, August 2012
e4
AFRICA
Case Report
HIV infection, pulmonary arterial hypertension and
pregnancy: a fatal triad
MYAT TUN LIN NYO, LEANN SCHOEMAN, RAVEENDRA SOOKHAYI, BONGANI M MAYOSI
Abstract
A 30-year-old pregnant HIV-seropositive woman presented
with symptoms and signs suggestive of severe pulmonary
arterial hypertension, with a fatal outcome. Histological
features of pulmonary arterial hypertension were present
at post mortem. This is the first report of histologically
confirmed HIV-associated pulmonary arterial hypertension
associated with pregnancy in Africa.
Keywords:
HIV infection, pulmonary arterial hypertension,
pregnancy
Submitted 25/10/11, accepted 5/3/12
Published online 29/5/12
Cardiovasc J Afr
; 2012;
23
: e4–e6
DOI: 10.5830/CVJA-2012-020
Case report
A 30-year-old black African woman presented at 32 weeks of
pregnancy (gravidity 2 and parity 1) complaining of shortness of
breath, orthopnoea and a dry cough for a period of two months.
She was known to be human immunodeficiency virus (HIV)
seropositive with a CD
4
cell count of 252 cells per
μ
l, for which
she was taking zidovudine. She had no history of hypertension,
heart or lung disease.
On admission, her blood pressure was 120/80 mmHg, pulse
110 beats per minute and respiratory rate 30 breaths per minute.
She had a raised jugular venous pressure, praecordial signs of
pulmonary hypertension (i.e. systolic right parasternal lift, and
loud pulmonary component of the second heart sound) with
tricuspid incompetence and pulsatile hepatomegaly.
Examination of the chest was normal. The chest radiograph
revealed cardiomegaly with a right ventricular configuration and
clear lung fields, while the ECG displayed sinus tachycardia,
right-axis deviation, right ventricular hypertrophy and T-wave
inversion in leads V1–4 (Fig. 1).
Portable echocardiography showed a dilated right atrium
and right ventricle with no structural valvular lesions. A full
echocardiographic study with estimation of pulmonary arterial
pressure by Doppler was not performed because the patient was
too ill to be transported to the cardiac clinic echocardiography
laboratory. Small wedge- and crescent-shaped sub-segmental
perfusion defects were reported in both right and left upper lobes
on radionuclide lung perfusion scan. A diagnosis of pulmonary
embolism with pulmonary hypertension was made and she was
treated with a continuous infusion of unfractionated heparin.
She remained tachypnoeic despite therapeutic anticoagulation
over the ensuing six days. On the seventh day, she became
hypotensive, requiring intravenous inotropic support with
adrenaline infusion. Intra-uterine foetal death was diagnosed
at this stage. Labour was induced, and she delivered a stillborn
infant six hours later. An hour after delivery she suffered a
cardiac arrest and all resuscitation efforts were unsuccessful.
Post mortem examination excluded major pulmonary
embolism, pulmonary infarcts or pneumothorax. No deep-vein
thromboses were present in the calves or pelvic venous plexus.
The diagnostic finding was plexiform lesions of the pulmonary
vasculature indicative of advanced HIV-associated pulmonary
arterial hypertension (PAH) (Fig. 2A–D). Right ventricular
hypertrophy was present, in keeping with cor pulmonale.
Department of Medicine, Groote Schuur Hospital and
University of Cape Town, Cape Town, South Africa
MYAT TUN LIN NYO, FCP (SA)
BONGANI M MAYOSI, DPhil, FCP (SA),
Department of Obstetrics and Gynaecology, Groote Schuur
Hospital and University of Cape Town, Cape Town,
South Africa
LEANN SCHOEMAN, FCOG (SA)
Division of Anatomical Pathology, Department of Clinical
Laboratory Sciences, University of Cape Town, Cape Town,
South Africa
RAVEENDRA SOOKHAYI, MB BCh
Fig. 1. Sinus tachycardia, right-axis deviation, right
ventricular hypertrophy and T-wave inversion in leads
V1 –4.
