Cardiovascular Journal of Africa: Vol 27 No 3 (May/June 2016)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 3, May/June 2016 AFRICA e5
A case of enoxaparin-induced thrombocytopaenia during
treatment of acute myocardial infarction
Snag Yup Lim, Se Ryeon Lee, Yong Hyun Kim, Jin Seok Kim, Seong Hwan Kim, Jeong Chun Ahn,
Woo Hyuk Song
Abstract
Heparin-induced thrombocytopaenia is a life-threatening
complication, affecting the morbidity and mortality of the
patient if not properly treated. We report a case of a
75-year-old female patient who experienced enoxaparin-
induced thrombocytopaenia during medical treatment of
acute ST-segment elevation myocardial infarction due to
thrombotic total occlusion in the large right coronary artery.
Keywords: heparin, thrombocytopaenia, myocardial infarction
Submitted 12/9/15, accepted 17/2/16
Published online 12/4/16
Cardiovasc J Afr 2016; 27: e5–e8
DOI: 10.5830/CVJA-2016-010
Thrombocytopaenia often occurs in critically ill patients. While
therearemany reasons for it, heparin-induced thrombocytopaenia
(HIT) is one of the most fatal complications, characterised
by the occurrence of thrombocytopaenia in conjunction with
thrombotic manifestations after exposure to unfractionated
heparin (UFH) or low-molecular-weight heparin (LMWH).1 The
incidence of the HIT syndrome in patients exposed to heparin
varies widely, depending on the preparation of the heparin and
its concentration, varying from 0.2 to 5%.2
Clinical presentation of the HIT syndrome ranges from
asymptomatic thrombocytopaenia to a variety of intravascular
thromboses and embolisms after exposure toheparin. Thrombosis
can affect both the arterial and venous system, however, venous
thromboembolic complications are much more serious than
arterial thrombotic events. Without alternate anticoagulation,
the risk of thromboembolic complications can be seen in 30
to 75% of patients, and about 10 to 20% of patients suffer
disseminate intravascular coagulation (DIC).3 The mortality rate
associated with the HIT syndrome (HITS) is approximately 5 to
10%, usually secondary to thrombotic complications.4
The risk of HITS is higher in women and surgical patients
compared with medical patients, and five- to 10-fold higher
in patients receiving UHF compared to LMWH.5 Although
rare, LMWH-induced thrombocytopaenia can occur and some
cases have been reported in acute coronary syndrome. Here,
we report a case of a patient who experienced enoxaparin-
induced thrombocytopaenia during medical treatment of acute
myocardial infarction.
Case report
A 75-year-old female visited the emergency department with
chest pain of 12 hours’ duration. She had no other significant
medical or family history except mild arthritis in both knees.
Her initial electrocardiogram showed a normal sinus rhythm
with Q wave and ST-segment elevation in leads II, III and aVF.
The echocardiogram demonstrated hypokinesia of the inferior
wall of the left ventricle.
In the laboratory tests, the haemoglobin level was 12.7 g/dl,
white blood cell count was 13.4 × 103 cells/μl and the platelets
were 302 × 103 cells/μl. Initial coagulation studies showed a
normal range. The initial level of CK-MB was 85.4 U/l and
troponin-I was 20.2 ng/ml. Her clinical diagnosis was acute
ST-segment elevation myocardial infarction of the inferior wall.
An emergent coronary angiogram (CAG) revealed total
thrombotic occlusion of the proximal right coronary artery
(RCA) (Fig. 1). The RCA was engaged with a 7-Fr guiding
catheter (AL1, Cordis, Miami Lakes, Florida, USA) and
predilatation was carried out with a Sprinter 3.0 × 20-mm
balloon (Medtronic, Minneapolis, MN, USA) after a loading-
dose injection of intracoronary abciximab.
After the procedure, the total thrombotic occlusion was still
present, so we repeated thrombus aspiration with a thrombus
extraction catheter (Thrombuster, Kaneka Medical Corp, Japan)
and repeated the ballooning. The thrombotic occlusion did not
improve and we decided on the second-stage procedure after
one week of enoxaparin therapy in the intensive care unit.
The patient was treated with aspirin, clopidogrel, statin and
enoxaparin for one week.
A follow-up CAG (Fig. 2) and intravascular ultrasound
(IVUS) were done after seven days of enoxaparin therapy, and it
still revealed thrombi in the large RCA, despite the enoxaparin
Department of Internal Medicine, Ansan Hospital, Korea
University, Dan Won-Gu, Ansan, GyoungGi-Do, Korea
Snag Yup Lim, MD, PhD
Se Ryeon Lee, MD
Yong Hyun Kim, MD
Jin Seok Kim, MD
Seong Hwan Kim, MD
Jeong Chun Ahn, MD
Woo Hyuk Song, MD,
Case Report