Vol.2, No.9, 1085-1086 (2010) Health
doi:10.4236/health.2010.29159
Copyright © 2010 SciRes. Openly accessible at http://www.scirp.org/journal/HEALTH/
Myocardial infarction in antiphospholipid antibody
syndrome
Davide Lazzarini*, Luca Morolli, Jonathan Montomoli, Giorgio Ioli
Third Department of Medicine, Santarcangelo di Romagna, Azienda USL di Rimini, Rimini, Italy; *Corresponding Author:
davide. [e-mail]
Received 1 December 2009; revised 13 May 2010; accepted 15 May 2010.
ABSTRACT
A 52-year-old man was admitted to hospital with
chest pain after physical activity. Emergency
coronary angiography showed multiple throm-
boembolic occlusions in the anterior descen-
ding coronary artery and in the right coronary
artery. Further testing revealed anticardiolipin
and 2-glicoprotein antibodies (the patient had
been diagnosed for ulcerative colitis and poly-
myalgia rheumatica). Heparin and nitrate were
administered intravenously in addition to oral
aspirin and metoprolol. Soon after, the patient
referred a withdrawal of chest oppression, and
his general clinical condition rapidly stabilised.
A follow-up examination was performed 9 mon-
ths later the discharge: he had resumed most of
his activities and sieric concentration of lupus
anticoagulant antibodies and anticardiolipin an-
tibodies, IgM isotype, were decreased.
Keywords: Antiphospholipid Antibody Syndrome;
Myocardial Infarction; Anticardiolipin Antibodies;
2-Glicoprotein Antibodies
1. INTRODUCTION
Antiphospholipid antibody syndrome is a disorder of co-
agulation characterized by recurrent vascular thrombosis,
pregnancy loss and thrombocytopenia associated with
persistently elevated levels of antiphospholipid antibodies.
Antiphospholipid antibodies are a heterogenous group of
immunoglobulins IgG, IgM or, less frequently IgA.
Antiphospholipid antibody syndrome is present if there
are at least one of the clinical criteria (vascular thrombo-
sis, pregnancy morbidity) and one of the laboratory cri-
teria (lupus anticoagulant, anticardiolipin antibody, anti
2-glicoprotein antibodies) [1]. Antiphospholipid anti body
syndrome falls into two main classifications: PRIMARY,
if there are no other autoimmune disorder such as syste-
mic lupus eythematosus (the cause of primary antipho-
spholipid syndrome in unknowm, but some factors are
associated with developing antiphspholipid antibodies,
such as infections, certain drugs or genetic predisposi-
tions); SECONDARY, if there are other autoimmune
disorders [2], such as systemic lupus erythematosus.
2. CASE REPORT
A 52-year-old man was admitted to our hospital with a
20-hour history of angina pectoris and dyspnoea. He
referred chest pain following physical activity for seve-
ral days.
Family medical history was insignificant.
The patient had been diagnosed for ulcerative colitis
(1995) and polymyalgia rheumatica (2000). In 2001 the
patient tested positive for lupus anticoagulant antibodies.
Further testing revealed elevated titlers of anticardiolipin
antibodies (89 U/ml ; NV = < 28 U/ml); 2-glicoprotein
antibodies (100 MU/ml; NV = < 17 MU/ml) and rheu-
matoid factor (190 U/ml ; NV = < 15 U/ml). Both the an-
ticardiolipin and the 2-glicoprotein antibodies were
IgM isotypes. No clinical symptoms of venous thrombo-
sis were found. In 2002, the lupus anticoagulant antibo-
dies were absent, and the patient was diagnosed for
ischemic dilated (congestive) cardiomyopathy with occ-
lusion of the distal portion of the anterior descending
coronary artery. Prior to hospitalization the patient was
taking prednisone 5 mg diem, lysin acetylsalicylate 75
mg diem and mesalazin 4 g periodically.
On clinical examination, the patient had a normal
body temperature, a blood pressure of 100/60 mmHg, a
heart rate of 78 beats/min and a respiratory rate of 22
breath/min. Heart beats were regular without murmurs,
bruits or gallops, while lung auscultation revealed fine
and coarse crackles. He reported muscle aching and a bit
of stiffness in the neck, shoulders and upper arms. The
rest of his examination was normal.
The electrocardiogram showed a QS pattern without
ST elevation in leads V1-V6, DII and aVF. An emergency

D. Lazzarini et al. / HEALTH 2 (2010) 1085-1086
Copyright © 2010 SciRes. Openly accessible at http://www.scirp.org/journal/HEALTH/
1086
echocardiogram demonstrated hypokinesis of the anterior,
lateral and septal walls.
Emergency coronary angiography showed multiple
thromboembolic occlusions in the distal circumflex and
anterior descending coronary artery and in the marginal
branch of the right coronary artery. Haemoglobin was 11
g/dl (NV = 12 g/dl); white blood cell count was 13 ×
103/l (NV = 8 – 10 × 103/l) and platelets were 317 ×
103/l (NV = 150 – 400 × 103/l). Partial Thromboplastin
Time was 27.3 sec ( NV = 25 – 39 sec) and the Interna-
tional Normalized Ratio was 1.3 (NV = 0.8 – 1.2).
Creati-nine Kinase－MB peaked at 140 U/l (NV = 5 –
130 U/l).
Heparin and nitrate were administered intravenously
in addition to oral aspirin and metoprolol. Soon after, the
patient referred a withdrawal of chest oppression, and
his general clinical condition rapidly stabilised. The
patient was discharged from the hospital on the seventh
day with only aspirin therapy at 325 mg/die [3].
A follow-up examination was performed 9 months
later. The patient was well and had resumed most of his
activities. The clinical examination was normal. The C-
reactive protein level was 6.76 mg/l, and sieric concen-
tration of lupus anticoagulant antibodies and anticardio-
lipin antibodies, IgM isotype, were 30.5 U/ml.
3. DISCUSSION
We believe this case report to be of some interest because
it underlines some unusual aspects of secondary antipho-
spholipid antibody syndrome such as the absence of
venous thrombosis, multiple thromboembolic occlusions
of coronary arteries without interest elsewhere [4,5], the
temporary absence of the lupus anticoagulant antibodies
and the absence of thrombocytopenia. Another interes-
ting fact is the contemporary presence of antiphospholi-
pid antibody syndrome and polymyalgia rheumatica,
independent diseases rarely present in the same patient
[6].
The diagnosis of definite antiphospholipid antibody
syndrome requires the presence of at least one of the
clinical criteria and at least one of the laboratory criteria.
However, no limits are placed on the interval between
the clinical event and the positive laboratory findings [7].
In this patient the antiphospholipid antibody syndrome
was diagnosed by the presence of one clinical (episodes
of coronary thrombosis with angina) and two laboratory
criteria (anticardiolipin IgM antibodies present in the
blood on two occasions at least six weeks apart; lupus
anticoagulant antibodies detected in the blood on two
occasions at least six weeks apart).
This case-report underlines the presence of antiphos-
pholipid antibody as a risk factor in ischemic cardiopathy.
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