CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 3, April 2012
AFRICA
e3
Spontaneous coronary artery dissection associated with
Leriche syndrome
CY KARABAY, MM CAN, IH TANBOGA, SM AUNG, A KALAYCI, C GECMEN, C KIRMA
Abstract
Spontaneous coronary artery dissection (SCAD) is a rare
cause of acute coronary syndrome. SCAD has been observed
in three groups of patients; those with coronary atheroscle-
rosis, women in the peripartum period, and those with an
idiopathic cause. SCAD may also be associated with other
conditions. Herein, we present a 44-year-old man who devel-
oped SCAD concomitant with Leriche syndrome.
Keywords:
spontaneous coronary artery dissection, Leriche
syndrome
Submitted 13/4/10, accepted 15/5/11
Cardiovasc J Afr
2012;
23
: e3–e5
DOI: 10.5830/CVJA-2011-012
Spontaneous coronary artery dissection (SCAD) is a rare cause
of acute coronary syndrome and sudden cardiac death.
1
SCAD
has been described in young women during the peripartum period
and in women using oral contraceptive pills.
1
The majority of
cases of SCAD appear to be idiopathic, although dissections have
been linked to Marfan’s syndrome, atherosclerotic cardiovascular
disease, blunt chest trauma, intense physical exercise, use of
contraceptives, Kawasaki disease, systemic lupus erythematosus
and other conditions. The management of these patients has
been controversial. Here, we present a 44-year-old man who
developed SCAD concomitant with Leriche syndrome.
Case report
A 44-year-old man presented to our emergency department
with pain in the chest and left arm of two days’ duration. He
had hypertension, hyperlipidaemia and a 20-pack-year history
of smoking but no history of coronary artery disease. He
had intermittant claudication of approximately three months’
duration.
His ECG showed pathological Q waves and deep T waves on
Cardiology Clinic, Kartal Kosuyolu Heart and Research
Hospital, Istanbul, Turkey
CY KARABAY, MD,
MM CAN, MD
IH TANBOGA, MD
SM AUNG, MD
A KALAYCI, MD
C GECMEN, MD
C KIRMA, MD
the precordial leads. Transthoracic echocardiography revealed
hypokinesia of the anterior, anteroseptal and apical walls of the
left ventricle with an ejection fraction of 40% (by Simpson’s
method). Concurrent biochemical markers were consistent with
myocardial necrosis (TnI: 17.1 ng/dl, reference: 0–0.1 ng/ml).
On physical examination, the bilateral femoral arteries could
not be palpated. Coronary angiography was performed via the
brachial artery due to the absence of pulsations of the femoral
arteries. Coronary angiography showed a flap-like filling defect
in the middle third of the left anterior descending artery (LAD)
(Fig. 1) but no plaque was detected in the LAD. We did not
perform IVUS to exclude plaques with positive remodelling.
An atherosclerotic plaque was noted in the distal segment of the
right coronary artery (RCA). Aortography showed the occlusion
of the abdominal aorta at the infra-renal level (Fig. 2).
The levels of AT III, proteins C and S, plasminogen,
fibrinogen, and factor V Leiden were evaluated for thrombophilia
and found to be normal. Markers of autoimmune disorders
such as complement, cryoglobulins, antinuclear, antineutrophil,
cytoplasmic, anti-DNA and antiphospholipid antibodies were
also found to be negative. Therefore atherosclerosis was assumed
to be the underlying pathology of the distal aortic occlusion.
Cardiac positron emission tomography, performed after
the patient had stabilised, revealed no viable myocardium. We
planned medical treatment for the coronary artery disease and
aorto-bifemoral bypass for the peripheral disease.
Fig. 1. Coronary angiography showing flap-like filling
defect in the middle third of the left anterior descending
artery (arrow).
Case Report
