CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 1, February 2012
e16
AFRICA
Coronary muscular bridge mimicking acute stent
thrombosis
CY KARABAY, AC AYKAN, A GÜLER, E ALIZADE, A KALAYCİ, R ZEHIR, C DUNDAR
Abstract
A patient who develops hypotension or angina pectoris after
intravenous inotropic agents should be assessed for dynamic
left ventricular outflow obstruction or the presence of a
muscular bridge. In this case report, we present a patient
with low ejection fraction who developed hypotension and
angina pectoris with inotropic therapy after coronary inter-
vention. We performed a coronary angiogram to exclude
stent thrombosis but a muscular bridge was found in the
segment distal to the stent.
Keywords:
coronary myocardial bridge, dynamic LVOT obstruc-
tion, stent thrombosis
Submitted 4/12/10, accepted 16/2/11
Cardiovasc J Afr
2012;
23
: e16–17
DOI: 10.5830/CVJA-2011-005
The coronary arteries normally run through epicardial apidose
tissue but sometimes they may partially course through the
myocardium. This congenital condition is known as myocardial
bridge (MB). The segment of the coronary artery covered by the
MB is called a tunnelled artery. It has an angiographic or patho-
logical incidence of 0.5 to 2.5% and 15 to 85%, respectively.
1
The left anterior descending coronary artery (LAD) is usually
affected.
2
Generally, myocardial bridge is a benign condition, but it
may cause angina, ischaemia, infarction, arrhythmia and sudden
death.
3
The symptoms are considered to be caused by coronary
ischaemia attributed to a reduction in blood flow subsequent to
coronary compression by the MB during systole or by delayed
arterial relaxation in diastole, or both.
4
Case report
Here we report a case of muscular bridge mimicking acute stent
thrombosis. A 54-year-old hypertensive patient was admitted
to a local hospital with acute anterior myocardial infarction.
Emergency coronary angiography was performed, which showed
thrombosis in the proximal segment of the LAD. After adminis-
tration of 600 mg clopidogrel and 5 000 units unfractioned hepa-
rin, a 3.0
×
25-mm paclitaxel eluting stent was deployed in the
LAD at 12 atm and, simultaneously, a 2.0
×
15-mm balloon at 12
atmwas applied to the diagonal branch, using the kissing method.
The patient was referred to our clinic for further intensive
care because of hypotension (80/60 mmHg) and bilateral basal
crepitate rales (Killip class II). On admission to the clinic, he
complained of chest pain and the physical examination showed
bilateral basal crepitate rales. He was tachycardic (110 beats/
min) and hypotensive (75/45 mmHg).
We did not find any dynamic change in the ECG. Decreased
left ventricular function (hypokinesia of the anterior, anteroseptal
and apical wall) with a left ventricular ejection fraction of 46%
(with biplane Simpson method) and no pericardial effusion were
apparent on transthoracic echocardiography. His haemogram
was normal without a decline in the haematocrit.
Intravenous fluid therapy and a dopamine infusion at a rate of
10 mcg/kg/min as an inotropic agent were started on the patient.
After titration of the dopamine dose to 20 mcg/kg/min, his blood
pressure declined progressively to 60/30 mmHg and there was a
dynamic change in the ECG (appearance of biphasic T waves in
the precordial leads).
We again performed transthoracic echocardiography to
exclude dynamic left ventricular outflow tract obstruction
(LVOT). It demonstrated akinesia of the anterior, anteroseptal
and apical regions, with an ejection fraction of 36% (with biplane
Simpson method) and there was no obstruction in the LVOT.
As the situation suggested acute stent thrombosis, the patient
was immediately transferred to the angiography laboratory.
Coronary angiography showed a patent stent without any disrup-
tion of the coronary blood flow. A muscular bridge was located
in the middle segment of the LAD, which was causing 80%
stenosis.
The clinical scenario suggested that the sustained drop in
arterial blood pressure and occurrence of chest pain with the
change in ECG was due to the myocardial bridge. By causing
tachycardia, increasing the myocardial oxygen demand and
contractility of the myocardium, dopamine had augmented the
ischaemic effect of the myocardial bridge, which further caused
the sustained hypotension, occurrence of chest pain, segmentary
wall motion abnormality and ishaemic change in the ECG.
As beta-blockers are the mainstay of therapy for a muscular
bridge,
5
we stopped the dopamine infusion, and administered 10
mg intravenous esmolol, together with intravenous fluids. After
Cardiology Clinic, Koşuyolu Heart and Research Hospital,
İstanbul, Turkey
CY KARABAY, MD, karabaymd @ yahoo.com
AC AYKAN, MD
A GÜLER, MD
E ALIZADE, MD
A KALAYCİ, MD
R ZEHIR, MD
C DUNDAR, MD
Case Report
