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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 3, May/June 2017
AFRICA
e7
suggest that bridging of the major coronary arteries may produce
myocardial ischaemia, coronary thrombosis and myocardial
infarction, as well as predispose the patient to atherosclerosis
or sudden death.
7,8
When symptoms occur in the presence of
myocardial bridges, they are ischaemic in nature. The diagnosis
of myocardial bridging of the LAD should be realised in patients
who have exertional angina and myocardial perfusion defect but
no coronary risk factors, especially those who are young, as in
the presentation of our patient.
The prevalence of bridging has been reported to be around
25% in necropsy studies and around 2% in angiographic studies.
Variation at autopsy may in part be attributable to the care taken
in preparation and the selection of hearts. A higher prevalence
has been observed in patients with hypertrophic cardiomyopathy
and recipients of cardiac transplants.
1,9,10
Our patient’s echo-
cardiographic examination revealed no hypertrophy.
The site, length and severity of bridging and resultant
coronary stenosis vary from patient to patient. Myocardial
bridges are located at a depth of 1–10 mm with a typical length
of 10–30 mm. Our patient had a 12-mm bridging segment of
the LAD.
For the treatment of angina caused by myocardial bridging,
beta-blockers and calcium channel blockers are preferred for
negative chronotropic and inotropic effects. We administered
metoprolol as a beta-blocker to our patient and he is presently
asymptomatic. Surgical therapy is advised for patients with
persistent symptoms and proven ischaemic changes, and for
those with high risk, such as ventricular arrhythmias, aborted
sudden death, or non-fatal myocardial infarction. There are few
reports of survival rates but, when studied, five-year survival
ranges between 85 and 98%. Our patient was followed up with
medical therapy.
The early repolarisation pattern is not always identified
on routine ECG due to the intermittent nature of early
repolarisation. For example, among 542 persons with baseline
early repolarisation who underwent repeat ECG examination
five years later, early repolarisation (
≥
0.1 mV) was not
observed in approximately 20%.
2,5
No systematic evaluation
has been undertaken reporting the prevalence of concealed
early repolarisation in the general population, and the clinical
importance, if any, of concealed early repolarisation remains
unclear. We believe that early repolarisation pattern in our
patient was due to ischaemia caused by myocardial bridging and
was not concealed.
Conclusion
Differentiating ST-segment elevation caused by acute myocardial
infarction from all other aetiologies, especially acute pericarditis–
myocarditis, and early repolarisation, can be challenging. In our
patient, anginal chest pain was thought to be due to myocardial
bridging of the LAD artery, considering the possibility of a
systolic narrowing of the coronary artery with subsequent
ischaemia. Early repolarisation pattern in the inferior leads was
deemed to result from ischaemia caused by myocardial bridging,
which is the main point of this case. Ischaemia caused by
myocardial bridging should also be considered in the differential
diagnosis of early repolarisation in young patients.
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