Cardiovascular Journal of Africa: Vol 24 No 2 (March 2013)

CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 2, March 2013

e12

AFRICA

patients with normal coronary arteries without predisposing

factors for coronary artery disease. In these patients, the acute

release of inflammatory mediators can induce either coronary

artery spasm without an increase in levels of cardiac enzymes

and troponins, or coronary artery spasm progressing to acute

myocardial infarction with raised cardiac enzymes and troponins.

The type II variant (coronary thrombosis) includes patients

with culprite but quiescent pre-existing atheromatous disease.

In these patients, the acute release of inflammatory mediators

can induce coronary artery spasm with normal levels of cardiac

enzymes and troponins, plaque erosion, or rupture, manifesting

as acute myocardial infarction.

Until now, KS was found to be related to poisons, venoms,

drugs and contrast agents. Among these, antibiotic-related acute

coronary syndrome is rare. It has been reported commonly only

with penicillins in the course of an anaphylactic shock where

coronary hypoperfusion and epinephrine-induced vasospasm

were strongly proposed to explain the underlying mechanism of

myocardial injury.

3,4

However, allergy-induced acute coronary events in the

absence of anaphylaxis are increasingly encountered in clinical

practice, suggesting mast cell-based vasospasm as the principal

mechanism.

It is also hypothesised that there is a threshold

level of mast cell content above which it could provoke

coronary artery spasm and plaque rupture. This threshold level

is closely associated with the allergen concentration, the patient’s

sensitivity and the route of antigen entrance.

3,6

There are studies reporting that IgE antibodies with different

specificities can have an additive effect, and corresponding

antigens can trigger mediator release when the patient is

simultaneously exposed to them. This suggests that atopic

individuals are more vulnerable to coronary artery spasm than

normal people.

3,5

The management of KS may be challenging for clinicians, and

unfortunately guidelines have not been established yet. Patients

with KS need treatment with steroids, antihistamines, fluid

resuscitation, possibly epinephrine, oxygen and antithrombotics

before transfer to the cardiac catheterisation laboratory.

The treatment should both dilate coronary vessels and

suppress the allergic reaction. Vasodilator drugs, including

nitrates and calcium channel blockers, should be considered as

first-line therapy in young and previously healthy individuals,

since vasospasm is the primary mechanism.

Acute coronary syndrome protocol should be followed in

patients with the type II variant. These patients should be

followed up in cardiology and allergy clinics following hospital

discharge. A full cardiology work-up, including a 12-lead ECG,

echocardiogram and cardiac risk-factor modification is necessary.

In our patient, myocardial injury occurred in the absence of

an anaphylactic reaction, strengthening the suspicion of mast

cell-based pathophysiology. On the other hand, his chest pain

developed suddenly without any apparent allergic reaction,

suggesting a possible local effect of ampicillin and amoxicillin,

individually or in combination, directly on the coronary mast

cells. This sole cardiac involvement may represent another aspect

of allergic reactions, ranging from urticaria to anaphylaxis.

Reasons for the variability in clinical manifestations of this

syndrome are currently under research. The absence of coronary

lesions on the angiogram and a positive skin-prick test for

B-lactams indicated coronary spasm and type 1 variant of KS

in our case.

To the best of our knowledge, this is the first case in the

literature describing the association between this syndrome and

penicillin simultaneously administered orally and parenterally.

This report, as well as others,

show that this unique disease should

be entertained when acute-onset chest pain is accompanied by

allergic symptoms, electrocardiographic changes, and increased

levels of markers of myocardial damage.

Conclusion

All patients admitted to emergency departments with chest pain,

ST-segment changes on electrocardiography and/or increased

markers of myocardial necrosis should be investigated for

allergic insults.

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