Cardiovascular Journal of Africa: Vol 22 No 1 (January/February 2011) - page 39

CARDIOVASCULAR JOURNAL OF AFRICA • Vol 22, No 1, January/February 2011
AFRICA
37
with medical therapy and referred for coronary artery bypass
grafting.
Discussion
KD is a febrile disorder of unknown cause with multiple
systemic manifestations, affecting primarily infants and young
children.
4
First described in Japan by Kawasaki in 1967 as acute
mucocutaneous lymph node syndrome, it has been reported with
increasing frequency around the world. Involvement of the heart
with acute myocarditis and coronary angiitis occurs in 25 to 50%
of the patients during the acute phase, accounting for most of the
mortality. However, 50% of the aneurysms regress spontaneous-
ly over a one- to two-year period, and therefore adult ischaemic
heart disease secondary to KD is infrequent and occurs mostly
in young adults.
4
Obtaining a history of childhood Kawasaki disease is quite
difficult because the diagnosis of acute KD is based on clinical
criteria only, without specific laboratory testing, and therefore
requires a high index of suspicion. In young adults, diagnosis is
based on typical features in two-dimensional echocardiography
and coronary arteriography. The former consists of local wall
motion abnormalities as a result of prior MIs and ectasia or frank
aneurysms of the proximal coronary arteries.
5,6
Echocardiography is particularly helpful in the paediatric
population, both for initial diagnosis and for long-term follow
up.
5,6
Coronary arteriography typically reveals multivessel aneu-
rysmal disease alternating with segmental stenoses, coronary
ectasia, calcifications, rich collateral circulation, and varying
degrees of left ventricular dysfunction as a sequela of multiple
MIs or myocarditis, or both.
4,6
Conclusion
We believe that our patient had KD rather than atherosclerotic
CAE, for the following reasons. (1) He had extensive triple-
vessel disease at a very early age. He was a non-smoker without
any other risk factors for atherosclerotic coronary artery disease
(CAD). This would favour KD because patients with CAE have
the typical risk profile of atherosclerotic CAD.
1-3,6
(2) Our patient
had ectasia involving all three vessels, which is rare in athero-
sclerotic CAE, but typical of KD.
1-4
In our patient, echocardiog-
raphy failed to reveal features of KD because the very proximal
left main and right coronary arteries were spared. This is not
uncommon in KD.
4,6
However, coronary arteriography clearly
demonstrated the typical findings of KD.
References
1. Hartnell GG, Parnell BM, Pridie RB. Coronary artery ectasia: its preva-
lence and clinical significance in 4993 patients.
Br Heart J
1985;
54
:
392–395.
2. Swaye RH, Fisher LD, Litwin P,
et al
. aneurysmal coronary artery
disease.
Circulation
1983;
67
:134–138.
3. Swanton RH, Thomas ML, Coltart DJ,
et al
. Coronary artery ectasia
– a variant of occlusive coronary atherosclerosis.
Br Heart J
1978;
40
:
393–400.
4. Kato H, Kawasaki T, Fujiwara H,
et al
. Adult coronary artery disease
probably due to childhood Kawasaki disease.
Lancet
1992;
340
:
1127–1129.
5. Kitamura S, Kawasima Y, Fujita T,
et al.
Aortocoronary bypass grating
in a child with coronary artery obstruction due to mucocutaneous lymph
node syndrome. Report of a case.
Circulation
1976;
53
: 1035–1040.
6. Shapira OM, Shemin RJ. Aneurysmal coronary artery disease.
Atherosclerotic coronary artery ectasia or adult mucocutaneous lymph
node syndrome.
Chest
1997;
111
: 796–799.
Letter to the Editor
Dear Sir
The review article by Owira and Ojewole
1
cites, among others,
the influence of grapefruit (juice) on amiodarone pharmacoki-
netics and pharmacodynamics. Some apparent inconsistencies
are worthy of note.
Amiodarone is not a ‘prodrug’ only. It has inherent phar-
macodynamic effects. Its major N-dealkylation metabolite,
N-desethylamiodarone (N-DEA) appears to possess even greater
pharmacodynamic effects, notably with regard to cardiac elec-
trophysiology.
The statement that concomitant ingestion of grapefruit juice
‘led to clinical prolongation of QT intervals and torsades de
pointes’ is misleading and not substantiated by the articles
cited.
2,3
On the contrary, the grapefruit-initiated inhibition of
N-DEA formation resulted in decreased cardiac electrophysio-
logical effects. It is not clear whether ‘accumulation’ of amiodar-
one resulting from inhibition of conversion to N-DEA has clini-
cal implications, but reduction in N-DEA concentrations may
compromise the anti-arrhythmic action of amiodarone.
A further observation concerns the incorrect title of the article
by Libersa
et al
.,
3
which creates the impression that amiodarone
metabolism is dramatically induced by grapefruit juice. The
converse is true.
The authors of reference number 2 above (number 14 in the
article) are incorrectly written. It should be Tsutomu U, instead
of Urano T, and Ryuichi H, instead of Hasegawa R.
FRANK OTTO MULLER, MB ChB, FFPM,
Director: R&D, Integrow Health (Pty) Ltd, George, South Africa
References
1. Owira P MO, Ojewole J AO. The grapefruit: an old wine in a new glass?
Metabolic and cardiovascular perspectives.
Cardiovasc J Afr
2010;
21
:
280–285. 
2. Saito M, Hirata-Koizumi M, Matsumoto M,
et al
. Undesirable effects
of citrus juice on the pharmacokinetics of drugs.
Drug Safety
2005;
28
:
677–694. 
3. Libersa CC, Brique SA, Motte KB,
et al
. Dramatic inhibition of amiodar-
one metabolism induced by grapefruit juice.
Br J Clin Pharmacol
2000;
49
: 373–378.
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