CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 3, April 2012
e8
AFRICA
plaque, thereby leading to acute STEMI.
3,9,11
Despite divergent
results on STEMI risk in small studies on carriers of the 4G allele
of PAI-1, a large-sized meta-analysis has showed a relationship
between PAI-1 4G/4G and the development of STEMI.
3
Several platelet allo-antigen systems reside on glycoproteins
IIb and IIIa, of which the HPA-1 system is important. However,
there are conflicting data about the relationship between HPA-1
polymorphisms and STEMI.
12,13
HPA1a or HPA-1b phenotypes
may induce platelet aggregation and binding to fibrinogen,
thereby increasing the risk of STEMI.
12
Coronary spasm can lead to acute STEMI with normal
coronary arteries, in association with thrombotic complications,
especially in patients with variant angina. Its ergonovine-
induced prevalence may increase by 20 to 55% in acute
coronary syndromes.
14
We did not provoke coronary spasm with
ergonovine because of its potential risks; however, there was a
catheter-induced spasm in the right coronary artery.
Accordingly, we concluded that coronary spasm was most
likely to have induced the occurrence of acute STEMI in
the presence of a prothrombotic state in our case. However,
it is unclear whether multiple gene polymorphisms without
simultaneous evaluation of their phenotypes may be associated
with arterial thrombotic events.
Conclusion
Multiple gene polymorphisms associated with the prothrombotic
state may contribute to the development of acute STEMI in
adolescents who have a tendency to coronary spasm. Dual
antiplatelet or anticoagulant therapy in addition to a calcium
antagonist may be considered in such patients with recurrent
cardiac events.
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