Discussion:
Acute MI in the teenage years of life is a rare phenomenon. Data on AMI
in young adults is limited to few case reports3. In
these cases the etiology of MI was either hypercoagulable state,
autoimmune disease or coronary spasm, dissection or coronary
embolization2-8.
S. Osula reported a case of 16 year old boy presenting as AMI,but
the etiology was hypercoagulable state resulting from nephrotic
syndrome3. A case of 23 years old male presenting with
AMI was reported by Mustafa cetin. Etiology of AMI in this case
was Behcet‘s disease4. Vale PR reported a case
of spontaneous coronary artery dissection involving the left circumflex
artery in a young adult male presenting with a myocardial infarction
after exercise6. L Abid et al found primary
antiphospholipid syndrome (APLS) as a causative factor of AMI in two
young adults7. Coronary artery embolism was the cause
of acute MI in the setting of an existing ASD in a case reported byJonathan Kei2 . A case of AMI in a boy of age
similar to our patient was reported by S. Ouali et al . In this
case, coronary artery disease was associated with aneurysmal dilatation
in the carotid, vertebral and right renal arteries and it was diagnosed
as aortoarteritis.9
None of these case reports attributed AMI to atherosclerosis. In the
present case AMI occurred in a teenaged girl, who is non-smoker, non
drug abuser, no evidence of hypercoagulability, autoimmune disease and
coronary anomalies. Absence of these factors, a very strong family
history of CAD and presence of plaque in LAD were strong indicators
towards atherosclerosis as the cause of AMI in this patient.
To the best of our knowledge, this is the first case report of AMI in a
teenage girl occurring because of atherosclerosis. The data regarding
the incidence of atherosclerosis CAD in this age is limited but the
reported incidence (15–19 years) is 2% (all males) (8). There is no
reports of atherosclerosis causing AMI in teenaged girl.