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.