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Abstract
Myocardial infarction is extremely rare in children. However, chest pain suspected to be cardiac in origin by the parents is a very common presenting symptom in pediatric emergency services. In this case, an electrocardiogram is very important in the differential diagnosis of cardiogenic complaints and should be carefully considered.
Keywords: Children, electrocardiography, myocardial infarction, percutaneous coronary intervention
How to cite this article: Introduction 
Myocardial infarction (MI) is extremely rare in children, so accurate incidence has not been recorded. However, chest pain suspected to be cardiac in origin by parents is a very common presenting symptom in pediatric emergency services. Hence, an electrocardiogram (ECG) is very important in the differential diagnosis of cardiogenic complaints. Identifying MI in children is more difficult than in adults and the differential diagnosis is age-dependent.[1],[2] Herein, we present an interesting case of MI and the successful lifesaving percutaneous coronary intervention (PCI), in a 10-year-old previously healthy girl.
Case Report A previously healthy 10-year-old girl presented to the hospital emergency service with chest pain and respiratory distress. She was conscious and her general condition was good on admission. On physical examination, gallop rhythm was noted. The initial 12-lead ECG revealed significant ST-segment depression in leads V3-V6 and pathological Q-waves in V2 [Figure 1]. Posterior-anterior chest radiography revealed bilateral and basally accented pulmonary edema [Figure 2]. Based on this data, she was consulted with us and referred to our hospital. The patient was brought to our center as intubated because she had an arrest on the way. A two-dimensional echocardiogram revealed dilated left atrium and ventricle with a left ventricular ejection fraction of 56% with hypokinesia of the left anterior descending (LAD) territory on admission. Therefore, she was quickly taken to the angiography unit and an emergent cardiac catheterization was performed. A selective coronary angiogram was performed using the left and right 5-French 4-cm Judkins diagnostic catheters. The catheterization showed a normal left main coronary artery (LMCA) but severe stenosis of LAD, involving both the ostium and the proximal segment. At the same time, LAD and the left circumflex (LCX) arteries had multiple atherosclerotic plaques. Retrograde collateral circulation from the right coronary artery (RCA) was shown. There was also severe atherosclerotic stenosis in the midportion of RCA [Figure 3]. A floppy guidewire (ChoICE, Boston Scientific) was advanced distally over the guiding catheter in RCA, predilatation was done with a 2 × 8 percutaneous transluminal angioplasty balloon and 2.75 × 19 mm coronary stent (Ephesos, Alvimedica) was implanted. A better dilatation and stent apposition was provided with a 3 × 8 noncompliant balloon at high pressure. The stenosis was still not fully opened, but LCA started to fill retrograde gradually [Figure 4]. We could not benefit from intravascular ultrasound or optical coherence tomography during PCI as we intervened urgently but planned to make it in the follow-up if the stent fails. The patient was consulted with cardiovascular surgery in terms of bypass surgery during the process and was considered unsuitable for surgery. The procedure was terminated, and she was taken to the intensive care unit. Anticoagulant, antithrombotic, anticongestive, antiarrhythmic, and also inotropic therapy started immediately. Very high levels of troponin I, about 2000 times of the reference range, were noticed in the laboratory. Within the following 24 h, she was extubated. A detailed and careful history was taken, but neither family history nor laboratory tests led us to the cause. Hence, she was consulted with other departments such as rheumatology, nephrology, endocrinology-metabolism, and examined in detail. Hypercholesterolemia (total cholesterol: 121 mg/dl, low-density lipoprotein: 75 mg/dl, high-density lipoprotein: 41 mg/dl, triglyceride: 151 mg/dl, and lipoprotein [a]: 27 mg/dl), hyperhomocysteinemia (homocysteine: 3.3 mmol/L), thrombophilias-prothrombotic disorders (antithrombin 3, free protein S, and protein C), collagen vascular diseases induced coronary arteritis (Takayasu's arteritis, polyarteritis nodosa, ANCA-associated vasculitis, and giant-cell arteritis), and idiopathic or inherited cardiomyopathies were ruled out. Cardiac magnetic resonance imaging and myocardial perfusion single-photon emission computed tomography revealed the early ischemia in the LCX and LAD territory. Unfortunately, we could not clarify the cause of MI. She was discharged after 2 weeks. At the first follow-up, at 1 month, we learned that her father died at the age of 50 from acute MI during this period. As a follow-up, selective coronary angiography was performed on the 6th month after PCI, and we found that restenosis did not develop. At 18 months following PCI, she was stable, had no complaints, had good exercise tolerance, and had only minor abnormalities on Holter recordings.
Figure 1: (a) ST-segment depression in leads V3-V6 and pathological Q-waves in V2 on admission and (b) electrocardiogram at discharge with pathological Q-waves in V2-V3
Figure 3: Injections of both left and right coronary arteries before PCI. The left side shows the hypoplastic LAD and LCX and the arrows show the stenotic portion of RCA. LAD: Left anterior descending, LCX: Left circumflex, RCA: Right coronary artery, PCI: Percutaneous coronary intervention
Figure 4: Percutaneous stenting of RCA and contrast injection after PCI. RCA: Right coronary artery, PCI: Percutaneous coronary intervention Discussion Acute MI is a rare cause of morbidity and mortality in childhood. It is often difficult to find the underlying reason in patients without coronary abnormalities. Although our patient had coronary involvement, we could not make a diagnosis despite our efforts.
Non-ST elevation MI is rarely accompanied by pathologic Q-waves in adults, but such a relationship has not been reported in children. Nakanishi et al. defined infarction criteria based on the amplitude, and the duration of pathological Q-waves on ECG rather than ST changes in children.[3] The development of Q-waves is the hallmark of acute MI that heralds infarction in children.[1],[4] Our patient's ECG revealed pathologic Q-waves in V2 and aVR along with ST-segment depressions in V3-V6. Hence, we thought of anteroseptal MI rather than myocarditis in diagnosis and planned an emergency catheterization.
PCI is a safe and effective procedure, often used for the treatment of complications after Kawasaki disease or pediatric congenital heart surgery.[5] Although there is no evidence base to guide treatment decisions for children with MI, adult guidelines recommend keeping the total ischemic time at 120 min or less, preferably 60 min or less. In this case, the direct PCI time for the first medical contact is 90 min or less, which is associated with improved morbidity and mortality.[6] In our patient, although RCA was diffusely stenotic, the localized and severe stenotic lesion in the distal part was suitable for PCI. However, a similar approach was not valid for the severe, ostial, and long segmental stenotic branches of LMCA.[7] During and after catheterization, she was consulted about coronary artery bypass grafting as an early management strategy, but it is decided to be ineligible in the pediatric surgery council.
Normal pediatric ECG variants and some nonischemic cardiac disorders can mimic MI, so it is important to separate them from MI in children. Hence, pediatricians should always be careful and alert about the presence of abnormal Q-waves and characteristic ST changes.
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Conflicts of interest
There are no conflicts of interest.
References 
Correspondence Address:
Assoc. Prof. Dr. Mnevver Tuğba Temel
Department of Pediatric Cardiology, Faculty of Medicine, University of Gaziantep, 27310 Gaziantep
Turkey
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/apc.apc_160_21
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