Skip to main content

Advertisement

ADVERTISEMENT

Clinical Images

Child Myocardial Infarction and Follow-Up Outcome after
Revascularization

Mohammad A. Rahman, MD, Habib Chaudhury, MD, Nurul Aga, MD
January 2008


Case Presentation. A 13-year-old girl from very poor socioeconomic conditions presented with a 15-day history of chest discomfort and shortness of breath at rest. Her electrocardiogram (ECG) revealed Q-wave and ST-elevation in the chest leads suggestive of myocardial infarction (MI). She was admitted but not administered thrombolytics due to her late presentation. She was normotensive, non-diabetic and a non-smoker. The patient had a family history of coronary heart disease (CHD) (Figure 1). Her body mass index was 16.4 kg/m2. Echocardiography revealed an anterior MI with inferior and posterior wall hypokinesia and a global ejection fraction of 35%. Doppler sonography of the carotid arteries revealed atherosclerotic plaque (Figure 2). Fasting plasma glucose, total cholesterol, LDL-cholesterol, HDLcholesterol, triglyceride, apolipoprotein A1, homocysteine, prothrombin time, fibrinogen, protein C, protein S, C-reactive protein and ANA were within normal limits; her plasma apolipoprotein B was reduced (48 mg/dL) and the ESR was raised. She was positive for anti-chlamydial Ab (IgG), but negative for anti-H pylori Ab (both IgM and IgG). She was diagnosed with CHD and an anterior MI with Canadian Cardiovascular Society Class IV angina. The patient was treated with an antiplatelet agent, low-molecular weight heparin (enoxaparin sodium), beta-blocker, ACE-inhibitor, furosemide, nitrates, statins, and coronary angiography was scheduled.

The coronary angiogram revealed a normal left main coronary artery, 100% stenosis in the patient’s left anterior descending coronary artery (LAD) just after its origin, a normal left circumflex artery (LCX) (Figure 3) and 85% stenosis in her mid-right coronary artery (RCA) (Figure 4). A 6 Fr 3.5 XB guide catheter (Cordis Corp., Miami Lakes, Florida) was engaged in the left main coronary artery and we attempted to introduce a BMW 0.014 inch guidewire (Guidant Corp., Indianapolis, Indiana) into the LAD, but it failed to cross. Next, a Cross-It 200 wire (Guidant) was inserted into the LAD. The LAD was predilated with a 1.5 x 15 mm balloon at 8 atm. The Cross-It 200 wire was exchanged for an ATW Marker Wire (Cordis). After dilatation in the proximal and mid segments, 2 bare-metal stents (2.5 x 18 mm at the proximal LAD and 2.5 x 13 mm at the mid LAD) were deployed in the proximal and mid segments with overlapping struts. There was no significant residual narrowing, but sluggish flow to the distal LAD remained (Figure 5). To treat the RCA, a 6 Fr 3.5 JR guide catheter was engaged, and a ATW marker wire crossed beyond the mid RCA lesion. Predilatation of the RCA was performed using a 2 x 15 mm balloon at 6 atm. A Cypher Select 2.75 x 18 mm stent (Cordis) was then deployed across the lesion at 11 atm. The final angiogram showed a good result (Figure 6). Post-percutaneous coronary intervention (PCI) medication included an eptifibatide bolus,then infusion for 24 hours, followed by low-molecular weight heparin for 5 days. After 7 days, the patient was discharged on aspirin, clopidogrel, ACE-inhibitor and carvidelol, and warfarin sodium was prescribed for 3 months.

After 6 months, although the patient was asymptomatic, we decided to perform a follow-up angiography that showed excellent patency of the Cypher stent in the RCA, and there was 45–50% in-stent stenosis at the mid-segments of the LAD stents (mild-tomoderate grade of intimal proliferation). Coronary angiography findings were supported by a follow-up stress thallium scan (Figure 7). The computed tomographic angiogram after 2 years and 4 months showed patent RCA and LAD stents (Figure 8). The patient will be followed clinically for a period of more than 30 months.
Discussion. The angiographic pattern of coronary artery narrowing and Doppler study carotid arteries confirmed this to be a case of atherosclerotic CHD. The occurrence of MI in children, although rare, has usually been reported to be due to secondary causes such as an arterial congenital anomaly (i.e., agenesis or anomalous origin of the left coronary artery, absence of the left coronary artery), vasculitis (e.g., Kawasaki’s disease), embolism, hyperlipidemia, as well as a hypercoagulability state (long-lasting nephrotic syndrome) and myocarditis.1–8

However, none of the secondary causes were found in this case. MI due to atherosclerotic CHD without any secondary cause (arteriosclerosis) in a child has not been previously reported. The conventional and emerging risk factors have been thoroughly looked into in thiscase. To our knowledge, this may be the youngest child presenting with MI due to atherosclerotic coronary artery narrowing and treated with PCI. The possible etiology for such an aggressive atherosclerotic coronary artery narrowing could be dyslipidemia (increased small low-density lipoprotein [LDL]) along with malnutrition and infection. Low Apo B level, indicating the risk of high small-density LDL particles, is a CHD risk, although cholesterol and triglyceride levels are within normal limits.9 This case demonstrates “real-world” revascularization with PCI of a 13-year-old girl who had 100% LAD stenosis just after its origin and 85% stenosis of the RCA in the distal part, with an excellent outcome at more than 2 and one-half years post-PCI. This case underscores the need for further study of the etiology of MI due to atherosclerotic CHD in early childhood. The origin of adult CHD in utero and in early childhood has been an area of considerable interest for the last decade.10,11 With better understanding of the role of chronic inflammation of vascular endothelium in atherosclerosis, it was observed that atherosclerostic CHD is not restricted to adults.12–16 However, literature on the outcomes and guidelines of PCI in children is limited.17 Revascularization by PCI in childhood CHD is challenging in terms of limited recommendations for such cases. Questions that remain to be answered include: (1) what will be the fate of the stent in the growing child; (2) how long should aspirin and clopidogrel be continued; and (3) what advice may be given regarding longterm safety regarding the use of clopidogrel, and specifically, the safety of child-bearing? This case points to the need for thorough brainstorming on such issues.

References
1. Isaka N, Nakano T. Myocardial infarction in childhood. Ryoikibetsu Shokogun Shirizu 1996;12:679–683.
2. Gredilla Diaz E, Rodriguez Perez E, Perez Ferrer A, et al. Acute myocardial infarction in childhood. Report of 2 cases. Rev Esp Anestesiol Reanim 2002;49:373–376.
3. Silva JM, Oliveira EA, Marino VS, et al. Premature acute myocardial infarction in a child with nephrotic syndrome. Pediatr Nephrol 2002;17:169–172.
4. Rigollaud JM, Jimenez M, Vallot M, et al. Myocardial infarction in a child with an anomalous left coronary artery arising from the right coronary sinus. Value of echocardiography. Arch Mal Coeur Vaiss 2001;94:499–503.
5. Deodhar AP, Tometzki AJ, Hudson IN, Mankad PS. Aortic valve tumor causing acute myocardial infarction in a child. Ann Thorac Surg 1997;64:1482–1484.
6. De Caro E, Ribaldone D. Acute myocardial infarction and residual impairment of coronary perfusion: Unusual complications of mitral endocarditis in a paediatric patient. G Ital Cardiol 1996;26:427–429.
7. Hopp L, Gilboa N, Kurland G, et al. Acute myocardial infarction in a young boy with nephrotic syndrome: A case report and review of the literature. Pediatr Nephrol 1994;8:290–294.
8. Vieira EJ, Tuppy GH, Kawamura T. Acute myocardial infarction in a 5-year old child — Mucocutaneous lymph node syndrome (Kawasaki disease). A case report. Arq Bras Cardiol 1986;46:49–52.
9. Sniderman AD. How, when, and why to use apolipoprotein B in clinical practice. Am J Cardiol 2002;90(Suppl):48i–54i.
10. Barker DJ, Bagby SP. Developmental antecedents of cardiovascular disease: A historical perspective. J Am Soc Nephrol 2005;16:2537–2544.
11. McGill HC Jr, McMahan CA, Herderick EE, et al. Origin of atherosclerosis in childhood and adolescence. Am J Clin Nutr 2000;72(5 Suppl):1307S–1315S.
12. Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr 2006;83:456S–460S.
13. Charakida M, Deanfield JE, Halcox JP. The role of nitric oxide in early atherosclerosis. Eur J Clin Pharmacol 2006;62(Suppl 13):69–78.
14. Strong WB, Rao PS, Steinbaugh M. Primary prevention of atherosclerosis: A challenge to the physician caring for children. South Med J 1975;68:319–327.
15. Berenson GS, Srinivasan SR, Hunter SM, et al. Risk factors in early life as predictors of adult heart disease: The Bogalusa Heart Study. Am J Med Sci 1989;298:141–151.
16. Biadaioli R, Bertini G, De Martino M, et al. Risk factors for atherosclerosis in childhood. Evaluation of total blood cholesterol and triglycerides in children of parents with myocardial infarction before age 45. Minerva Pediatr 1982;34:683–689.
17. Windhagen-Mahnert B, Paul T, Offner G, et al. Severe stenosis of the right coronary artery in a 15-year-old girl with type IIa hypercholesterolemia: Successful treatment with stent implantation. Z Kardiol 1997;86:727–731.


Advertisement

Advertisement

Advertisement