Discussion

Chest pain is a common finding in children and adolescents. Chest pain caused by heart disease is rarely seen among childhood, varies from 1 to 4%.^{Reference Selbst, Ruddy, Clark, Henretig and Santulli1,Reference Saleeb, Li, Warren and Lock2} Cardiac cause may be associated with life-threatening conditions and risk of sudden cardiac death.^{Reference Reddy and Singh3,Reference Friedman and Alexander4} Cardiac chest pain is seen in the precordial region, accompanied by palpitations or syncope, which can spread to the back, neck, jaw, or arms. In our patient, he had a chest pain suggesting cardiac-related chest pain which was no change with position nor respiration, described as a pressure in the chest and radiated in his left shoulder, left arm, and back. Cardiac causes of chest pain are cardiomyopathy, myo/pericarditis, pulmonary hypertension, arrhythmias, severe aortic/pulmonic stenosis, mitral valve prolapses, pulmonary embolus, cocaine uses, sympathomimetic overdose, and congenital/acquired coronary anomalies.^{Reference Selbst, Ruddy, Clark, Henretig and Santulli1–Reference Reddy and Singh3} The underlying cardiac disease should be suspected when sudden onset of pain or characteristics of chest pain with post-cardiac surgery and family members with sudden and early death histories. Our patient had a history of stenting due to aortic coarctation and aortic root replacement owing to aortic stenosis. Although troponin I levels taken after chest pain were normal, chest pain caused by cardiac reason was a high suspicion as a result of underlying cardiac history and characteristic of chest pain.

Acute coronary syndrome is extremely rare in childhood and adolescents. Etiologic factors for myocardial infarction in paediatric population are congenital/acquired coronary artery abnormalities (Kawasaki disease, myocardial bridging, anomalous origin of the coronary artery, fistulas, atresia, or stenosis of coronary artery), CHD, thrombosis susceptibility, poor coronary perfusion associated with perinatal asphyxia, hypoxia and sepsis, inflammatory conditions (myocarditis, systemic lupus erythematosus), genetic disorders (homocystinuria, progeria, mucopolysaccharidosis), and familial hypercholesterolemia.^{Reference Reddy and Singh3,Reference Osula, Bell and Hornung5}

Because of the thrombogenicity of mechanical valves, patients with prosthetic mechanical valve may develop acute coronary syndrome. In aortic root replacements like Bentall operation, coronary steal complications such as kinking or pseudo aneurysms should be assessed. Mechanical heart valves are long-lived, and anticoagulant therapy is necessary and may cause bleeding or embolic complications if dose adjustment is not performed properly. In children, difficulties of dietary control and blood clotting tests need close monitoring.^{Reference Khitin, Sade, Bradley, Crawford, Widener and Stroud6,Reference Levis, Schultz and Lee7} Typical chest pain, ischaemic electrocardiogram findings with raised cardiac enzymes in patients with mechanical valves, and acute coronary syndrome should be suspected. Echocardiography showed normal systolic functions and no wall motion abnormality. When the patient’s history is deepened, it was learned that he was not using his medicine properly. It is important to take a detailed history of adolescent patients’ compliance with drug use. In addition, low international normalised ratio level led us to perform coronary angiography for coronary thrombus.

Management of acute coronary syndrome requires an urgent and careful approach. Close monitorisation of haemodynamic parameters (blood pressure, ECG and arrhythmia monitoring, pulse and saturation control) should be done. Oxygen treatment should be given if necessary and pain relief should be performed. Medical treatment with thrombolysis (streptokinase), antiplatelet drugs, and anticoagulation can be used. Percutaneous transluminal coronary angioplasty and stenting may be required in selected cases to reperfusion of coronary artery.^{Reference Nakazone, Tavares, Machado and Maia8,Reference Kiernan, Flynn and Kearney9} In our patient, the combination of anticoagulant and antiplatelet was sufficient in the treatment of thrombosis, and no additional interventional therapy was needed.