**5. Cardiac enzymes**

got extremely high value for the diagnosis of MI [1, 21]. However, in Paediatric patients, the determination of Q-wave in just one derivation could even be sufficient to determine MI [21]. While these Q-waves show infarct of the myocardial wall, high R waves in V1 and/or V2 (negative Q-waves) may represent true posterior wall MI. On the ECG of approximately half of cases, pathological Q-waves have a tendency to regress with time. In newborn infants, the presence of Q-waves in derivations DII, DIII and AVF may be normal. Furthermore, if ECG leads are placed on the upper part of the chest, Q-waves can be incorrectly shown in V5–6 that can cause misinterpretation of an integral part of the evaluation of coronary artery disease [16]. Elevation of the J point that joins the QRS and the ST segment is the first finding of myocardial ischaemia [7]. Compared to baseline, an elevation of 1–2 mm of the J point and the ST segment can be determined in myocardial ischaemia. An elevation of >2 mm should rouse suspicion of MI [7]. When the clinician has suspicions on the resence of pathological Q-wave, ECG in deep inspirium can be helpful. There is a change in the voltage of the Q-waves in physiological cases while there is no change of voltage at deep inspirium in pathological Q waves [7]. Towbin et al. reported that the presence of Q-waves wider than 35 msn on ECG was the most valuable finding for MI and a diagnosis of transmural MI diagnosis should not be made in patients

Towbin et al. evaluated the ECG and clinical findings in the pre-MI records of 37 patients who died because of MI. In this retrospective study, it was reported that findings of MI were determined on the pre-mortem ECG records of 28 children who suffered fatal acute MI, while it was reported in 9 cases who died because of chronic MI [3]. It was also reported by the same authors that when MI was determined in a hypertrophic heart, the infarction was determined at the hypertrophic ventricle. This showed that in PMI, the presence of hypertrophy was a risk factor for MI. At least one of the criteria shown in the **Table 2** was determined to be present in 30 patients included into the study by Towbin et al [2]. Furthermore, no finding was determined on ECG in approximately 19% of the cases in that study, ECG was not sufficient to make a diagnosis of PMI alone. The evaluation of the patient should be made together with

Furthermore, Nakanishi et al. showed that deep Q-waves were a good marker for MI in Kawasaki patients. It was also determined in the same study that T-wave inversion in deriva-

**5.**ST segment elevation [≥2 mm] and prolonged QT interval corrected for heart rate [>440 ms] with any other criteria.

**Table 2.** Electrocardiographic findings significant for MI in children, as reported by Towbin et al.

the anamnesis, physical examination, ECG and laboratory data.

tions II, III and AVF showed MI in the inferior wall [22].

**2.**Increased amplitude or duration [>35 ms] of pre-existing Q waves

**1.**New appearance of wide Q waves >35 ms in duration

**3.**New onset Q waves in serial tracings

**4.**Q waves notching

with no Q-wave abnormalities [2].

106 Myocardial Infarction

An increase in the level of enzymes released into circulation from cells exposed to injury is important in the diagnosis of MI. These enzymes are creatine kinase myocardial band (CK-MB) and troponin [7, 10]. In all Paediatric cases thought to have myocardial damage, the troponin level should be examined. Values more than 2 ng/ml value are especially more valuable for cardiac origin [17]. Even in cases of mild damage in myocardial cells, an increase in enzyme levels may be seen [19]. In addition, the events causing an increase in troponin levels must be known (**Table 3**) [6].
