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    • br Case report The patient was an month old boy

    2019-04-26


    Case report The patient was an 11-month-old boy. No abnormalities were observed throughout the embryonic stage and perinatal period. When he was 11 months and 10 day old, he suddenly developed pallor and poor responsiveness, with his eyes rolled back in his head, which continued for approximately 1min. He later developed a fever above 38°C and was brought to a nearby clinic, continually exhibiting mild clouding of consciousness. When he was brought to our emergency center on the same day, we suspected febrile seizure and performed an electroencephalogram (EEG). The results were normal, and he was discharged. Cardiac arrhythmia was detected the following day when he visited the outpatient unit of the pediatric department of our hospital, with the electrocardiogram (ECG) showing a wide QRS complex tachycardia. The patient was hospitalized for observation and further examination. Physical findings on admission showed that height was 78cm, body pkg inhibitor weight was 9745g, and blood pressure (during sinus rhythm) was106/60mmHg, with no other abnormality. Laboratory findings were as follows: CRP: 0.3mg/dl; CPK: 52 IU/l; CPK-MB: 14.0 IU/l; TP: 6.7g/dl; Alb: 4.4g/dl; GOT: 62 IU/l; GPT: 24 IU/l; LDH: 379 IU/l; ALP: 399 IU/l; Cr: 0.24mg/dl; BUN: 7mg/dl; Na: 138 mEq/l, K: 4.9mEq/l; Cl: 103 mEq/l; Troponin-T: (+); BNP: 767.0pg/ml; HANP: 330.0pg/dl; RBC: 6.02×106; Hct: 42.1; Hgb: 12.4; WBC: 14,600 (Segs: 33.0%; Bands: 1.0%; Lymph: 63.0%). ECG during sinus rhythm showed a pkg inhibitor rate of 110/min and right bundle branch block with extreme right axis deviation (Fig. 1(a)), while during tachycardia there were 2 kinds of QRS morphology on ECG. One had the QRS complex of left bundle branch morphology with tachycardia rate of 160/min, and the other had the QRS complex of right bundle branch with tachycardia rate of 172/min (Fig. 1(b) and (c)). Echocardiogram after hospitalization showed that the left ventricular muscle was edematous with increased intensity, and mild hypokinesis was noted. The ejection fraction of the left ventricle was 50%. The left ventricular end-diastolic diameter was 36mm, and the left ventricular end-systolic diameter was 29mm. Tachycardia occurred after midnight on the second day of hospitalization, which showed a wide QRS complex with both right and left bundle branch blocks. Blood pressure during tachycardia was around 80mmHg. A slight clouding of consciousness was observed, but it did not develop into a loss of consciousness. Intravenous administration of lidocaine and propranolol had no effect on this tachycardia; therefore, we started a continuous intravenous drip of procainamide. Because the blood sample that was taken on that day had tested positive for cardiac troponin T, we considered the possibility of myocarditis and administered gamma globulins. Tachycardia was temporarily controlled by continuous intravenous administration of procainamide, but recurred after 2 day and lasted. We increased the dose of intravenous procainamide. Tachycardia was controlled again, but after several days, tachycardia attacks recurred frequently. Tachycardia remained refractory even after raising the dose of procainamide to 90μg/kg/min. We observed no significant increase in CPK or CPK-MB throughout the clinical course.
    Electrophysiological findings and catheter ablation Three electrode catheters were inserted via the right femoral vein into the high right atrium (HRA), His bundle area (HBE), and right ventricle (RV), and 1 electrode catheter was inserted via the right femoral artery into the left ventricle (LV). Electrical stimulation was applied through the electrodes and the intracardiac electrograms were recorded. Both rapid pacing and programmed extrastimulation were applied during sinus rhythm and tachycardia at twice the diastolic threshold with a pulse width of 2ms. CardioLab (GE Healthcare, Little Chalfont, England) was used to record the intracardiac electrograms during EPS. Based on the above findings, we concluded that the mechanism of this tachycardia must be reentrant ventricular tachycardia caused by bundle branch reentry using the left bundle branch as the retrograde limb and the right bundle branch as the antegrade limb. The right bundle branch was considered the critical circuit of the ventricular tachycardia. Therefore, we started mapping the right bundle branch for catheter ablation. However, the hemodynamics compromised and the systolic pressure had dropped to 60mmHg due to ventricular tachycardia. Moreover, as more mapping procedures were performed, fewer tachycardia episodes were observed. Hence, we decided to perform catheter ablation of the right bundle branch during sinus rhythm. Because the patient had presented with an incomplete right bundle branch block pattern during the sinus rhythm, it was impossible to use the onset of right bundle branch block as the index for ablation efficacy. Therefore, we performed linear ablation of the right bundle branch using the right bundle branch potential as an indicator based on changes of duration and morphology of the QRS complex.