Successful catheter ablation of premature ventricular contractions triggering torsade de pointes in a small infant with histiocytoid cardiomyopathy: a case report

Figure 1. Electrocardiograms taken for the diagnosis and during ablation. (A) Twelve lead electrocardiograms after the accessory pathway ablation. (B) Torsade de pointes triggered by a short-coupled premature ventricular contraction (240 ms). (C and D) Two premature ventricular contractions (premature ventricular contraction 1 and premature ventricular contraction 2) that were triggering torsade de pointes. (E) Positive correlation between atrial pacing cycle length and coupling interval of the triggering premature ventricular contractions. The coupling interval of the triggering premature ventricular contraction was 265 and 237 ms during atrial burst pacing of 150 and 190 b.p.m., respectively. (F and G) Successful ablation of each premature ventricular contraction. The pre-potentials preceding the ventricular electrograms were recorded during both sinus rhythm and premature ventricular contractions. The arrows indicate the pre-potentials.

Figure 2. Fluoroscopy in the RAO and LAO views. (A) Right ventricular angiography. (B and C) Successful ablation of two premature ventricular contractions, premature ventricular contraction 1 and premature ventricular contraction 2. The origins of these two premature ventricular contractions were the apex and mid-level of the right ventricle. Electrode catheters were positioned at the bundle of His, right ventricle, left atrium, and persistent left superior vena cava. The inflow and outflow conduits of the left ventricular assist device were mounted in the left ventricular apex and aorta (A, B, and C).

Figure 3. Histological findings. (A) Haematoxylin–Eosin stain. The arrows indicate the clusters of vacuolated cells. These cells were surrounded by histiocytoid cells characterized by their large, round shape, pale eosinophilic or foamy cytoplasm, and irregular, centrally located round nuclei. (B) Desmin stain. The enclosed spaces contain histiocytoid cells lightly stained in blue. These histiocytoid cells were found throughout both ventricles. Fibrotic changes were hardly noted except in the endocardium. (C) Macroscopic view of the ablation site in the right ventricle. The arrow indicates the ablation site where the tissue has turned white. (D) Masson’s trichrome stain. Transmural lesions were replaced by fibrous tissues in the right ventricular wall but not in the epicardium.