DISCUSSION
Coronary artery injury is a rare but important complication of RFCA in the RVOT.[1,2] Given the anatomical proximity of coronary arteries to the RVOT,[3] high-power ablation in this structure should be avoided as should excessive contact force. The use of irrigated-tip catheters may additionally increase the risk of coronary artery injury as it favors deeper lesion creation. Indeed, irrigated-tip catheters have been implicated in reported cases of LAD injury from RVOT ablation.[1,2]
There were several reasons for the delayed recognition of ST-elevation in this case. Even though the procedure was performed under conscious sedation, the patient was asymptomatic. Careful monitoring of the ST-segment is particularly important in cases using general anesthesia as patient feedback is impossible, although as this example illustrates, caution is warranted in all cases. An awareness of the risk of coronary artery injury during RVOT ablation can be crucial as ST-segment changes are usually not the focus of attention during relevant procedures and can be subtle depending on which leads are being monitored in real-time. In this case, the attention paid to distinguishing between multiple morphologically similar VTs likely distracted us from changes in the ST-segment. Furthermore, the ST-segment changes were relatively minor in leads I, III, V1, and V6, which were the leads displayed alongside intracardiac electrograms (Fig. 2B).
That acute LAD occlusion resulted in monomorphic VTs is unusual; however, their occurrence only after the onset of ST-elevation and full suppression with cardiac reperfusion strongly argue for acute ischemia as the cause. Furthermore, the morphologies of VT 2 and VT 3 suggest LV exits close to the ischemic territory, with the QRS morphologies of VT 2 and VT 3 similar to that of VT 1 but with earlier precordial transitions. Traditionally, acute ischemia causes polymorphic VT or ventricular fibrillation, whereas monomorphic VT is typically associated with myocardial scar and reentry. In the present case, however, there was no evidence of scar in the expected culprit region and both VT 2 and VT 3 were preceded by heart rate accelerations and a lack of ventricular ectopics, which may suggest a non-reentrant mechanism. Although speculative, it is possible that acute ischemia increased automaticity or triggered activity by established mechanisms, such as increases in intracellular calcium, the production of free fatty acids and oxygen free radicals, acidosis, and increased catecholamine levels.[4]
To the best of our knowledge, this is the first reported case of ischemia-related VTs attributable to acute LAD occlusion from endocardial RVOT ablation. An awareness of the risk of acute coronary artery injury and resultant ischemia-related VTs during RVOT ablation could help avoid exacerbating this complication with further RFCA, particularly as the VT morphology changes can be subtle as was seen in the present case.