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.