The authors report no conflicts of interest for the published content. No funding was required or provided for this report.
Mapping and ablating premature ventricular complexes (PVCs) that originate near the great cardiac vein (GCV) and anterior interventricular vein (AIV) can pose several challenges related to the advancement and positioning of catheters within these veins, the delivery of effective lesions, and the risk of collateral injury to the left coronary arteries and left phrenic nerve. When ablation of these PVCs from inside the GCV/AIV is not possible, a systematic assessment of nearby vantage points, such as the left coronary cusp (LCC) and left ventricular (LV) endocardial breakout site, should be considered, in addition to the performance of a more invasive epicardial ablation procedure via a percutaneous pericardial puncture or thoracotomy. Several electrocardiographic, anatomic, and electrogram timing features have been shown to predict the likelihood of successful ablation from a non-epicardial site, such as the LCC or LV endocardium, but none of these spots is considered to be a perfect location. The case described here in this report is a demonstration of a safe and successful ablation of GCV PVCs from the LV endocardial breakout site using adequate power and lesion duration, even when the site was 17 mm away from the putative origin, and some previously described electrocardiographic and electrogram-based predictors of success suggested the outcome would not be positive.
In recent years, there have been considerable advances in our understanding of the various sites from which frequent monomorphic premature ventricular complexes (PVCs) can arise, and in the different ablative strategies to eliminate such PVCs. This case illustrates some of the obstacles in mapping and ablating frequent PVCs that originate near the great cardiac vein (CGV) and reviews some strategies to overcome them.
A 56-year-old male with hypertension, non-obstructive coronary artery disease, and non-ischemic cardiomyopathy (left ventricular ejection fraction (LVEF) of 45% to 50%) presented with symptoms of gradually progressive fatigue and intermittent lightheadedness for several months, and was found to have frequent monomorphic PVCs. A 24-hour Holter monitor revealed a PVC burden of 16%. In an attempt to suppress the PVCs, improve his cardiomyopathy, and ease his symptoms, metoprolol was started, but it had no significant effect on the PVCs. A decision was then made to pursue catheter ablation of the PVCs, with the presumption that they were a major contributor to the patient’s cardiomyopathy and symptoms. The PVC morphology (right bundle branch block (BBB) pattern and right inferior axis) pointed to an origin close to the left ventricular outflow tract (LVOT), while the maximum deflection index (MDI) of the PVC (0.61) and the presence of a Q-wave in lead I suggested an epicardial origin
Cardiomyopathy resulting from frequent ventricular ectopy is now a well-accepted occurrence, and this case is yet another illustration of how successful ablation of PVCs in this situation can improve LV systolic function. Certain sites appear to have a predilection for causing frequent PVCs (eg, right and left ventricular outflow tracts, atrioventricular annuli, regions adjacent to the coronary venous system, LV summit, cardiac crux, and papillary muscles); and several electrocardiographic criteria have now been developed to predict where they can be successfully ablated, enabling operators to plan a suitable mapping and ablation strategy and counsel the patient appropriately prior to the procedure. Among these criteria are the BBB pattern, axis, precordial transition, and MDI of the PVC. For example, an MDI ≥ 0.55, a Q-wave in lead I for a PVC from the anterior LV, and a broad initial R-wave in lead VI for a GCV/AIV PVC would all be suggestive of an epicardial origin.
Mapping and ablating within the coronary venous system can pose several challenges. The usual diagnostic catheters can be difficult to advance to the GCV or AIV and, occasionally, a prominent valve of Vieussens adds to this difficulty. One sometimes has to resort to a much smaller catheter (eg, a 2.5-French multipolar Pathfinder® catheter; Cardima, Inc., Fremont, CA, USA) to extensively map the GCV and AIV. The GCV and AIV are also in close proximity to the left coronary artery system, so even when an ablation catheter can be successfully positioned in the appropriate site in the CGV or AIV, it may not be safe to perform RF ablation. Coronary angiography must always be performed, because the risk of coronary artery injury increases substantially when the distance between the site of RF ablation and the artery is ≤ 4 to 5 mm.
The proximity of a vantage point to the origin of the PVC helps to determine the likelihood of successful ablation from that vantage point. When approaching a GCV/AIV PVC from the LCC, it is helpful to understand that the part of the GCV that is closest to the LCC is to the right of the more proximal segment of the GCV. Therefore, an origin close to the LCC, as compared with one farther from the LCC, would be expected to produce a deeper Q-wave in lead aVR than in lead aVL, and a taller R-wave in lead II than in lead III. Indeed, one study showed that a distance < 13.5 mm between the earliest GCV/AIV site and the closest point of the LCC, a Q-wave ratio in aVL/VR < 1.45, and an R-wave ratio in III/II < 1.13 were all predictors, albeit imperfect ones, of successful ablation from the LCC or adjacent endocardium below the LCC.
The LV endocardium below the aorto-mitral continuity is another vantage point for ablating GCV PVCs. In one study, all successful cases were characterized by an initial R-wave in the PVC in lead I, and an interval ≤ 7 ms between the earliest activations in the GCV and in the LV endocardium (ie, the “GCV-non-GCV interval”).
Frequent PVCs that originate near the GCV can be ablated successfully and safely from the LV endocardial breakout site, near the aorto-mitral continuity, even when the endocardial site is as far as 17 mm away from the putative epicardial origin, and some predictors of success based on electrocardiographic features and electrogram timing suggest otherwise.
Electrocardiogram showing the patient’s frequent PVCs.
Mapping within the coronary venous system.
Mapping in the LV endocardium near the aorto-mitral continuity.