Ventricular premature complexes (PVCs) are common cardiac arrhythmias, often benign but sometimes indicative of underlying structural heart disease or a precursor to more serious ventricular tachyarrhythmias. While most PVCs are managed medically, catheter ablation offers a curative option for symptomatic patients refractory to medical therapy or those with high-risk PVC characteristics. This article presents a detailed case study of left ventricular (LV) summit PVC ablation performed using a stepwise approach guided by a 3D electroanatomic mapping system, focusing on the challenges presented by the proximity of the ablation site to severe coronary artery stenosis. Furthermore, we will explore the broader context of LV summit ablation, including various ablation techniques, procedural considerations, and future directions in this evolving field.
Case Presentation:
A 68-year-old male presented with frequent, symptomatic PVCs originating from the left ventricular summit. His symptoms included palpitations, chest discomfort, and reduced exercise tolerance. Electrocardiogram (ECG) revealed frequent, morphologically consistent PVCs with a left bundle branch block (LBBB) morphology. Echocardiography showed mildly reduced left ventricular ejection fraction (LVEF) of 45% and no significant valvular disease. Coronary angiography revealed severe stenosis of the proximal left anterior descending (LAD) coronary artery. Medical management with beta-blockers and amiodarone provided minimal symptomatic relief. Given the persistent symptoms and the potential for malignant arrhythmia progression, the patient underwent catheter ablation.
Procedural Approach: Stepwise LV Summit Ablation
The procedure was performed using a 3D electroanatomic mapping system (CARTO® system, Biosense Webster, Inc.) to precisely locate and ablate the PVC origin. The patient was placed under general anesthesia. Access was obtained via the right femoral vein using a 6 Fr sheath. A diagnostic catheter was used to verify the PVC morphology and confirm the origin site. Due to the proximity of the target site to the severe LAD stenosis, a careful stepwise approach was employed to minimize the risk of coronary artery injury.
Step 1: Mapping and Identification of the PVC Origin:
High-density mapping of the left ventricle was performed using a 3D mapping catheter (e.g., an irrigated ablation catheter). The mapping strategy aimed to identify the earliest activation site of the PVC, which was located at the LV summit, adjacent to the LAD stenosis. This step was crucial for precise ablation targeting. The electrogram characteristics at the LV summit confirmed the origin of the PVC. The activation time and voltage maps were carefully analyzed to define the target ablation site.
Step 2: Ablation Strategy and Technique:
Given the proximity to the LAD stenosis, a cautious approach was chosen. A small, irrigated ablation catheter (e.g., 4 mm tip) was selected to minimize the risk of thermal injury to the coronary artery. Radiofrequency ablation was delivered in short bursts (e.g., 30-60 seconds) at low power settings (e.g., 20-30 watts) to avoid excessive heat generation. The temperature was continuously monitored to prevent exceeding safe limits. Intracardiac echocardiography (ICE) was utilized throughout the procedure to visualize the catheter position relative to the coronary artery and ensure the ablation was targeted precisely.
Step 3: Post-Ablation Verification:
Following each ablation attempt, the procedure was paused to assess the effectiveness of the ablation. This involved repeated mapping to confirm the absence of PVCs. The procedure was deemed successful once the PVCs were eliminated without inducing any new arrhythmias. The patient was monitored closely post-procedure for any signs of complications.
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