Electrophysiologic Mechanism of Deteriorating Cardiac Function in a Patient with Inappropriate CRT Indication and Frequent Ventricular Ectopy

Abstract

An 84 y/o man had worsened symptoms (NYHA class III, LVEF 25%) following implant of a biventricular (BiV) cardioverter defibrillator (Biotronik, Lumax 540) at another institution. He also had frequent premature ventricular contractions (PVCs, 35%) that interfered with cardiac resynchronization therapy (CRT) and triggered BiV pacing. At electrophysiology (EP) study, the left ventricular (LV) lead was discovered to be within the anterior interventricular vein. His native QRS (113 ms) was much narrower than during CRT; thus, BiV pacing was disabled to allow for native conduction. The dominant clinical PVC was mapped and successfully ablated from the coronary cusps. His symptoms improved dramatically within days of the procedure and programming change. Prior to ablation, Electrocardiographic Imaging (ECGI)1-2 was applied to noninvasively map and study the mechanisms of pacing induced dyssynchrony (Figure 1) and ineffectiveness of PVC-triggered pacing (Figure 2). Figure 1 QRS morphologies (12-lead ECG) and ECGI-reconstructed epicardial activation isochrones under native sinus rhythm (Panel A, left, and Panel B) and BiV Pacing (Panel A, right, and Panel C). Note that QRS in native sinus rhythm is much narrower than for ... Figure 2 QRS morphologies (12-lead ECG) and ECGI activation Isochrone maps during PVC-triggered BiV pacing (Panel A, left, and Panel B) and spontaneous PVC without pacing (Panel A, right, and Panel C). The activation maps are shown in posterior (top, POS) and ... This patient had a narrow QRS and consequently a predictable lack of benefit from CRT and inappropriate CRT indication. Moreover, his LV lead was anterior, which several studies have demonstrated not to be optimal for CRT. Inappropriate CRT in patients with synchronous LV activation could cause pacing induced dyssynchrony, leading to deteriorating LV function. 1, 3 In the context of heart failure, ECGI has been used to map the EP substrate2, to identify potential responders/nonresponders to CRT1, and to guide electrode placement4. Unlike the global body-surface QRSd, the ECGI derived cardiac electrical dyssynchrony (ED) index, computed as the standard deviation of all activation times on the LV, quantifies the spatial dispersion of activation over the LV (ED>28 ms is a marker of electrical dyssynchrony1). As shown in the ECGI image of Figure 1, pacing from the early-activated LV anterior wall during BiV created a functional line-of-block. This forced the activation front to propagate in a U-shaped pattern around the line-of-block, causing late dyssynchronous activation of the lateral LV base. The image in Figure 2 shows that during PVC-triggered pacing, the PVC site of origin was in close proximity to the anterior LV lead, but far from the RV sensing lead, which caused delayed sensing and pacing. Thus, BiV pacing triggered by PVC failed to capture the (already activated) ventricles and was ineffective. Because in many similar cases PVCs can impede the effective delivery of continuous CRT, PVC treatment (catheter ablation or antiarrhythmic drugs) to ensure high percentage of effective BiV pacing might be considered.