Left ventricular paced activation in cardiac resynchronization therapy patients with left bundle branch block and
Brian J Wisnoskey1, Niraj Varma1
1Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
Insights
Cardiac resynchronization therapy (CRT) pacing effects are unpredictable. Optimized CRT requires considering individual patient factors beyond standard measures for effective left ventricular (LV) pacing.
Area of Science:
- Cardiology
- Electrophysiology
- Medical Devices
Background:
- Cardiac resynchronization therapy (CRT) uses left ventricular (LV) pacing to synchronize delayed LV activation in patients with myocardial disease.
- Understanding intrinsic LV activation delays is crucial, but responses to LV stimulation and influencing factors remain unclear.
Purpose of the Study:
- To investigate how QRS duration, morphology, LV substrate, and electrode choice affect LV stimulation responses.
- To test the interactions between intrinsic LV activation and paced conduction times.
Main Methods:
- Evaluated intrinsic activation delay (qLV) and paced LV conduction times in 120 heart failure patients with LBBB undergoing CRT.
- Used device-based measurements at proximal and distal LV bipoles with quadripolar LV leads.
Main Results:
- Intrinsic qLV showed minimal variation, but 30% had conduction barriers, often functional and resolving with pacing.
- LV-paced conduction times were longer than intrinsic, unrelated to QRS morphology, and varied by electrode pair and etiology.
- Poor correlation was found between intrinsic activation delay (qLV) and LV-paced conduction time (R² = 0.278).
Conclusions:
- The impact of LV pacing in CRT is not reliably predicted by current standard measures.
- Individualized assessment during CRT optimization is essential for effective LV pacing.
Background:
Cardiac resynchronization therapy (CRT) uses left ventricular (LV) pacing to restore rapid synchronized LV activation when it is delayed in patients with myocardial disease.
Objective:
Although intrinsic LV activation delays are understood, little is known about reactions to LV stimulation and whether they are affected by QRS duration (QRSd), morphology, LV substrate, or choice of electrode pair. The purpose of this study was to test these interactions.
Methods:
In 120 heart failure patients with left bundle branch block (LBBB) and QRS >120 ms receiving CRT with quadripolar LV leads, device-based measurements of intrinsic activation delay (qLV) and paced inter- (and intra-) LV conduction times were evaluated at the proximal and distal LV bipoles.
Results:
During intrinsic conduction, qLV varied little between the proximal and distal pairs in patients with LBBB (n = 120; age 68 ± 11 years; 63% male; ejection fraction 25% ± 7%; 33% ischemic cardiomyopathy; QRSd 162 ± 19 ms). A minority (30%) had conduction barriers (ie, gradients) (ΔqLV 29 ± 8 ms vs 9 ± 5 ms in patients without gradients; P <.01), which occurred equally in ischemic and nonischemic patients. A majority were functional (and not scar-mediated), as they resolved with pacing in most patients (75%). Importantly, LV-paced conduction times were unrelated to baseline QRS morphology (LBBB 166 ± 30 ms vs RBBB control 172 ± 30 ms; P = NS), longer than intrinsic conduction (166 ± 30 ms vs 129 ± 28 ms; P <.01), and varied significantly by electrode pair (ie, small distances) and etiology. Correlation between intrinsic activation delay (qLV) and LV-paced conduction time was poor (R2 = 0.278; P <.05).
Conclusion:
LV-paced effect, which is core to CRT, is unpredictable based on conventionally used measures and should be considered during CRT optimization.
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