Response to cardiac resynchronization therapy is determined by intrinsic electrical substrate rather than by its modification.

Marc Strik, Sylvain Ploux, Peter R Huntjens, Uyên Châu Nguyên, Antionio Frontera, Romain Eschalier, Remi Dubois, Philippe Ritter, Nicholas Klotz, Kevin Vernooy, Michel Haïssaguerre, Harry J G M Crijns, Frits W Prinzen, Pierre Bordachar
Author Information
  1. Marc Strik: IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac, Bordeaux, France; Bordeaux University Hospital (CHU), Cardio-Thoracic Unit, F-33600 Pessac, France; Maastricht University Medical Center, Cardiovascular Research Institute Maastricht, Maastricht, the Netherlands. Electronic address: m.strik@maastrichtuniversity.nl.
  2. Sylvain Ploux: IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac, Bordeaux, France; Bordeaux University Hospital (CHU), Cardio-Thoracic Unit, F-33600 Pessac, France.
  3. Peter R Huntjens: IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac, Bordeaux, France; Bordeaux University Hospital (CHU), Cardio-Thoracic Unit, F-33600 Pessac, France; Maastricht University Medical Center, Cardiovascular Research Institute Maastricht, Maastricht, the Netherlands.
  4. Uyên Châu Nguyên: Maastricht University Medical Center, Cardiovascular Research Institute Maastricht, Maastricht, the Netherlands.
  5. Antionio Frontera: IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac, Bordeaux, France; Bordeaux University Hospital (CHU), Cardio-Thoracic Unit, F-33600 Pessac, France.
  6. Romain Eschalier: Centre Hospitalier Universitaire Clermont-Ferrand, Clermont-Ferrand, France.
  7. Remi Dubois: IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac, Bordeaux, France; Bordeaux University Hospital (CHU), Cardio-Thoracic Unit, F-33600 Pessac, France.
  8. Philippe Ritter: IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac, Bordeaux, France; Bordeaux University Hospital (CHU), Cardio-Thoracic Unit, F-33600 Pessac, France.
  9. Nicholas Klotz: IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac, Bordeaux, France; Bordeaux University Hospital (CHU), Cardio-Thoracic Unit, F-33600 Pessac, France.
  10. Kevin Vernooy: Maastricht University Medical Center, Cardiovascular Research Institute Maastricht, Maastricht, the Netherlands; Radboud University Medical Center, Nijmegen, the Netherlands.
  11. Michel Haïssaguerre: IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac, Bordeaux, France; Bordeaux University Hospital (CHU), Cardio-Thoracic Unit, F-33600 Pessac, France.
  12. Harry J G M Crijns: Maastricht University Medical Center, Cardiovascular Research Institute Maastricht, Maastricht, the Netherlands.
  13. Frits W Prinzen: Maastricht University Medical Center, Cardiovascular Research Institute Maastricht, Maastricht, the Netherlands.
  14. Pierre Bordachar: IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac, Bordeaux, France; Bordeaux University Hospital (CHU), Cardio-Thoracic Unit, F-33600 Pessac, France.

Abstract

BACKGROUND: Electrocardiographic mapping (ECM) expresses electrical substrate through magnitude and direction of the activation delay vector (ADV). We investigated to what extent the response to cardiac resynchronization therapy (CRT) is determined by baseline ADV and by ADV modification through CRT and optimization of left ventricular (LV) pacing site.
METHODS: ECM was performed in 79 heart failure patients (4 RBBB, 12 QRS < 120 ms, 23 non-specific conduction delay [NICD] and 40 left bundle branch block [LBBB]). 67 patients (QRS ≥ 120 ms) underwent CRT implantation and in 26 patients multiple LV pacing site optimization was performed. ADV was calculated from locations/depolarization times of 2000 virtual epicardial electrodes derived from ECM. Acute response was defined as ≥10% LVdP/dt increase, chronic response by composite clinical score at 6 months.
RESULTS: During intrinsic conduction, ADV direction was similar in patients with QRS < 120 ms, NICD and LBBB, pointing towards the LV free wall, while ADV magnitude was larger in LBBB (117 ± 25 ms) than in NICD (70 ± 29 ms, P < 0.05) and QRS < 120 ms (52 ± 14 ms, P < 0.05). Intrinsic ADV accurately predicted the acute (AUC = 0.93) and chronic (AUC = 0.90) response to CRT. ADV change by CRT only moderately predicted response (highest AUC = 0.76). LV pacing site optimization had limited effects: +3 ± 4% LVdP/dt when compared to conventional basolateral LV pacing.
CONCLUSION: The baseline electrical substrate, adequately measured by ADV amplitude, strongly determines acute and chronic CRT response, while the extent of its modification by conventional CRT or by varying LV pacing sites has limited effects.

Keywords

MeSH Term

Aged
Aged, 80 and over
Arrhythmias, Cardiac
Body Surface Potential Mapping
Bundle-Branch Block
Cardiac Resynchronization Therapy
Electrocardiography
Female
Heart Failure
Humans
Male
Middle Aged
Treatment Outcome

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