Cardiac Resynchronization Therapy
Part 2—Issues During and After Device Implantation and Unresolved Questions
Jeroen J. Bax, MD*,*,
Theodore Abraham, MD, FACC
,
S. Serge Barold, MD, FACC
,
Ole A. Breithardt, MD
,
Jeffrey W.H. Fung, MD||,
Stephane Garrigue, MD, PhD¶,
John Gorcsan, III, MD, FACC#,
David L. Hayes, MD, FACC**,
David A. Kass, MD,
Juhani Knuuti, MD, PhD,
Christophe Leclercq, MD, PhD,
Cecilia Linde, MD, PhD,
Daniel B. Mark, MD, PhD, FACC||||,
Mark J. Monaghan, PhD¶¶,
Petros Nihoyannopoulos, MD, FRCP, FACC, FESC***,
Martin J. Schalij, MD*,
Christophe Stellbrink, MD and
Cheuk-Man Yu, MD||
* Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands
Johns Hopkins University, Baltimore, Maryland
University of South Florida, Tampa, Florida
University Klinikum Mannheim, Mannheim, Germany
|| The Chinese University of Hong Kong, Hong Kong, China
¶ Hopital cardiologique du Haut-Leveque, Pessac, France
# University of Pittsburgh, Pittsburgh, Pennsylvania
** Mayo Clinic, Rochester, Minnesota
Turku PET Center, University of Turku, Turku, Finland
Hopital Pontchaillou, Rennes, France
Karolinska University Hospital, Stockholm, Sweden
|||| Duke Clinical Research Institute, Durham, North Carolina
¶¶ King’s College Hospital, London, United Kingdom
*** Hammersmith Hospital, London, United Kingdom
Stadtische Kliniken Bielefeld, Bielefeld, Germany
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Figure 1 (Top) Ventricular activation sequence using three-dimensional noncontact mapping (EnSite 3000, Endocardial Solutions, Minneapolis, Minnesota) in a patient with dilated (non-ischemic) cardiomyopathy (left ventricular [LV] ejection fraction [EF] 30%, New York Heart Association [NYHA] functional class III) with a QRS duration of 154 ms who responded to cardiac resynchronization therapy (CRT). The propagation wavefront splits when encountering a conduction block located at the LV anterior wall, resulting in delayed activation of the lateral wall. (Bottom) The virtual electrograms over the line of block are displayed. Note the fragmented or double potential electrograms. The LV lead was positioned at the basal lateral region of LV (white arrow, top). One year after CRT, the LVEF was 42%, and the patient was in NYHA functional class I. LAT = lateral.
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Figure 2 (Top) Ventricular activation sequence (right anterior oblique view [Ant]) using three-dimensional noncontact mapping (EnSite 3000, Endocardial Solutions) in a patient with ischemic cardiomyopathy (left ventricular [LV] ejection fraction [EF] 35%, New York Heart Association functional class III) with a QRS duration of 148 ms who did not respond to cardiac resynchronization therapy (CRT). (Bottom) Ventricular activation sequence (posterior view [POST]). There was no line of block or acute change in propagation direction of the depolarization wavefront detected by the mapping system. Of note, there were differences in the electrocardiogram (ECG) pattern between this patient and the patient displayed in Figure 1, indicating that the surface ECG fails to predict the activation sequences in these patients. The prolonged LV activation time in this patient may be due to the relatively slow conduction velocity in the myocardium. The LV lead was positioned in the posterolateral vein. One year after CRT, the LVEF was 34% and the clinical status of the patient unchanged.
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Figure 3 The incidence of responders to cardiac resynchronization therapy in patients with sinus rhythm (left) is higher than in patients with atrial fibrillation (right) (data based on reference 21). Black = non-responders; white = responders.
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Figure 4 Consequences of optimization of atrioventricular (AV) delay during biventricular pacing at stable heart rate. The QRS complex resulting from P1 is wide due to apical right ventricular pacing (165 ms). The aortic pre-ejection time interval (Pre-Ao1) is long; the aortic systolic phase is also long due to the wide QRS complex. The second QRS complex resulting from P2 is narrowed due to biventricular pacing leading to a shorter aortic pre-ejection time interval (Pre-Ao2) compared with Pre-Ao1. Consequently, time duration of the aortic systolic phase is reduced, and the E-wave corresponding to P3 occurs earlier (compared to P1 and P2) with a greater amplitude, indicating a better LV filling phase. Pre-Ao3 is even shorter than Pre-Ao2 due to the addition of an AV delay optimization during P3, resulting in a greater cardiac output (CO) during P3 compared with the one obtained during P2, in which biventricular pacing was delivered without AV delay optimization.
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Figure 5 Changes in mitral regurgitation according to different pacing modes. (A) Spontaneous sinus rhythm showing severe mitral regurgitation. (B) Simultaneous biventricular pacing, showing significant reduction in mitral regurgitation. (C) Further reduction of mitral regurgitation after biventricular pacing with optimized interventricular delay (left ventricular pre-activation of 20 ms).
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Figure 6 Immediate effect of cardiac resynchronization therapy (CRT) on the severity of mitral regurgitation. Color-coded Doppler echocardiography shows moderate mitral regurgitation during no pacing (CRT OFF, A) and the estimated left ventricular (LV)peak +dP/dt is 361 mm Hg/s (CRT OFF, B). During CRT, the mitral regurgitant jet is smaller, corresponding to mild mitral regurgitation (CRT ON, C). The simultaneously acquired LVpeak +dP/dt by continuous-wave Doppler echocardiography has improved significantly to 823 mm Hg/s (CRT ON, D).
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Figure 7 Cardiac resynchronization therapy (CRT) appears to have no effect on basal (resting) blood flow (measured quantitatively by positron emission tomography using O15-labeled water) (left) or blood flow reserve (measured after adenosine vasodilation, right). (Data based on reference 50).
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Figure 8 Cardiac resynchronization therapy (CRT) significantly increased basal myocardial efficiency (based on assessment by positron emission tomography using C11 acetate) (left), and a similar trend was observed during dobutamine stress (although not significant, right). (Data based on reference 50). Open bars = CRT on; solid bars = CRT off.
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Figure 9 Tissue Doppler imaging in a patient with heart failure and narrow QRS complex, showing left ventricular (LV) dyssynchrony in multiple segments (top, middle, and bottom panels) as illustrated by the temporal difference in peak systolic velocity during the ejection phase (arrows). (Top) Tissue Doppler imaging velocity tracings obtained in the interventricular septum (yellow and light blue curves) and lateral wall (red and green curves). Earliest activation (peak systolic velocities, first arrow) is in the septum, and latest activation in the lateral wall (peak systolic velocities, second arrow). Thus, significant LV dyssynchrony is present between the septum and the lateral wall. (Middle) Tissue Doppler imaging velocity tracings obtained in the anterior wall (red and green curves) and inferior wall (yellow and light blue curves). Earliest activation (peak systolic velocities, first arrow) is in the anterior wall, and latest activation in the inferior wall (peak systolic velocities, second arrow). Thus, significant LV dyssynchrony exists between the anterior and inferior wall. (Bottom) Tissue Doppler imaging velocity tracings obtained in the anteroseptal wall (red and green curves) and posterior (yellow and light blue curves). Earliest activation (peak systolic velocities, first arrow) is in the anteroseptal wall, and latest activation in the posterior wall (peak systolic velocities, second arrow). Thus, significant LV dyssynchrony is present between the anteroseptal and posterior wall. AVC = aortic valve closure; AVO = aortic valve opening.
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Figure 10 The incidence of left ventricular (LV) dyssynchrony in patients with narrow QRS complex (<120 ms) or wide QRS complex (>150 ms). The LV dyssynchrony is expressed as the extent of dyssynchrony between the septum and lateral wall. Considering LV dyssynchrony >60 ms as significant, the incidence of LV dyssynchrony was 27% in patients with narrow QRS complex as compared to 70% in the patients with wide QRS complex. (Data based on Bleeker et al. [60]).
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Copyright © 2005 by the American College of Cardiology Foundation.
