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- •Contents
- •1 General Description of Types and Modes of Pacing
- •Abstract
- •References
- •2 Left Ventricle Systolic Function Evaluation in Patients with Implanted Devices
- •Abstract
- •2.1 Evaluation of Classical Parameters of Systolic Function in Patients with Implanted Devices
- •2.2 LV Volumes Measurement
- •2.3 LVEF
- •2.4 LV Mass
- •2.5 LV Regional Function Segmentation of the LV
- •2.6 Visual Assessment
- •2.8 Conclusion
- •References
- •3 Left Ventricle Diastolic Function Evaluation in Patients with Implanted Devices
- •Abstract
- •3.1 Conclusions
- •References
- •4 Lead Position Evaluation in Patients with Implanted Devices
- •Abstract
- •4.1 Conclusion
- •References
- •5 Right Ventricle Function Evaluation in Patients with Implanted Devices
- •Abstract
- •5.2 Conclusions
- •References
- •6 Mitral Regurgitation Echocardiographic Evaluation in Patients with Implanted Devices
- •Abstract
- •6.2 FMR Mechanisms in Patients with CRT and Heart Failure
- •6.3 Effects of CRT on FMR
- •6.7 Conclusions
- •References
- •7 Tricuspid Valve Evaluation in Patients with Implanted Devices
- •Abstract
- •7.1 Conclusion
- •References
- •8 Echocardiographic Follow-Up the Patients with Implanted Devices
- •Abstract
- •8.1 Patients with Pacemakers Evaluation After the Implant
- •8.2 CRT Patients Evaluation After Implant
- •8.3 Conclusions
- •References
- •9 Echocardiography-Guided Optimization of Atrioventricular and Interventricular Delay in Patients with Implanted Devices
- •Abstract
- •9.1 Conclusion
- •References
- •10 Echocardiographic Evaluation of Complications After Intracardiac Devices Implantation
- •Abstract
- •10.1 Myocardial Perforation
- •10.3 Lead Thrombosis
- •10.4 Tricuspid Valve Damage
- •10.5 Conclusion
- •References

46
3 Left Ventricle Diastolic Function Evaluation in Patients …
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Lead Position Evaluation in Patients with Implanted Devices
4
Abstract
Patients with CRT have an epicardial lead
for LV and two endocardial leads, one in the
right ventricle and one in the right atrium.
Patients with dual chamber pacemakers
have an electrode in the right ventricle and
another in the right atrium. Patients with a
single-chamber pacemaker present a lead at
the level of the right ventricle. Patients with
ICD with or without pacemaker represent
another category. Echocardiography is essential for right ventricle lead position identification, especially before a planned upgrade.
In CRT patients, the lead must be implanted
far from the fibrosis area and will be evaluated in non-responders. The right atrial lead
position usually necessitates transesophageal
echocardiography.
Patients with cardiac resynchronization therapy
(CRT) have an epicardial lead for left ventricle
(LV) and two endocardial leads, one in the right
ventricle (RV) and one in the right atrium (RA).
Patients with dual chamber pacemakers have
an electrode in the RV and another in the RA.
Patients with a single chamber pacemaker present a lead at the RV level. Another category of
patients is those with implanted cardio defibrillator (ICD) with or without a pacemaker.
Echocardiography is an essential imaging
tool for identifying lead positions in implanted
patients (Kydd et al. 2012; Smiseth et al. 2012).
Some studies indicated echocardiography in
guiding RV septal lead deployment, but this
approach is still under research. RV lead might
be responsible for LV dyssynchrony in patients
with a single or dual-chamber pacemaker. This
group necessitates three- and six-month reevaluations after the implantation, using tissue
Doppler and Speckle tracking echocardiography,
to identify LV subclinical dysfunction or HF and
decide the moment of CRT upgrading (Kydd
et al. 2012; Smiseth et al. 2012).
Echocardiography in patients with CRT is
essential in identifying the best site for a lead
position.
• For LV lead—LV fibrosis and scar area
identification
• LV area with the latest activation
identification
• For the RV lead—the best-recommended
position is at the septum level (Fig. 4.1,
Supplementary material 1), avoiding the
RV apex (Kydd et al. 2012) (Fig. 4.2,
Supplementary material 2).
Supplementary Information The online version
contains supplementary material available at
https://doi.org/10.1007/978-3-031-64079-7_4.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
D.-M. Toader, Echocardiographic Evaluation of Patients with Implanted Devices,
https://doi.org/10.1007/978-3-031-64079-7_4
49

50
Fig. 4.1 Apical four-chamber view right ventricle focused in a patient with CRT and right ventricle lead at the septum level
4 Lead Position Evaluation in Patients with Implanted Devices
Fig. 4.2 Apical four-chamber view right ventricle focused in a patient with CRT and right ventricle lead at the apex
Echocardiography for LV lead positioning
identifying in patients with CRT
arrow 2) This movement is followed by inferolateral wall contraction (Fig. 4.3, arrow 3) and is con-
comitant with passive septal stretch. (Fig. 4.3, arrow
Patients with typical left bundle branch block
(LBBB) present an abnormal sequence of mechanical activation. The early septum contraction, named
septal flush (Fig. 4.3, arrow 1), is concomitant with
the passive stretch of the infero-lateral wall. (Fig. 4.3,
4) This sequence of contraction results in apical
rocking (Supplementary material 3) and an inefficient contraction (Kydd et al. 2012).
Mechanical dyssynchrony can be present because of coronary artery disease with

514 Lead Position Evaluation in Patients with Implanted Devices
Fig. 4.3 Abnormal motion in a patient with dilated cardiomyopathy and left ventricle branch block: arrow 1:
septal flush, arrow 2: concomitant with passive stretch of
myocardial stunning or hibernation, scar,
or fibrosis. (2) Intraventricular dyssynchrony
produces abnormal LV loading, capable of
metabolic changes that may exacerbate the
syndrome of heart failure.(Chakir et al. 2008)
Correcting mechanical dyssynchrony is the
key mechanism of benefit from CRT.(Kass
2009; Aiba et al. 2009; Gorcsan et al. 2012)
Depending on the coronary venous anatomy,
the LV pacing lead is placed in an epicardial
location via a transvenous approach (Kass 2009;
Aiba et al. 2009). The optimum LV lead position is at the site of maximal mechanical dyssynchrony and away from the transmural scar
(Ypenburg et al. 2007).
The LV lead position is an essential determinant of CRT response (Ypenburg et al. 2007;
Khan et al. 2009; Thebault et al. 2012; Adelstein
et al. 2014). For a good CRT response rate and
survival benefit, optimal LV lead position must
be achieved (Delgado et al. 2011). Pacing the
segments with late contraction in patients with
LBBB results in earlier electrical stimulation,
an earlier mechanical activation, and an efficient
LV contraction (Kydd et al. 2012). Important
infero-lateral wall, arrow 3: infero-lateral wall contraction, arrow 4: concomitant with passive septal stretch
determinants of reverse remodeling after CRT
are the extent of myocardial scar tissue and the
position of the LV lead (Ypenburg et al. 2008).
Identification of LV Area of Scar
The presence of a large LV scar is a strong independent predictor of poor clinical outcome and
lack of CRT response. Identifying the presence and localization of the scar area is essential because patients with ischemic heart disease
have a poor response to CRT (Delgado et al.
2011; Ypenburg et al. 2008).
LV systolic strain measured by speckle
tracking echocardiography (STE) is an imaging technique useful for areas of scar identification (Delgado et al. 2011; Bleeker et al. 2006;
Becker et al. 2011). The scar position is also
important in CRT response prediction (Becker
et al. 2006; Shanks et al. 2011; Molhoek et al.
2004).
This method uses offline analysis by frame-
by-frame tracking of speckles within the myocardium (Suffoletto et al. 2006; Voight et al.
2015). The semi-automated process requires the

52
4 Lead Position Evaluation in Patients with Implanted Devices
manual definition of the myocardium. The region
of interest must incorporate the total thickness
of the myocardial wall. After tracking results,
the time-strain curve (Fig. 4.4). Strain describes
the deformation or fractional change in the length
of a myocardial segment and is expressed as percentages. Strain is positive when it reflects the
lengthening or thickening and is negative when
it reflects the shortening or thinning. (Fig. 4.5)
The strain rate describes the speed of deformation (Suffoletto et al. 2006; Voight et al. 2015)
(Fig. 4.6).
Echocardiographic reverse remodeling is significant in patients with nonischemic heart failure.
(Woo et al. 2005) Pacing an LV segment containing transmural scar is associated with higher
mortality, hospital admissions for heart failure,
and reduced LV reverse remodeling (Ypenburg
et al. 2007; Khan et al. 2009; Bleeker et al. 2006;
Wikstrom et al. 2009; Ghio et al. 2009).
The precise mechanisms underlying scar formation in patients without coronary artery disease are unclear, although distinct patterns are
recognized. The scar pattern is subendocardial
or transmural in patients with coronary artery
disease. The scar is located in the midwall or
subepicardium in patients with nonischemic cardiomyopathies. The impact of patterns of fibrosis on outcomes in CRT is not yet established
(Kydd et al. 2012).
High values of the peak strain identify viability in animal models (Popovic et al. 2007;
Adelstein and Saba 2007). In patients with prior
myocardial infarction, with preserved ejection
fraction, segmental longitudinal strain identified
a cutoff value of −13% for transmural infarc-
tion (sensitivity 80%; specificity 83% Gjesdal
et al. 2007; Duckett et al. 2012) Exercise-related
changes in longitudinal strain may indicate the
presence of contractile reserve and therefore
predict reverse remodeling following CRT but
studies to demonstrate this approach are awaited
(Lancellotti et al. 2009; Becker et al. 2009).
The two-dimensional (2D) circumferential
and radial strain has also been used to iden-
tify segments with a transmural scar and predict
Fig. 4.4 Bullseye display representation obtained by speckle tracking echocardiography: posterolateral scar (blue) in
a patient with dilated cardiomyopathy, CRT, and posterolateral old myocardial infarction

534 Lead Position Evaluation in Patients with Implanted Devices
Fig. 4.5 Longitudinal strain obtained with 2D speckle
tracking echocardiography in apical four-chamber view
in a patient with dilated cardiomyopathy and CRT;
dyssynchronous aspect of the red curve, which corresponds to the anterolateral basal segment of the left ventricle. (arrow)
Fig. 4.6 Strain rate obtained with 2D speckle tracking echocardiography in apical four-chamber view of a patient
with dilated cardiomyopathy and CRT

54
4 Lead Position Evaluation in Patients with Implanted Devices
CRT outcome (Kydd et al. 2012) (Fig. 4.7). The
placement of LV lead away from segments of
scar, identified by low amplitude radial strain,
has a positive impact on LV remodeling following CRT (Kydd et al. 2012). A regional radial
strain < 5% (Delgado et al. 2011; Bleeker et al.
2006; Becker et al. 2011) and a peak systolic
radial strain < 16.5% (Delgado et al. 2011) by
speckle tracking echocardiography identifies the
presence of a myocardial scar and may help the
lead placement away from this area (Delgado
et al. 2011; Bleeker et al. 2006; Becker et al.
2011, 2006).
With three-dimensional (3D) STE, the
deformation or strain can be performed in multiple planes, and all the segments can be assessed
simultaneously with single-beat acquisition,
without beat-to-beat variability or out-of-plane
motion, with the sequential assessment of basal,
mid, and apical regions (Nesser et al. 2009;
Bordachar et al. 2010) (Fig. 4.8).
A greater scar density in segments immediately adjacent to the LV lead tip has an inverse
relationship with improved ejection fraction following CRT (Adelstein and Saba 2007; Becker
et al. 2007). The septal scar in patients with
ischemic cardiomyopathy is associated with a
poor response to CRT, both acutely and at six
months (Duckett et al. 2012; Boogers et al. 2011).
Peak radial strain imaging at the mid myocardial level in ischemic and nonischemic HF
patients > 9.8% indicates the absence of transmural scar. Guided lead placement to either
targeted or adjacent segments is followed by a
positive response to CRT, a 15% reduction in LV
end-systolic volumes, improved functional class,
and reduced mortality or heart failure hospitalization (Khan et al. 2009).
Circumferential strain may offer an alternative to radial strain in patients with significant
scar. The utility of speckle tracking to guide
CRT is still under research (Kydd et al. 2012). In
patients with ischemic disease, the epicardial
circumferential strain could distinguish transmural from nontransmural scar better than fullthickness circumferential strain (Becker et al.
2009; Singh et al. 2011) (Fig. 4.9) Peak sys-
tolic circumferential strain > −11.1% by STE
identified transmural scar for the LV lead position. The absence of transmural scar at the LV
lead position resulted in significantly greater LV,
reverse remodeling, and functional improvement
at 12 months follow-up (Delgado et al. 2011).
The pacing of a scarred area produces an
electrical capture, and similar sensing and pacing thresholds may be present in patients with
and without scar but without mechanical capture and myocardial thickening. This is followed
Fig. 4.7 Abnormal curves of CS (a) and RS (b) in a patient with old lateral infarction and CRT. (arrows)

554 Lead Position Evaluation in Patients with Implanted Devices
Fig. 4.8 3D echocardiography strain measurement: longitudinal strain (a), circumferential strain (b), radial strain (c),
in a patient with dilated cardiomyopathy and CRT
Fig. 4.9 Layer-specific strain analysis: decrease circumferential strain at all myocardium levels in a patient with
dilated cardiomyopathy, CRT, and myocardial infarction
by dyssynchrony and no LV hemodynamic
improvement after CRT (Lambiase et al. 2004;
Ansalone et al. 2002).
Myocardial areas without viability are akinetic or dyskinetic. CRT response will be
harmful if the LV lead is placed in a nonviable segment. The LV lead position remote from
the area of the latest mechanical activation will
a: endocardial (a), mid-level (b), epicardial (c), versus
normal values b: endocardial (d), mid-level (e), epicardial (f)
not improve the dyssynchrony or symptoms
(Veire et al. 2006; Murphy et al. 2006).
Longitudinal systolic strain dyssyn-
chrony index (SDI) represents the differ-
ence between peak end-systolic longitudinal
strain for each segment and is linked to wasted
energy (Fig. 4.10). Delayed segments, with
maximum contraction after aortic valve closure
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