**6. Cardiac resynchronization therapy guided by cardiovascular magnetic resonance**

Cardiovascular magnetic resonance (CMR) is well known for its unprecedented image quality for cardiac structures as well as for functional assessment of cardiac functions. In addition, it has been introduced to CRT communities as a unique diagnostic tool in differentiating between the various causes of LV dysfunction. CMR is well known to be an excellent evaluating tool for critical factors in the potential response to CRT like a myocardial scar, the total amount of scar (scar burden), and scar location and its relationship to the pacing stimulus. The intricate arrangements of human heart myocardial fibers are a complex anisotropic fiber structure showing longitudinal, circumferential, and oblique layers that form a mechanical link between remote areas of the myocardium [68–71]. Electrically heterogeneous conduction from endocardium to mid-myocardium and epicardium is also a feature of the human heart [72]. Conduction disturbances, superimposing in this inherent anatomical, functional, and electrical heterogeneity of the myocardium is expected to yield multiple areas of dyssynchrony [72, 73]. This finding raises the possibility that deploying an LV lead over a single site of late wall motion may not correct global cardiac dyssynchrony. By the same token, multiple LV leads may be preferable to one LV lead in some patients (**Figure 2**) [74].

#### **Figure 2.**

*CMR radial wall mapping illustrating inward wall motion with colors ranging from blue to green and to red. Bull's eye with a homogenous red color throughout denotes complete synchrony, where the bull eye with homogenous blue color denotes complete synchrony. Heterogenous color coding denotes dyssynchrony of radial motion where blue is representing early (global systolic phase) activation and red representing late (global diastolic phase) inward radial wall motion (from Foley et al. [74, 75]).*

*CRT Past, Present, and Future Directions: Toward Intelligent Responders Selection… DOI: http://dx.doi.org/10.5772/intechopen.101608*

With its unique discriminative and diagnostic accuracy, CMR has become the gold standard for the in vivo assessment of myocardial scarring. The cutoff point for scar burden, where more is associated with poor response to CRT, is different between different investigators but in general, we consider scar burden less than 15–33% is a potentially good indicator for better response to CRT [76, 77]. Another delicate feature of CMR contribution to CRT management is that CMR can be a fine assessment tool for diagnosing the substrate of heart failure. It is well known that myocardial infarctions can be silent in about one-third of patients and coronary angiography study can be normal after myocardial infarction. In addition, wall motion abnormalities are not equivalent to myocardial ischemia. Unparalleled anatomical imaging, combined with late gadolinium enhancement (LGE)-CMR findings, makes CMR an ideal radiation-free diagnostic tool for the actual heart failure substrate. Scarring in the subendocardial or transmural distribution along arterial territories is typical for infarcted myocardium. Lack of localized myocardial scarring is characteristic of non-ischemic cardiomyopathy or less often, by mid-wall LGE, characterized fibrosis. Myocarditis, sarcoidosis, and arrhythmogenic right ventricular cardiomyopathy are characterized by the patchy distribution of LGE. Amyloidosis and Anderson-Fabry diseases are characterized by diffuse LGE.

### **7. Cardiac resynchronization therapy guided by computed tomography**

Although CMR is an excellent diagnostic tool for evaluating CRT response evaluation, the frequent presence of pacemakers in this group of patients renders its use limited especially in countries where MRI-compatible devices are not available. Non-response to CRT might be caused by factors other than dyssynchrony of electrical activation. Important hidden factors that must gain attention for non-responders are myocardial scar, myocardia hypocontractility, and suboptimal left ventricular (LV) lead location. All of these factors can be investigated with computed tomography (CT). Late iodine enhancement computed tomography (LIE-CT) was found to be an important elegant diagnostic modality in this regard. Théo Pezel et al. investigated CT dyssynchrony measurements for which the LV short-axis images from the multiphase reformatted reconstructions were used [78]. CT dyssynchrony indices used in their investigation were: global and segmental time to maximal wall thickness, global and segmental time to maximal inward wall motion, and time to minimum systolic volume. The dyssynchrony they measured were not the baseline dyssynchrony but the persistent dyssynchrony despite biventricular stimulation. LV lead malpositioning is a serious potentially avoidable reason for non-responders group. Pre-determination of LV lead positioning might be approached by invasive angiogram during implantation and CT coronary angiography. Short axis of the heart is used to determine LV lead final position as anterior, anterolateral, lateral, inferolateral, or inferior. In the long axis of the heart searched positions are basal, mid, or apical. Théo Pezel et al. evaluated concordance of the lead location to regional LV mechanical contraction, where they calculated the mean times to maximal wall thickness and maximal wall motion of each segment using an 8-segment model. Identification of the segment of the myocardium with the latest mean times to either maximal wall thickness or wall motion was determined. Greater global dyssynchrony, as measured by the time to maximal wall thickness, time to peak inward wall motion, and time-to-minimum systolic volume was found between non-responders. Greater segmental dyssynchrony between the anterior and inferior segments, between the inferoseptal and anterolateral segments, and between the anteroseptal and inferolateral segments was found between non-responders. In addition, in the non-responders, the LV

lead location was less often concordant with the region of maximal wall thickness (9% vs. 72%, p = .001) [78].

In addition, CT was found to be an appropriate diagnostic tool to follow up the association of LV wall thickness and the ability to reverse LV remodeling and mitral regurgitation improvement after CRT [79].
