Cardiac resynchronization therapy guided by cardiovascular magnetic resonance
© Leyva; licensee BioMed Central Ltd. 2010
Received: 4 June 2010
Accepted: 9 November 2010
Published: 9 November 2010
Cardiac resynchronization therapy (CRT) is an established treatment for patients with symptomatic heart failure, severely impaired left ventricular (LV) systolic dysfunction and a wide (> 120 ms) complex. As with any other treatment, the response to CRT is variable. The degree of pre-implant mechanical dyssynchrony, scar burden and scar localization to the vicinity of the LV pacing stimulus are known to influence response and outcome. In addition to its recognized role in the assessment of LV structure and function as well as myocardial scar, cardiovascular magnetic resonance (CMR) can be used to quantify global and regional LV dyssynchrony. This review focuses on the role of CMR in the assessment of patients undergoing CRT, with emphasis on risk stratification and LV lead deployment.
European Society of Cardiology guidelines for cardiac resynchronization therapy (2010 Update).*
CRT preferentially by CRT-D is recommended to reduce morbidity or to prevent disease progression
NYHA class II
LVEF ≤ 35%, QRS ≥ 150 ms
CRT-P/CRT-D is recommended to reduce morbidity and mortality
NYHA class III/IV
LVEF ≤ 35%, QRS ≥ 120 ms
Optimal medical therapy
CRT-P/CRT-D should be considered to reduce morbidity
NYHA class III/IV
LVEF ≤ 35%, QRS ≥ 130 ms
Permanent dependency induced by AV nodal ablation
CRT-P/CRT-D should be considered to reduce morbidity
NYHA class III/IV
LVEF ≤ 35%, QRS ≥ 130 ms
Slow ventricular rate and frequent pacing
Concomitant Class I pacemaker indication
CRT-P/CRT-D is recommended to reduce morbidity
NYHA class III/IV
LVEF ≤ 35%, QRS ≥ 120 ms
CRT-P/CRT-D is recommended to reduce morbidity
NYHA class III/IV
LVEF ≤ 35%, QRS < 120 ms
CRT-P/CRT-D is recommended to reduce morbidity
NYHA class II
LVEF ≤ 35%, QRS < 120 ms
American College of Cardiology/American Heart Association/Heart Rhythm Society guidelines for cardiac resynchronization therapy (2008).*
NYHA Class III/IV
LVEF ≤ 35%, SR
QRS ≥ 120 ms
Optimal medical therapy
NYHA Class III/IV
LVEF ≤ 35%,
Optimal medical therapy
Frequent dependence on
NYHA Class III/IV
LVEF ≤ 35%
QRS ≥ 120 ms
Optimal medical therapy
NYHA Class I or II
LVEF ≤ 35%
Optimal medical therapy
Dvice implant with anticipated
frequent ventricular pacing
Appropriate diagnosis and management of heart failure not only involves an accurate assessment of myocardial and valvular function, but also of heart failure etiology. Additional aspects that are relevant to CRT are mechanical dyssynchrony, scar burden and scar localization in the vicinity of the LV pacing stimulus. With its ability to provide a one-stop assessment of all these aspects of cardiac structure and function, cardiovascular magnetic resonance (CMR) is gaining credence as a routine imaging modality for patients undergoing CRT. This review focuses on the available evidence for using CMR in the diagnostic work-up and implantation in patients undergoing CRT. The potential for further development is also explored.
Responders and non-responders to CRT
The terms 'responder' and 'non-responder' are frequently used in relation to CRT. Yet, there is no consensus on what should be considered a response . Some authors use clinical variables, such as an improvement in NYHA class or walking distance, whereas others use composite measures, such as freedom from hospitalizations or left ventricular reverse remodelling. Whilst the notion of response is conceptually attractive, we should consider the response rate to pharmacological therapy for heart failure. For example, an improvement in ≥ 1 NYHA classes is only observed in 46.7% of patients treated with enalapril,  21% of patients treated with bisoprolol and 41% of patients treated with spirinolactone . In relation to placebo, the responder rates with these drugs are 24.9% for enalapril, 6% for bisoprolol and 8% for spironolactone.
If we are to use 'response' in managing patients undergoing CRT, composite measures are probably the most useful. The combination of changes in NYHA class and LV reverse remodelling, for example, is easily quantifiable and clinically useful. We should consider, however, that the lack of a symptomatic benefit does not necessarily imply absence of a prognostic benefit.
Dyssynchrony as the target in CRT
Conducting tissue disturbances give way to conduction through the slower-conducting myocardium, delays in ventricular activation, wasted work,  a reduction in cardiac output  and LV end-systolic dilatation . According to the most popular paradigm of CRT, cardiac dyssynchrony arising from such disturbances contributes to the syndrome of heart failure and its correction leads to a clinical benefit. This paradigm, which dictates that pre-implant dyssynchrony is a sine qua non for a benefit from CRT, has driven the unrelenting search for a dyssynchrony measure as a predictor of response to and outcome of CRT.
In the pursuit for a reliable CMR measure of dyssynchrony, we must consider the extensive body of evidence in relation to dyssynchrony and CRT provided by echocardiography. Amongst the earliest and the simplest echocardiographic measures of dyssynchrony to emerge was the septal-to-posterior wall motion delay,  which is the absolute time difference between peak septal and peak posterior wall motion towards the centre of the LV. Amongst the most complex is the absolute difference or the standard deviation of the time-to-peak systolic wall motion on tissue Doppler imaging in various (usually 12) myocardial segments . These and multiple other measures raised great expectations as predictors of response to and outcome of CRT in early single-centre studies [18, 20, 21]. Their utility were further tested in the Predictors of Response to CRT (PROSPECT) trial, a multicentre study in which 12 echocardiographic parameters of dyssynchrony were assessed by a blinded core laboratory in 498 patients with standard CRT indications . In this study, the ability of echocardiographic measures to predict clinical response varied widely, with sensitivities ranging from 6% to 74% and receiver-operator characteristics curves of ≤ 0.62. Importantly, the interobserver coefficient of variation for these measures were as high as 72.1% for the septal-to-posterior wall motion delay and 33.7% for the standard deviation of the time-to-peak systolic wall motion of 12 myocardial segments on tissue Doppler imaging . Essentially, the PROSPECT study found that no single echocardiographic measure of dyssynchrony improved patient selection for CRT beyond current guidelines. In CARE-HF,  the first and only randomized controlled study of CRT to include measures of dyssynchrony in patients selection, no single echocardiographic measure of dyssychrony emerged as a clinically applicable predictor of outcome. After much expectation, echocardiographic measures of dyssynchrony have not gained credence in selecting patients for CRT [23–26].
Normal QRS duration
The purist view is that there is no treatable dyssynchrony at a QRS < 120 ms and an LVEF > 35%. Dyssynchrony, however, is a biological phenomenon and as such, is expected to behave as a continuous rather than as a dichotomous variable [27, 28]. Not surprisingly, therefore, cardiac dyssynchrony is detectable in patients with a QRS ≤ 120 ms [29–35] and higher LVEFs [36, 37]. Using CMR, we have shown that up to 91% of patients with a QRS < 120 have radial dyssychrony . (Additional File 1; Movie 1) It seems reasonable to suppose, therefore, that at least some patients with a QRS < 120 ms might benefit from CRT. Although several observational studies have reported a benefit in patients with a QRS < 120 ms, [39–41] the recently reported Resynchronization Therapy in Narrow QRS (RethinQ) study, a randomized controlled trial, showed no benefit in terms of peak oxygen consumption . This study, however did not use an implantation technique that avoids pacing LV scar. Whether or not CMR-guided CRT (avoiding scar) is effective in patients with a QRS < 120 ms remains to be explored.
Does the magnitude of pre-implant dyssynchrony affect the CRT response?
Assessing dyssynchrony with CMR
Except for the UK NICE,  no guideline group has adopted a criterion of mechanical dyssynchrony in relation to CRT. Importantly, NICE has not specified which measure of mechanical dyssynchrony should be adopted, nor what cut-off to apply. In the absence of a consensus, therefore, measures of mechanical dyssynchrony cannot be used to decide on eligibility for CRT, even in the UK. The question remains, however, as to whether measures of mechanical dyssynchrony can be used for risk stratification and for guiding LV lead deployment.
Steady-state free precession (SSFP)
To accurately assess myocardial displacement and deformation (strain and strain rate), the imaging region of interest must be tracked through the cardiac cycle. In CMR, tacking can be achieved using myocardial tagging techniques which, in effect, label areas of myocardium. Essentially, tags, which are created by manipulating magnetization. , act as fiducial markers that conform to the myocardium in which they are placed. This not only permits accurate quantification of myocardial displacement, but also of strain and strain rate . Commonly used sequences include spatial modulation of magnetization (SPAMM) and complimentary spatial modulation of magnetization (CSPAMM). The latter is more time-consuming, but it allows tags to be analysed in diastole as well as in systole.
Three-dimensional motion and strain
Various CMR techniques can be used to assess dyssynchrony from myocardial velocity measurements. In this respect, we should note the limitations of velocity-based measurements in the assessment of dyssynchrony, as demonstrated by echocardiographic studies [23, 58].
Velocity-encoded CMR has shown some promise in the assessment of dyssynchrony . In a small study, Marsan et al found a strong correlation between tissue Doppler imaging and velocity-encoded CMR with respect to longitudinal myocardial peak systolic and diastolic velocities and time to peak systolic velocity at the level of left ventricular septum and lateral walls. (r = 0.97, p < 0.001)  Similar findings emerged from a study of patients with idiopathic dilated cardiomyopathy .
Strain-encoded (SENC) CMR has recently emerged as a technique for directly imaging strain without the need for post-processing . It uses a standard tagging sequence that tags myocardium at end-diastole with a sinusoidal tag pattern which modulates the longitudinal magnetization orthogonal to the imaging plane. Myocardial deformation leads to changes in the local frequency of the tag pattern in proportion to strain. As well as providing real-time quantitative strain measures, SENC has a higher spatial resolution than standard tagging and allows acquisition of both circumferential and longitudinal myocardial strain data. So far, however, this promising technique has not been applied to CRT.
Atrioventricular and interventricular dyssynchrony
The above CMR techniques are useful for the assessment of intraventricular dyssynchrony. Interventricular dyssynchrony, however, is also relevant in CRT. In a study of 45 patients undergoing CRT, Muellerleile et al found that the interventricular mechanical delay, derived from velocity-encoded CMR, was comparable to pulsed-wave echocardiography in predicting responders to CRT .
The role of atrioventricular dyssynchrony in predicting the response to CRT has not been studied. Arguably, correction of atrioventricular dyssynchrony should relate to a favourable response. Whilst atrioventricular dyssynchrony is easily measured with echocardiography, this is still challenging for CMR.
Dyssynchrony and LV pacing site
Several studies have shown that the anatomical position of the LV lead during CRT, assessed using fluoroscopy, has no bearing on the response to and outcome of CRT [64–66]. Small echocardiographic studies using tissue Doppler imaging,  tissue synchronization imaging (TSI),  three-dimensional echocardiography,  and speckle tracking,  however, have shown that a better response to CRT can be achieved if the LV lead is deployed in the area of latest activation or contraction. There is, nevertheless, a wide interindividual variation with respect to the site of latest activation [67–70].
Using the combination of pressure-volume loops and myocardial tagging to assess the ideal LV position in pacing-induced failing canine hearts, Helm et al found that LV sites yielding 70% of the maximal dP/dtmax increase covered approx. 43% of the LV free wall . The distribution and size of these pacing sites correlated with the three-dimensional dyssynchrony mapping derived from myocardial tagging. Essentially, this study provided proof of concept that myocardial tagging can be used to locate the ideal site for LV lead deployment in CRT. Importantly, however, this animal model did not involve myocardial infarction. Rademakers et al, on the other hand, have recently devised an animal model of heart failure involving myocardial infarction . This model revealed that CRT can improve resynchronization and LV pump function to a similar degree in infarcted than non-infarcted hearts, but optimal lead positioning and timing of LV stimulation was crucial. In clinical practice, it is likely that combining three-dimensional myocardial tagging with an assessment of scar will be useful in guiding LV lead deployment.
If deploying the LV lead in an area of late activation or contraction is indeed important, it is in the interest of the CRT implanter to know how many areas there are and where they are. In this respect, we should consider that the myocardium is a complex anisotropic fibre structure, consisting of longitudinal, circumferential and oblique layers that form a mechanical link between remote areas of the myocardium [72–74]. The myocardium is also electrically heterogeneous from endocardium to mid-myocardium and epicardium . Conduction disturbances, superimposed on the inherent anatomical, functional and electrical heterogeneity of the myocardium is likely to lead to multiple areas of dyssynchrony [76, 77].
Additional file 3: Movie 3. Colour-coded endocardial wall motion throughout the cardiac cycle in a healthy subject, derived from SSFP imaging. Note the homogeneity of colour (early wall motion in blue and late wall motion in red) throughout the cardiac cycle. (WMV 748 KB)
Additional file 4: Movie 4. Colour-coded endocardial wall motion throughout the cardiac cycle in a patients with heart failure and a left bundle branch block, derived from SSFP imaging. Note the heterogeneity of colour (early wall motion in blue and late wall motion in red) throughout the cardiac cycle. (WMV 740 KB)
Myocardial scar and CRT
The effectiveness of almost all cardiac therapies is dependent on myocardial viability. Such is certainly the case for revascularization [79–84] and pharmacological therapy . With respect to CRT, the total amount of scar (scar burden), its location and relationship to the pacing stimulus have been shown to be important in determining response and outcome. It is by virtue of unique anatomical resolution and the contrast between scarred and non-scarred myocardium achievable[81, 86, 87] that CMR has become the gold-standard for the in vivo assessment of myocardial scarring.
Several studies have shown that scar burden relates to a poor response to and outcome from CRT. In a LGE-CMR study of 28 patients undergoing CRT, White et al found that scar burden was higher in the non-responders versus responders group (median 24.7% vs. 1.0%, respectively, p = 0.0022) . In a study of 45 patients with ischemic cardiomyopathy, we showed that scar burden correlated negatively with changes in 6-min walking distance (r = -0.54, p < 0.0001) and positively with changes in quality of life scores (r = 0.35, p = 0.028; high scores denote a poorer quality of life). The response (defined as survival for one year following implantation free of hospitalizations plus an improvement by ≥ 1 NYHA classes or by ≥ 25% in 6-min walking distance) in patients with < 33% scar was 2.3 times greater than in patients with ≥ 33% scar . In a further study of 62 patients undergoing CRT, we found that the presence of a LV free wall scar was as an independent predictor of the composite endpoints of cardiovascular death or hospitalization for worsening heart failure [HR: 3.06, P < 0.0001)] as well as the endpoint of cardiovascular death [HR: 2.63, P = 0.0016)] after a mean follow-up period of 2 years. These findings are in keeping with those of a study using 201Tl single photon emission computed tomography (SPECT),  in which scar burden was shown to correlate negatively with changes in LVEF after CRT (r = -0.53; P < 0.0001).
The cut-off of scar burden above which CRT becomes ineffective is difficult to identify from the various studies. This is partly due to the adoption of different criteria for response to CRT and the inclusion of varying proportion of patients with ischemic and non-ischemic cardiomyopathy. For example, in our study of only patients with ischemic cardiomyopathy,  a scar volume of 33% was the best cut-off for predicting a favourable response: the responder rate in patients with < 33% scar was 2.3 times greater than patients with ≥ 33% scar. In contrast, White et al, who studies patients with ischemic (52%) and non-ischemic cardiomyopathy, found a scar burden < 15% as the best cut-off for predicting a clinical response . Taken together, these studies of myocardial scarring and CRT support the hypothesis that there is a limit of scar burden above which resynchronization becomes ineffective.
Scar location and relationship to LV pacing site
Following the finding that pacing LV free wall scar is detrimental in CRT is the use of LGE-CMR to guide LV lead deployment has become standard practice in some centres. In the author's implanting experience, scarring over the entire LV free wall is a rare occurrence and it is unusual not to have coronary sinus tributaries over non-scarred myocardium.
Heart failure is a complex syndrome that can hardly be quantified in terms of a single parameter. Accordingly, it is perhaps folly to consider that one single parameter can be used to predict the response and outcome of CRT. Clearly, the outcome of heart failure and CRT are intimately dependent on a panoply of factors, not all of which relate to hemodynamic or imaging parameters. It is this which provides the biological rationale for using composite predictors. The statistical attraction is that composite predictor tends to dampen the background noise of sampling error .
CMR and etiology of heart failure
Heart failure is not a diagnosis without qualification of etiology . The etiology of heart failure influences prognosis and the choice of therapy, including device therapy. In this respect, the 2007 UK National Institute of Clinical Excellence (NICE) guidance stipulated that CRT-D should only be considered if there is a history of a myocardial infarction, or 'a familial cardiac condition with a history of sudden death, including long QT syndrome, hypertrophic cardiomyopathy, Brugada syndrome or arrhythmogenic right ventricular dysplasia, or have undergone surgical repair of congenital heart disease' . Idiopathic dilated cardiomyopathy, which accounts for most cases of non-ischemic cardiomyopathy, was not considered by NICE and therefore, falls under the guidance for CRT-P. In the UK, therefore, etiology is particularly important in choosing between CRT-P or CRT-D. Importantly, however, an ischemic etiology does not imply reduced prognostic benefit from CRT .
The diagnosis of ischemic cardiomyopathy has traditionally been made on the basis of a history of a myocardial infarction,  the finding of coronary artery stenoses on coronary angiography or of a regional wall motion abnormalities on echocardiography. It is well recognized, however, that myocardial infarctions can be silent (28% in men, 35% in women),  that coronary angiography can be normal after a myocardial infarction (8%) [109, 110] and that wall motion abnormalities are not exclusive to ischemic cardiomyopathy .
The sequences used to quantify T2* have proven to be unique in the identification and management of iron overload cardiomyopathy,  Sequences using T2-weighting have also been used to identify myocardial oedema, [116, 117] which may be useful in the assessment of myocarditis and acute coronary syndromes [110, 87].
CMR device compatibility
As discussed above, the principal role of imaging in CRT is in selecting patients and in guiding device implantation. Potential aspects of imaging after device implantation, such as residual dyssynchrony and relationship of myocardial scarring to the implanted LV lead may help identifying the reasons for a lack of response.
Several factors preclude the use of CMR in patients with devices . Radiofrequency-induced heating of the pacing leads has been shown to lead to temperatures as high as 60° in experimental settings . On the other hand, radiofrequency and magnetic gradients induce currents within the device generator  and these can interfere with detection and pacing algorithms. In addition, they can induce arrhythmias and alter pacemaker settings. These factors have indeed implicated in the reported deaths. Despite these concerns, several centres have recently reported favourably on the safety of CMR in patients with pacemakers [121, 122]. Continuous ECG, blood pressure and oxygen saturation monitoring during the scan, turning off the device in non device-dependent patients, setting the leads to a bipolar configuration and using low field, gradient and radiofrequency settings are among the precautionary measures taken. With regard to CRT-D and ICDs, experience is more limited. In balance, the strength of the evidence for a role of CMR in CRT is insufficient to justify scanning after implantation.
This year has seen the launch of the first CMR-safe pacemaker (Medtronic Inc, Minneapolis, US). The development of CMR-safe CRT-P and CRT-D devices would permit assessment of cardiac function, dyssynchorny and myocardial viability after device implantation. This is not only likely to help in clinical management but it will undoubtedly further our understanding of the mechanisms underlying CRT.
Intraoperative CMR in CRT
Recently, Schwatzman have shown how myocardial scar, imaged pre-operatively using LGE-CMR, can be fused with electroanatomic mapping data to guide LV lead implantation . Using this technique, activation time and virtual venography was used to target LV lead positions, and the electroanatomic mapping system was used to assist in lead manipulation. Further studies, however, are needed to determine whether other CMR-derived data, relating to coronary sinus anatomy,  mechanical activation, [125, 34] perfusion and viability can also be 'fused' with real-time CMR or conventional fluoroscopy to guide LV lead deployment.
This decade is likely to see an exponential growth in the use of CRT for patients with heart failure. CMR not only provides unparalleled quality of imaging for cardiac structure and function but it is also unique in differentiating between the various causes of LV dysfunction. It is on this basis that CMR is already considered as an ideal 'one-stop' investigation for patients with heart failure. In addition, perhaps the most clinically applicable aspect of CMR to CRT per se is its ability to precisely localise myocardial scar, which is known to be crucial in LV lead deployment. For these reasons, CMR has a clear role in the diagnostic and implantation pathway of patients undergoing CRT. Further studies are needed to clarify the utility of fusion imaging in guiding LV lead deployment. On the part of scanner manufacturers, further software development and validation is required, so as to make analysis of dyssynchrony, tagging and LGE data more accessible to the clinician. With the development of CMR-compatible devices, the use of CMR in CRT device optimization may one day become a reality.
Conflict of interests
The authors declare that they have no competing interests.
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