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ACC/AHA 2008 Performance Measures for Adults With ST-Elevation and Non-ST-Elevation Myocardial Infarction

ACC/AHA 2008 Guidelines for the Management of Adults With Congenital Heart Disease
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J Am Coll Cardiol, 2004; 43:248-256, doi:10.1016/j.jacc.2003.08.038
© 2004 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: ELECTROPHYSIOLOGY

Intra-left ventricular electromechanical asynchrony

A new independent predictor of severe cardiac events in heart failure patients

Hugues Bader, MD*, Stephane Garrigue, MD*,*, Stephane Lafitte, MD{dagger}, Sylvain Reuter, MD*, Pierre Jaïs, MD*, Michel Haïssaguerre, MD*, Jacques Bonnet, MD*, Jacques Clementy, MD* and Raymond Roudaut, MD{dagger}

* Hôpital Cardiologique du Haut-Lévêque, University of Bordeaux, Pessac, France
{dagger} Echocardiography Laboratory, Hôpital Cardiologique du Haut-Lévêque, University of Bordeaux, Pessac, France

Manuscript received February 11, 2003; revised manuscript received July 22, 2003, accepted August 5, 2003.

* Reprint requests and correspondence: Dr. Stephane Garrigue, Cardiac Pacing and Clinical Electrophysiology Department, Hopital Cardiologique du Haut-Leveque, 19 Avenue de Magellan, Pessac Cedex 33604, France.
stephane.garrigue{at}chu-bordeaux.fr


   Abstract
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 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES: We sought to assess the electromechanical parameters, using tissue Doppler echocardiography, as potential independent predictors of heart failure (HF) worsening.

BACKGROUND: Ventricular conduction disorders worsen the prognosis for HF patients. However, the relationships between the QRS width and morphology, hemodynamic parameters, and presence and magnitude of intra-left ventricular (LV) and inter-ventricular (V) asynchrony have not been well clarified.

METHODS: A total of 104 patients with an LV ejection fraction (EF) ≤45% and stabilized HF, without myocardial infarction (MI), underwent echocardiography coupled with tissue Doppler imaging and were followed for one year. The protocol analyzed the incidence of worsening HF (hospitalization for cardiac decompensation). Inter-V and regional electromechanical delays for the anterior, septal, inferior, and lateral LV walls were correlated with the QRS morphology and duration. The intra-LV and inter-V asynchrony values of these patients were compared with those of healthy subjects matched by gender and age criteria to determine the respective normal ranges.

RESULTS: The presence of intra-LV (but not inter-V) asynchrony was identified as an independent predictor of severe cardiac events (hazard ratio 3.39, p < 0.0001), independent of the LVEF and QRS width. Of patients with a QRS width <120 ms (55%; n = 57), 56% presented with major intra-LV asynchrony and 12% with inter-V asynchrony. Intra-LV asynchrony was observed in 84% of left bundle branch block patients, but also in 83% of right bundle branch block patients (p = NS). There was a poor correlation between the QRS width and intra-LV or inter-V asynchrony (r = 0.36, p = NS and r = 0.43, p = 0.05, respectively).

CONCLUSIONS: In HF patients without MI, patients with intra-LV asynchrony are those with a significantly higher risk of cardiac events, independent of the QRS width and LVEF. Accordingly, such patients should be more actively identified for early intensive treatment and survey.

Abbreviations and Acronyms
  AF = atrial fibrillation
  CHF = congestive heart failure
  ECG = electrocardiogram/electrocardiographic/ electrocardiography
  HF = heart failure
  LBBB = left bundle branch block
  LV = left ventricular
  LVEF = left ventricular ejection fraction
  MI = myocardial infarction
  RBBB = right bundle branch block
  TDI = tissue Doppler imaging
  V = ventricular

Heart failure (HF) is a major health problem, as, in Western countries, it affects nearly 16 million people, with an annual incidence of 1% (1–3). Although many abnormalities are best understood at the myocardial level, the consequences of cardiac pump failure on the loco-regional asynchronous contraction of the muscle wall have not been well characterized yet. More specifically, the bridge between the electrical ventricular activation time and the mechanical sequence of the systolic phase remains incompletely identified. Widening of the QRS complex on the surface electrocardiogram (ECG) usually indicates an impaired (or slowed) propagation of the electrical input, a finding frequently associated with increased morbidity and mortality in HF patients (4–6). However, when a portion of the heart is activated late (i.e., bundle branch block), the activation sequence changes markedly, generating regions of both early and delayed contraction, but without a close relationship between the topography of the bundle branch block on the surface ECG (right or left) and the topography and importance of loco-regional mechanical consequences (7–11). More so than the electrical activation sequence, the mechanical one during ventricular systole predominates in terms of hemodynamic variations and clinical consequences. Recent studies have revealed that intra-ventricular (V) conduction block with or without prolonged atrioventricular conduction adversely influences ventricular function due to discoordinate contraction (7,8,12–14). It has also been suggested that of HF patients with the same apparent intra-V conduction block visible on the surface ECG, some present with inter-V mechanical asynchrony while others have intra-left ventricular (LV) asynchrony (15–17). Accordingly, it is likely that these two ventricular mechanical dyssynchronizations may have different consequences in terms of clinical and hemodynamic outcome, especially in patients with HF. In the present study of HF patients without myocardial infarction (MI), we have aimed to assess the relationship between the QRS morphology and duration, with the resulting loco-regional mechanical consequences in terms of inter-V and intra-LV electromechanical disorders. The second step was to determine electromechanical parameter-independent criteria for worsening of HF in stable drug-treated patients.


   Methods
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 Abstract
 Methods
Results
 Discussion
 References
 
Study population and design.   We studied the relationships between the QRS complex morphology, duration, and degree of inter-V and intra-LV electromechanical asynchrony, as well as their impact on morbidity, in a patient population optimally treated for stable HF. They were consecutively recruited according to the following inclusion criteria: LV ejection fraction (LVEF) <45%, regardless of the QRS width and morphology; New York Heart Association functional class I, II, or III; and no chronic atrial fibrillation (AF), pacemaker, implantable cardioverter-defibrillator, or MI.

All patients had to undergo coronary angiography in the last one year before study inclusion. According to the results of angiography, the patients were classified in different subgroups.

Patients with significant coronary disease (at least one coronary thrombosis or one coronary stenosis ≥50%).   They were excluded if they presented with at least one of the following criteria: 1) presence of akinetic LV wall on echocardiography or left ventriculography (during the coronary angiography procedure); 2) QS aspect on the surface ECG in at least two derivations; 3) hospitalization with elevation of troponin I associated or not with percutaneous transluminal coronary angioplasty; 4) or artery thrombosis on angiography. Patients with significant stable coronary disease but without the aforementioned criteria were included in the subgroup of patients with dilated cardiomyopathy and coronary artery disease.

Patients without significant coronary disease.   They were included in the study and classified as patients with dilated cardiomyopathy and valvular disease if they presented with significant structural valvular disease but without any indication of surgical treatment during one-year follow-up. Patients with an indication for surgical treatment before and/or during follow-up were excluded.

Patients with a normal coronary angiogram and without structural valvular disease were included in this subgroup and classified as having idiopathic dilated cardiomyopathy.

After written, informed consent was obtained, the patients were definitely included in a prospective study and underwent echocardiography and 12-lead surface ECG. All of them were followed for one year, and every hospitalization record was collected from the inclusion date. Worsening HF was the primary event tested and was defined as hospitalization for clinical cardiac decompensation, unstable angina, and/or atrial or ventricular arrhythmias. We also collected hospital records for noncardiac events with no sign of cardiac decompensation during the hospitalization.

The ECGs were read by two independent observers unaware of the remaining clinical and laboratory information.

Healthy patients referred for a history of accessory pathway ablation at least five years ago, with neither cardiomyopathy nor cardiotropic drug treatment since at least five years, were used to determine the normal range of intra-LV and inter-V electromechanical delay. These control subjects were matched by gender and age criteria with the study population. Twenty-five healthy patients among 63 were randomly selected to comprise the control group.

Standard echocardiography.   All studies were performed with a commercially available ultrasonographic system equipped with a 2- to 3-MHz transducer (Acuson, Sequoia, Mountain View, California). Two-dimensional and M-mode echocardiograms were obtained, according to the American Society of Echocardiography guidelines. Global LV function was assessed from both M-mode tracings by measuring LV end-diastolic and end-systolic diameters and from two-dimensional apical views by measuring LV end-diastolic volume, LV end-systolic volume, and LVEF, using the modified biplane Simpson rule (inter-observer and intra-observer correlations for LV volume: 0.94 and 0.96, respectively).

Aortic and pulmonary Doppler flows were recorded in the pulsed mode from the apical four-chamber view and parasternal short-axis view, respectively. The aortic and pulmonary ejection delays were defined as the delay between the onset of the QRS complex on the surface ECG and the onset of the aortic and pulmonary waves. Inter-V electromechanical asynchrony was defined as the difference between the aortic and pulmonary ejection delays.

Tissue Doppler imaging.   Tissue Doppler imaging (TDI) was performed in the pulsed-wave Doppler mode from the apical view to assess longitudinal myocardial regional function, analyzing the septal, inferior, lateral, and anterior walls. The velocity profiles were recorded with a sample volume placed in the middle of the basal segment of each wall. Gain and filters were adjusted as needed to eliminate background noise and to allow for a clear tissue signal. The TDI signals were recorded at a sweep speed of 100 mm/s. From the Doppler spectrum, the electromechanical delay (defined as the delay between the onset of the QRS complex on the surface ECG and the onset of the systolic TDI wave) was measured by two blinded observers. Intra-observer and inter-observer correlations for these parameters were assessed in 10 patients and reached 0.99 and 0.97, respectively. Intra-LV electromechanical asynchrony was defined as the time difference between the shortest and longest electromechanical delays among the four LV walls. This parameter represents the interval between the earliest LV wall systolic motion and the latest one (Fig. 1).



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  		Figure 1 (A) A series of tissue Doppler imaging (TDI) echocardiograms in a patient with primitive dilated cardiomyopathy with complete left bundle branch block (QRS width of 150 ms) and left ventricular ejection fraction of 21%. Despite a long QRS duration (B), this patient presents with no intra-left ventricular electromechanical asynchrony, because the anterior (A), inferior (I), septal (S), and lateral (L) electromechanical delays (between the onset of the QRS and that of the S wave observed on the TDI echocardiogram) are within a range of 30 ms. Respective electromechanical delay (EMD) of one given LV wall, between the onset of the QRS complex and that of the S wave observed on the TDI echocardiogram.

 
Data analysis.   Statistical analysis was performed using the Statistica software (StatSoft, Tulsa, Oklahoma).

Control subjects were included in the study to characterize the range of intra-LV and inter-V electromechanical delays in the population with normal cardiac function and no history of cardiomyopathy. The Shapiro and Wilk test was used to verify that the distribution of the controls' variables followed a gaussian curve. Then, the normal range of the variables was defined as the following: the statistical alpha risk was fixed at 0.05, so that the physiologic range of the parameters should be included in the "mean ± 2 SD" range, which represents 95% of the control group distribution (18). Consequently, the upper limit for a statistically normal value of intra-LV and inter-V electromechanical delay was the respective "mean + 2 SD" value; any value above this limit in HF patients was considered statistically different from the control group's value, and accordingly, the patient was classified as presenting with significant inter-V and/or intra-LV electromechanical asynchrony, compared with the control group. The baseline characteristics are shown in Table 1. The mean QRS width was 95 ± 6 ms, with a mean LVEF ranging from 68% to 82%. As described in the Methods, 95% of the control subjects had an inter-V electromechanical interval below 38 ms (mean value + 2 SD), so that inter-V electromechanical asynchrony was defined as a value of inter-V electromechanical interval above 38 ms, with a statistical alpha risk of 0.05. Intra-LV asynchrony was defined as a value of intra-LV electromechanical interval above 40 ms (mean value + 2 SD), with a statistical alpha risk of 0.05. No control subject had left anterior or posterior hemiblock. The QRS axis was 52 ± 7°.


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  		Table 1 Baseline Characteristics of the Two Groups of Patients

 
Patients were grouped according to whether they had inter-V and/or intra-LV electromechanical asynchrony. The Fisher exact test was used for univariate comparisons between qualitative variables, whereas the Student t test was performed to assess comparisons between quantitative variables. A multivariate analysis with logistic regression was performed to isolate independent criteria of patients with inter-V or intra-LV electromechanical asynchrony. The level of significance was set at 0.05.

The Kaplan-Meier method was used to describe the hospitalization for worsening HF using event-free curves for the two groups (patients with and without inter-V electromechanical asynchrony and patients with and without intra-LV electromechanical asynchrony) by providing the number of hospitalizations due to worsening HF. The differences between curves were evaluated by the Mantel-Haenszel and Breslow tests, which mainly explore the early and late phases of survival curves, respectively (19).

The significance of the association between each clinical, echocardiographic, and ECG criterion and the cardiac event-free curve was assessed by multivariate Cox regression analysis, adjusted for age, gender, and LVEF.


   Results
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 Abstract
 Methods
 Results
Discussion
 References
 
Heart failure population (n = 104).   Eleven patients refused to undergo coronary angiography before being included in the study (when this exploration was dated past one year). Similarly, three patients presented with normal coronary arteries associated with the presence of regional akinesia and no history of MI. These three patients were excluded from the study, according to the inclusion criteria (see Methods). Finally, four patients also had to be excluded, as they presented with valvular disease that required surgery during follow-up. Accordingly, from a total population of 122 patients, 18 had to be excluded (14.7%), so 104 patients comprised the definitive population. The baseline characteristics are given in Table 1. The mean age and gender ratio were statistically similar to those of controls. Fourteen percent of patients were receiving amiodarone due to paroxysmal AF. The mean LVEF was 31 ± 9%, and 68% of the patients presented with primitive cardiomyopathy. Forty-seven percent of the patients had bundle branch block (Table 1), and the presence of primitive cardiomyopathy was significantly predominant for complete or incomplete bundle branch blocks, compared with an ischemic or valvular origin of cardiomyopathy (Table 2). In patients with complete right or left bundle branch block (RBBB and LBBB, respectively), there was significantly more intra-LV than inter-V asynchrony (p < 0.01) (Table 3). Ninety-one percent of complete LBBB patients and 82% of complete RBBB patients had inter-V or intra-LV electromechanical asynchrony (Table 3). Intra-LV asynchrony was present in 54% of patients with incomplete LBBB and 50% in patients with left anterior hemiblock (Table 3).


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  		Table 2 Distribution of the Conduction Disorders According to the Cardiac Disease

 

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  		Table 3 Distribution of the ECG Electrocardiographic Characteristics According to the Different Types of Electromechanical Ventricular Asynchrony in the Study Population

 
There was a significant but poor correlation between the QRS width and the intra-LV electromechanical interval in the whole population (R2 = 0.13, p < 0.05) and inter-V electromechanical interval (R2 = 0.19, p < 0.05). The aortic pre-ejection interval was not significantly correlated with either the end-diastolic LV diameter (r = 0.32, p = NS) or LVEF (r = –0.26, p = NS), whereas the correlation with the QRS width was found to be significant (r = 0.51, p = 0.05). Considering patients with a QRS width >120 ms, this correlation reached significance only for the intra-LV delay, but remained poor (R2 = 0.20, p < 0.05). In these patients, there was no significant correlation between the LVEF and intra-LV delay (R2 = 0.04, p = NS) or inter-V delay (R2 = 0.02, p = NS). This was also true when considering the whole population (R2 = 0.005, p = NS and R2 = 0.0007, p = NS, respectively). In the whole population, the LV wall with the longest electromechanical delay was the free wall for 32% of patients, anterior wall for 38%, inferior wall for 20%, and septal wall for 10%. In patients with complete LBBB, the distribution was 33%, 36%, 21%, and 10%, respectively (p = NS vs. whole study population).

Predictors for recurrent HF.   No patient died during the one-year follow-up. Twenty-one patients (20%) were hospitalized for noncardiac events. Only four patients first hospitalized for noncardiac events were transferred afterward to our cardiology department for cardiac decompensation. According to our criteria, these transfers were considered as worsening HF events. Eighty-six patients (83%) were hospitalized for cardiac decompensation. Among them, two (2%) were also hospitalized for unstable angina and four (4%) for palpitations related to a sustained episode of AF. By using the multivariate Cox regression analysis, three independent predictors of worsening HF requiring periodic hospitalizations were identified (Table 4): QRS width >140 ms (p = 0.022), LVEF <25% (p < 0.001), and the presence of intra-LV electromechanical asynchrony (p < 0.001) were found to be independent risk factors for decompensation. The last was significantly and strongly associated with a higher risk of early HF episodes (Fig. 2A). In contrast, inter-V electromechanical asynchrony (Fig. 2B) and the aortic pre-ejection interval were not found to be independent predictive factors for HF decompensation. Table 4 summarizes the results of the Cox regression analysis.


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  		Table 4 Multivariate Cox Regression Analysis for Identifying Patients With Rehospitalization

 


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  		Figure 2 (A) These congestive heart failure (CHF) event-free survival curves are for patients with and without intra-left ventricular electromechanical asynchrony. There were significantly more rehospitalizations for decompensation in patients with versus without intra-left ventricular asynchrony. (B) These CHF event-free survival curves are for patients with and without interventricular electromechanical asynchrony. The presence of interventricular asynchrony did not significantly influence the number of rehospitalization over one-year follow-up.

 
Predictors of intra-LV electromechanical asynchrony.   The univariate analysis is shown in Table 5. The mean QRS duration was found to be longer in patients with than in those without intra-LV asynchrony (133 ± 34 vs. 110 ± 23 ms; p < 0.001). Complete LBBB was significantly more frequent in patients with intra-LV asynchrony (57% vs. 22%; p = 0.01). Interestingly, the mean LVEF and proportion of patients with LVEF <25% were statistically similar in both groups (Table 5). Two independent criteria for identifying patients with intra-LV asynchrony were identified by using multivariate logistic regression: QRS width >140 ms (p = 0.02) and the fact that these patients were hospitalized during their follow-up (p < 0.001) (Table 6).


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  		Table 5 Comparison Between Patients With and Without Intra-LV Electromechanical Asynchrony

 

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  		Table 6 Multivariate Logistic Regression Analysis for Identifying Patients With Intra-LV Electromechanical Asynchrony

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
The results of our study have several important implications. First, they have shown that, independent of the LVEF and QRS width, congestive HF (CHF) patients with intra-LV asynchrony have a much higher risk of worsening and a more severe prognosis than patients without asynchrony. Second, the presence of inter-V electromechanical asynchrony does not influence the outcome of CHF patients. Third, more than half of CHF patients (even with primitive dilated cardiomyopathy) without complete bundle branch block have major intra-LV electromechanical asynchrony. Fourth, the QRS width and morphology are therefore not predictive of loco-regional asynchronous contraction abnormalities, unless superior to 140 ms. Fifth, no relationship was found between the type of bundle branch block and the type of electromechanical asynchrony. In our study, we decided to consider hospitalizations for unstable angina or arrhythmias as worsening HF events, as both conditions may be related to increased filling pressures that may lead to subendocardial ischemia and arrhythmias. We confirmed the data of a recent study (20) that nicely showed that the presence of intra-LV asynchrony is an independent factor of worsening HF and mortality. However, we provided further data on correlations between the QRS width and morphology with the degree and type of ventricular asynchrony. In addition, we used a noninvasive technique, whereas Fauchier et al. (20) used a radionuclide technique coupled with the Fourier analysis.

Prolonged ventricular activation, as shown by a wide QRS complex, is common in patients with dilated cardiomyopathy (21,22) and independently impaired systolic and diastolic LV function (8,22,23). Hesse et al. (24) have demonstrated that RBBB should be considered as an independent risk factor of mortality and, more importantly, to the same extent as LBBB. It may be suggested that a different conduction abnormality visible on the surface ECG could result in the same mechanical consequences (i.e., impaired LV function). In our study, 83% of RBBB patients presented with intra-LV electromechanical asynchrony, as compared with 84% of LBBB patients. Consequently, the same proportion of RBBB and LBBB patients was hospitalized for recurrent CHF during the period of follow-up. The surface ECG could identify patients with and without loco-regional contraction abnormalities only when the QRS width was >140 ms, which represents a minority of HF patients (34% in our population). The proportion of patients with inter-V asynchrony alone was small for both types of bundle branch block, enhancing the potential link between the QRS width and presence of intra-LV (and not inter-V) mechanical disorders. The fact that a QRS width >140 ms was found to be independently related to CHF-induced rehospitalization, clearly confirms this notion. However, the presence of intra-LV electromechanical asynchrony was also found as a true independent factor of rehospitalization; this is explained by the fact that in 56% of patients with a QRS width <120 ms, intra-LV asynchrony was present, playing a determinant role in terms of cardiac events. These data are new and obtained by use of the TDI technique. It also explains why the correlation between the QRS width and intra-LV (or inter-V) electromechanical delay was poor (although significant). This observation raises important issues, especially regarding the potential mechanisms of mechanical ventricular asynchrony in patients without complete bundle branch block on the surface ECG. In animal models, dilated hearts with an altered ejection fraction are more susceptible to ventricular conduction slowing, mainly due to heterogeneous interstitial fibrosis, which alters inter-cellular electrical coupling and also intra-cellular calcium handling (25–27). Consequently, the Purkinje tissue could be altered distally and/or heterogeneously in very delimited areas of the ventricular myocardium, without substantially increasing the QRS duration on the surface ECG. In patients with stable ischemia without MI, loco-regional alterations might also slow the ventricular conduction and delay the electromechanical sequence.

In patients with complete LBBB, it has been thought that the LV is activated through the septum from the RV, where activation is assumed to be normal (28). This was verified for LV electrical activation; however, mechanical contraction sequences of the different LV walls may not always follow the electrical input propagation, including patients with idiopathic dilated cardiomyopathy. Our study shows that the longest electromechanical delay concerns the LV free wall only in 33% of such patients with complete LBBB. This observation is consistent with recent studies (29–31) and confirms that for the same QRS width and morphology, electromechanical asynchrony can substantially differ, particularly the sequence of LV wall contraction (10,11,32–34).

In HF patients with complete LBBB and idiopathic dilated cardiomyopathy, Ansalone et al. (30) observed with the pulsed-wave DTI echocardiographic technique that the lateral wall was not the latest activated one in every patient. Indeed, the authors observed that it concerned the lateral wall for 35% of their patients and the anterior wall for 26%. Our results, with different patient inclusion criteria, are not so different. For our patients with RBBB, the most delayed LV wall was the anterior for seven (70%) of the 10 patients, whereas for patients with complete LBBB, the most delayed wall was lateral in 27 patients (67%). For patients with incomplete LBBB, this percentage reached only 42% (n = 16). These data suggest that only patients with complete LBBB present mostly with the lateral LV wall as the latest activated one, compared with patients with complete RBBB or incomplete LBBB.

Because the presence of intra-LV asynchrony independently and strongly influences the long-term follow-up of CHF patients, this abnormality should be identified and quantified in every CHF patient. For that purpose, echocardiographic TDI appears to be determinant, as it is a noninvasive and reproducible technique. This technique may be used to identify patients who have a severe prognosis with frequent cardiac decompensation. Identifying CHF patients with intra-LV asynchrony may also be helpful for the therapeutic strategy. Today, despite optimal individualized treatment against HF, no new pharmacologic drug has been found to preclude or even mitigate electromechanical ventricular asynchrony. Therefore, the presence of such asynchrony (independent of the QRS width) should be used to select patients who are likely to respond to cardiac resynchronization, as this nonpharmacologic therapy has been shown to reduce the degree of LV mechanical asynchrony, even in patients with RBBB (29–31,35,36).

Study limitations.   Because coronary angiography was required before including the patient in the present protocol, this likely affected the patient selection, and the results might not be transferred to patients with new diagnosed HF in the outpatient clinic. Indeed, 18 patients had to be excluded from the study, which might have resulted in lost information.

The definition of abnormal intra-LV and inter-V electromechanical asynchrony relies on our control group. Although this group was small (n = 25), every control subject was randomly selected and matched by gender and age criteria with the study group, thus providing robustness and reliability to the statistical analysis. No survival curve could be performed, as no CHF patient died during the follow-up. Because we selected CHF patients without an excessively low LVEF (only 27% of patients had LVEF ≤25%), this result is not surprising over only one-year follow-up. Accordingly, it might turn out that a longer follow-up period would modify the weight of ventricular asynchrony in terms of the morbidity/mortality incidence. Finally, the pulsed-wave TDI echocardiographic technique did not permit us to differentiate passive from active LV wall motion. Although passive motion mostly concerns patients with MI (which is not our study group), strain rate techniques would have certainly helped in identifying true wall contraction.

Conclusions.   In patients optimally treated for HF, the QRS width appears to be poorly correlated with the presence of inter-V and intra-LV electromechanical asynchrony. Even the type of bundle branch block does not predict the location and degree of ventricular electromechanical asynchrony. Intra-LV asynchrony is predictive of HF worsening, independent of the QRS width and LVEF. In addition, this new prognostic factor may select patients who are potential responders to nonpharmacologic HF treatment specifically conceived to reduce the degree of intra-LV electromechanical asynchrony.


   References
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 Abstract
 Methods
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 Discussion
 References
 

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