STATE-OF-THE-ART PAPER
Significance of QRS Complex Duration in Patients With Heart Failure
Amir Kashani, MS, MD* and
S. Serge Barold, MD, FACC ,*
* Section of Cardiology, Yale University School of Medicine, New Haven, Connecticut
Division of Cardiology, University of South Florida College of Medicine, Tampa, Florida
Manuscript received November 1, 2004;
revised manuscript received December 26, 2004,
accepted January 12, 2005.
* Reprint requests and correspondence: Dr. S. Serge Barold, 5806 Mariner’s Watch Drive, Tampa, Florida 33615. (Email: ssbarold{at}aol.com).
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Abstract
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Prolongation of QRS ( 120 ms) occurs in 14% to 47% of heart failure (HF) patients. Left bundle branch block is far more common than right bundle branch block. Left-sided intraventricular conduction delay is associated with more advanced myocardial disease, worse left ventricular (LV) function, poorer prognosis, and a higher all-cause mortality rate compared with narrow QRS complex. It also predisposes heart failure patients to an increased risk of ventricular tachyarrhythmias, but the incidence of cardiac or sudden death remains unclear because of limited observations. A progressive increase in QRS duration worsens the prognosis. No electrocardiographic measure is specific enough to provide subgroup risk categorization for excluding or selecting HF patients for prophylactic implantable cardioverter-defibrillator (ICD) therapy. In ICD patients with HF, a wide underlying QRS complex more than doubles the cardiac mortality compared with a narrow QRS complex. There is a high incidence of an elevated defibrillation threshold at the time of ICD implantation in patients with QRS 200 ms. Mechanical LV dyssynchrony potentially treatable by ventricular resynchronization occurs in about 70% of HF patients with left-sided intraventricular conduction delay, a fact that would explain the lack of therapeutic response in about 30% of patients subjected to ventricular resynchronization according to standard criteria relying on QRS duration. The duration of the basal QRS complex does not reliably predict the clinical response to ventricular resynchronization, and QRS narrowing after cardiac resynchronization therapy does not correlate with hemodynamic and clinical improvement. Mechanical LV dyssynchrony is best shown by evolving echocardiographic techniques (predominantly tissue Doppler imaging) currently in the process of standardization.
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Abbreviations and Acronyms
| | CI = confidence interval | | CRT = cardiac resynchronization therapy | | ECG = electrocardiogram | | HF = heart failure | | HR = hazard ratio | | ICD = implantable cardioverter-defibrillator | | LBBB = left bundle branch block | | LV = left ventricle/ventricular | | LVEF = left ventricular ejection fraction | | NYHA = New York Heart Association | | RBBB = right bundle branch block | | VT = ventricular tachycardia |
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As long ago as 1962, there was speculation regarding the prognosis of QRS prolongation in patients with heart failure (HF) (1). Thereafter, a few studies reported mortality rates of 50% to 70% (over 50 to 60 months of follow-up) in patients with HF with left ventricular (LV) conduction delay (2–4) but others could not corroborate these findings (5). The conflicting results of these older studies may have been related to the prevailing unstandardized diagnosis and management of HF. Since then, important therapeutic advances have generated new questions about the significance of QRS prolongation in patients with HF.
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Incidence
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Prolongation of QRS (120 ms) occurs in 14% to 47% of patients with HF (Table 1) and is generally accepted as occurring in approximately 30% (4,6–19). Left bundle branch block (LBBB) occurs more commonly than right bundle branch block (RBBB) (25% to 36% vs. 4% to 6%, respectively) (13,20,21). There are a number of possible causes for the varying reported incidence of QRS prolongation in the HF population. The definition of QRS prolongation is not uniform; some studies set the limit at 120 ms and others at 150 ms. No two studies used the same methodology to measure QRS duration (Table 1) (4,6–11,13,14,17). Indeed, a variety of methodologies were applied to measure QRS duration: computer-reported measurements, average of several complexes, or widest complex on electrocardiogram (ECG). Some reports either were vague or simply did not state how QRS durations were measured.
Although all of the studies in Table 1 were conducted in patients with HF, there is obviously some heterogeneity among studied populations. Some patients with HF may not have had true LV systolic dysfunction, particularly in studies in which the LV ejection fraction (LVEF) was not determined. Some study populations consisted of patients with advanced HF (11,15), others involved HF patients with implanted defibrillators (a group that generally has more severe disease than the populations in most other reports) (14), whereas others focused on clinically stable outpatients (13).
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LV function and clinical status
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Prolongation of QRS (120 ms) is a significant predictor of LV systolic dysfunction in patients with HF (4,8,10,11,22). In contrast, the significance of QRS prolongation has not yet been evaluated in HF with a normal LVEF and diastolic dysfunction. In patients with HF, an inverse correlation exists between QRS prolongation and LVEF (Table 1) (4,8,10,11,13,18). In a study of nearly 3,500 patients with HF, Shenkman et al. (7) found a stepwise increase in the prevalence of systolic LV dysfunction as QRS complex duration increased progressively above 120 ms. A more recent study conducted in 343 patients with HF reported LVEF of 41%, 36%, 29%, and 25% in patients with QRS durations of <100 ms, 100 to 119 ms, 120 to 149 ms, and 150 ms, respectively (10). These observations in patients with HF are in keeping with the findings of Murkofsky et al. (23), who analyzed 226 patients (without typical bundle branch block, pacemaker, or stated HF) referred for radionuclide exercise ventriculography. The study indicated a high likelihood of an abnormal LVEF <45% with a QRS >0.10 s. The specificity increased for each 0.01-s increase in QRS duration so that it increased to over 99% with a QRS increment from >0.10 s to >0.12 s (23).
Moderate or severe mitral regurgitation was seen in 8% and 20% of patients with HF with QRS <120 ms and 120 ms, respectively. Increasing QRS duration was also associated with more severe tricuspid regurgitation (10).
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Progression of QRS duration
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As a rule, QRS duration increases as LV function worsens (4,8,10,13,24). One HF study indicated that the incidence of QRS prolongation (>120 ms) increased from 10% to 32% and 53% when patients moved from New York Heart Association (NYHA) functional class I to class II and III, respectively (24). In a study of 5,517 outpatients with HF, QRS prolongation was seen more frequently in patients with advanced NYHA functional class (32.8% of patients with complete LBBB vs. 26.4% without complete LBBB were in NYHA class III to IV) (21). Gasparini et al. (25) reported similar findings in a study of 158 patients with severe HF undergoing biventricular pacemaker implantation: 86% of patients with QRS >150 ms were in NYHA functional class III or IV versus 60% of patients with QRS <150 ms (p = 0.002). According to Xiao et al. (26), who analyzed a series of patients with dilated cardiomyopathy of mixed etiology admitted to a tertiary center (not necessarily for a procedure), QRS prolongation progresses at an annual rate of 5 ms in a population presumed to have HF and who received appropriate therapy for it, although HF diagnosis was not specifically indicated by the investigators. Larger increases in QRS duration occur in patients with early mortality. In the study by Xiao et al. (26), the time from reaching a QRS of 160 ms to death was 9.8 ± 18 months in patients without an implanted pacemaker versus 31 ± 16 months in patients with a pacemaker (26). The significance of these observations is unclear unless one postulates that ventricular pacing was intermittent because impaired LV dysfunction is related to the cumulative percent of ventricular pacing (27–30).
One study of 56 patients with symptomatic HF (followed up from 180 to 7,660 days; mean, 1,755 days) and necropsy-proven idiopathic dilated cardiomyopathy documented an increase in QRS duration from an average of 0.10 s to an average of 0.13 s in 76% of patients before death (20). These results are consistent with those of other reports in cardiomyopathy (ischemic or non-ischemic) and patients with HF identifying QRS prolongation as a poor prognostic indicator (4,26).
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Mortality
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Patients with HF with QRS prolongation have higher all-cause mortality and possibly a higher incidence of sudden death (or cardiac death) than those with narrow QRS complexes (4,9,11,13,31,32) (Table 2). In fact, mortality rates progressively increase as intraventricular conduction delay increases. In one study, QRS <0.12 s, QRS 0.12 to 0.16 s, and QRS >0.16 s correlated with 20%, 36%, and 58% mortality at 36 months, respectively (9).
Kalra et al. (8) investigated the optimal QRS duration that separates patients with HF into those with a relatively benign versus a poor prognosis (i.e., increased mortality or heart transplantation). Patients with a QRS 0.12 s had a three-fold increased risk for the combined end point of death or transplantation. Also, five-year survival was significantly lower in this patient population when compared with patients with HF with QRS <0.12 s (47% vs. 84%; p < 0.0001) (8).
In patients with B-type natriuretic peptide levels >400 pg/ml, QRS prolongation was found to be a significant univariate and multivariate predictor of all-cause death, cardiac death, and pump failure death (33). In a study of 82 patients with HF and dilated cardiomyopathy, change in QRS duration over time (0.5 ms/month) was a multivariate predictor of cardiac death or need for heart transplant at one year (34). In another study, QRS duration was the only electrocardiographic parameter with independent prognostic value for adverse outcomes (22). In 100 patients with HF referred for cardiac transplantation, 55% of patients with QRS duration 0.12 s (vs. 24% with QRS <0.12 s) went on to transplantation or death (11). The time course of the transplantation patients was not stated.
In a substudy of the Multicenter Unsustained Tachycardia Trial (MUSTT) (35), Zimetbaum et al. (36) analyzed ECGs from 1,638 patients (approximately 70% had HF) who did not receive antiarrhythmic drugs or implantable cardioverter-defibrillators (ICDs). Seventy-five percent of the patients with LV hypertrophy had clinical congestive HF, and so did 62% of those without LV hypertrophy. The primary end point was cardiac arrest or arrhythmic death. Multivariate analyses identified nonspecific intraventricular conduction delay (defined as QRS 0.11 s but morphologically different from LBBB or RBBB) as a predictor of arrhythmic or cardiac arrest (hazard ratio [HR], 1.44; 95% confidence interval [CI], 1.11 to 1.88) and total (HR, 1.47; CI, 1.22 to 1.78) mortality. The LBBB was also a significant predictor of arrhythmic (HR, 1.49; CI, 1.02 to 2.17) and total (HR, 1.61; CI, 1.26 to 2.08) mortality. The RBBB, however, was not associated with increased arrhythmic or total mortality (36).
Prolongation of QRS and severe cardiomyopathy (defined as LVEF <30%) have an additive effect on mortality. The highest mortality rates are seen in patients with HF with QRS prolongation and LVEF <35% secondary to both ischemic and non-ischemic etiologies (4,7).
In 1995, Silverman et al. (32) reported that QRS prolongation had a different prognostic value in patients with chronic HF with non-ischemic versus ischemic cardiomyopathy. They found that a prolonged QRS carried a significantly worse prognosis only in patients with non-ischemic cardiomyopathy. These results are at variance from the observations of Iuliano et al. (4), who found no significant difference (median follow-up, 45 months) in mortality or sudden death in patients with non-ischemic cardiomyopathy and QRS >0.12 s versus QRS <0.12 s. However, Iuliano et al. (4) reported a significantly higher all-cause and sudden-death mortality rate in patients with HF with ischemic cardiomyopathy and a longer QRS duration. Comparing the groups with QRS 0.12 s versus QRS  0.12 s (median follow-up, 45 months), the mortality was 51% vs. 34% and the sudden death rate was 25% vs. 17%, respectively (4).
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Ventricular tachycardia
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The aforementioned data raise the question of whether ventricular tachycardia (VT) accounts for the increased mortality in patients with HF with QRS prolongation. A wide QRS complex predisposes patients with HF to bundle branch re-entrant VT (bundle branch to bundle branch), a relatively rare arrhythmia that occurs predominantly in patients with dilated cardiomyopathy and a wide QRS complex in the form of LBBB or a nonspecific intraventricular conduction delay resembling LBBB (37–39). Although many patients with this form of VT receive ICDs because of the risk of other types of VT, the diagnosis of bundle branch re-entry VT is important because it can be easily eliminated by ablation of the right bundle branch.
Horwich et al. (40) studied 777 patients using electrophysiologic studies for assessment of VT inducibility. The percentage of patients with HF was not specified. Sustained monomorphic VT was induced in 49% and 23% (p <0.0001) of patients with QRS 120 ms and <120 ms, respectively, with bundle branch re-entrant VT in a minority, and multivariate analysis showed that QRS duration was an independent risk factor for VT inducibility. In fact, the risk of inducible sustained monomorphic VT increased by 2.4% for each 1 ms increase in QRS duration. This suggests that intraventricular conduction delay with or without a scarred myocardium can act as a substrate for re-entrant VT.
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ICD trials
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Multicenter Automatic Defibrillator Implantation Trial II (MADIT-II).
In MADIT-II, Moss et al. (41,42) studied the effect of prophylactic cardioverter-defibrillator implantation in patients with NYHA functional class I to III, LVEF 30%, and a myocardial infarction one or more months before enrollment in the study. The patients were characterized as having substantial LV dysfunction (mean baseline LVEF was about 23%), and 70% were in NYHA functional class I or II HF. The actual incidence of clinical HF was not mentioned, but it was probably common in this highly selected patient population. We believe that the MADIT-II observations can be extrapolated to the general HF patient population. Three clinically relevant categories of QRS duration (<0.12 s, 0.12 to 0.15 s, >0.15 s) were analyzed. There was a trend toward better reduction in mortality with ICD therapy in patients with the wider QRS complexes, but it was not statistically significant. Moss et al. (42) then extended their analysis of the MADIT II data to include each of six QRS durations (<0.09 s, 0.09 to 0.10 s, 0.11 to 0.12 s, 0.13 to 0.14 s, 0.15 to 0.16 s, >0.16 s). Similar HRs (mortality reduction) were found across all six QRS durations, suggesting that QRS duration is not an effective risk stratification factor for ICD therapy in the MADIT II population.
In addition to the reduction in mortality results, the MADIT II investigators also noted a slightly higher rate of hospitalization for HF in the ICD group compared with control patients (19.8% vs. 14.9%, respectively) (41). The higher hospitalization rate might have been attributable to mechanical LV dyssynchrony induced by chronic right ventricular pacing (27,28,30). Indeed, preliminary data from the MADIT II trial suggested that HF is related to the percentage of ventricular pacing (43), hence the importance of minimizing right ventricular pacing, especially in patients who do not need it.
Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT).
The SCD-HeFT was a randomized, placebo-controlled study designed to determine whether amiodarone or a single-chamber ICD programmed to shock only (no back-up pacing) would reduce all-cause mortality when compared with placebo (double-blind to drug therapy) in patients with dilated cardiomyopathy (ischemic or nonischemic), NYHA functional class II and III HF, and LV dysfunction (LVEF 35%) (44–46). A total of 2,521 patients were enrolled with randomization to ICD (n = 829), amiodarone therapy (n = 845), or placebo (n = 847). The median age of patients was 60 years (range, 19 to 90 years). Unlike the MADIT II trial, the SCD-HeFT study incorporated patients with nonischemic cardiomyopathy as well as those with ischemic HF. Most importantly, both patient groups were found to benefit from ICD therapy. When stratifying the ECG data in the ICD versus placebo groups, ICD therapy was associated with a significant reduction in the risk of mortality compared with placebo, regardless of the ECG measure, including QRS duration <120 ms or 120 ms. Another analysis found that although ICD shock rates were highest in patients with a longer QRS duration, patients with a narrow QRS also experienced a significant number of shocks, suggesting that treatment is warranted for this group also at higher risk.
A subset of MADIT II-like patients enrolled in SCD-HeFT (approximately 80% of the ischemic patients in SCD-HeFT met MADIT II criteria) showed the same reduction in mortality with ICD therapy regardless of QRS duration. Thus, for the SCD-HeFT population, no ECG measure seems to be specific enough to provide subgroup risk categorization for either excluding or selecting patients for ICD therapy.
On the basis of the MADIT II and SCD-HeFT data, the Centers for Medicare and Medicaid recently abandoned their restrictions on Medicare reimbursement for ICDs in patients with a prior myocardial infarction and LVEF of 30% or less and QRS duration 120 ms (47).
Despite the above considerations, a wide QRS complex remains an important prognostic marker in ICD patients with HF. In a recent study over 24 months in ICD patients with HF, those with a wide underlying QRS complex showed more than double the cardiac mortality than those with a narrow QRS complex (14). In view of two recent meta-analyses suggesting that resynchronization decreases mortality (48,49), it is tempting to postulate that the mortality in ICD patients with a wide QRS complex might have been reduced by upgrading their devices to biventricular ICDs. The association of a wide QRS complex with more advanced disease in ICD patients is also reflected in the high incidence of an elevated defibrillation threshold at the time of ICD implantation in patients with QRS 200 ms, requiring the use of high-output ICDs (50).
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Cardiac resynchronization
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Growing experience with cardiac resynchronization therapy (CRT) has highlighted the limitations of a wide QRS complex as a surrogate for mechanical LV dyssynchrony (51–83). Widening of the QRS complex was a major entry criterion in the recent trials and other studies of biventricular pacing in patients with HF with LVEF 35% (Table 3). The QRS duration in the major trials ranged from >120 to >150 ms (63,67,77,84).
Electrocardiographic parameters.
QRS duration and mechanical dyssynchrony
Barring a very wide spontaneous QRS complex, which probably increases the likelihood of associated mechanical LV dyssynchrony (54), the latter is not necessarily related to electrical dyssynchrony judged by QRS duration (Table 3). Indeed, the correlation is weak. Some patients with a wide QRS and a severely depressed LVEF may show no area of substantial mechanical delay (85). Thus, the predictive value of the basal QRS complex is poor for responders and nonresponders. (Table 3: responders consist of patients who had a statistically significant decrease in NYHA functional class (or equivalent) and/or increase in LVEF (or equivalent), and nonresponders consist of those who showed no change in these two indexes). This may explain why 20% to 30% of the patients in the major trials did not have a response to CRT (86–89). In this respect, Bleeker et al. (85) evaluated the role of the QRS complex as a marker of mechanical LV dyssynchrony (based on septal-to-lateral conduction delay) in 90 patients with severe HF (LVEF <35%, NYHA functional class III to IV). Severe mechanical LV dyssynchrony was defined as an electromechanical delay >60 ms between the septum and the lateral wall based on tissue Doppler imaging, the technique that has thus far been used the most frequently to determine LV mechanical dyssynchrony. The >60 ms value was based on previous observations that a delay >60 ms between the peak systolic velocity of the septum and lateral wall was highly predictive of response to CRT. Severe mechanical LV dyssynchrony was observed in 27% of the patients with a narrow QRS complex (>120 ms), in 60% of patients with a QRS duration 120 to 150 ms, and in 70% of patients with QRS >150 ms. Thus, 30% to 40% of patients with a wide QRS (predominantly reflecting left-sided conduction delay) complex did not show mechanical LV dyssynchrony, a figure that correlates with the reported percentage of nonresponders to CRT selected on the basis of QRS duration. For this reason, echocardiographic assessment with quantification of LV dyssynchrony is emerging as a superior predictor of CRT outcome than the widened QRS complex (53–55,62,69,73,85,86,89–91).
RBBB
So far, the experience of CRT in a small number of patients with RBBB and systolic HF is mixed, and it is likely that benefit may be restricted to patients with demonstrable mechanical LV dyssynchrony by echocardiography (92).
Narrow QRS complex <120 ms
It is possible that patients with HF with a narrow QRS complex (<120 ms) may benefit from CRT if they have echocardiographic mechanical LV dyssynchrony. This question is presently under intensive clinical investigation (55,93).
QRS narrowing after cardiac resynchronization
The paced QRS complex often narrows after resynchronization, but there is no correlation between QRS narrowing and the clinical response (Table 3). In some cases the QRS complex after CRT may actually lengthen or remain unchanged despite substantial improvement in mechanical LV dyssynchrony. Increased QRS duration with CRT does not necessarily reflect the presence of ventricular areas with slow conduction resulting in more heterogeneous myocardial activation. With mono-chamber LV pacing, there is an obvious discrepancy between QRS duration (compared with baseline) and hemodynamic and clinical improvement (94). Thus, in patients with HF, the paced QRS duration cannot be assumed to reflect a more heterogeneous propagation pattern of LV activation and prolonged duration of mechanical activation.
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Conclusions
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A wide QRS complex reflecting left-sided intraventricular conduction delay in patients with HF is associated with more advanced myocardial disease, worse LV function, poorer prognosis, and a higher all-cause mortality rate compared with patients with a narrow QRS complex. The influence of a wide QRS complex on the incidence of cardiac or sudden death is unclear because of limited observations. A progressive increase in QRS duration worsens the prognosis. In patients with systolic HF, the presence of a left-sided conduction delay alone can no longer be automatically equated with the presence of mechanical LV dyssynchrony, which is actually present in only about 70% of cases. Mechanical LV dyssynchrony is best shown by evolving echocardiographic techniques (predominantly tissue Doppler imaging) currently in the process of standardization. Echocardiographic parameters will complement or even replace QRS complex duration as a criterion for CRT patient selection. The duration of the basal QRS complex does not reliably predict the clinical response to ventricular resynchronization, and QRS narrowing after CRT does not correlate with hemodynamic and clinical improvement.
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Abstract
Incidence