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Keywords:

  • acute heart failure;
  • electrocardiogram;
  • mortality;
  • right bundle branch block

Abstract.

  1. Top of page
  2. Abstract.
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusions
  8. Conflict of interest statement
  9. Acknowledgements
  10. References

Objectives.  Risk stratification in acute congestive heart failure (ACHF) is poorly defined. The aim of the present study was to assess the impact of right bundle brunch block (RBBB) on long-term mortality in patients presenting with ACHF.

Methods and results.  The initial 12-lead electrocardiogram was analysed for RBBB in 192 consecutive patients presenting with ACHF to the emergency department. The primary endpoint was all-cause mortality during 720-day follow-up. This study included an elderly cohort (mean age 74 years) of ACHF patients. RBBB was present in 27 patients (14%). Age, sex, B-type natriuretic peptide levels and initial management were similar in patients with RBBB when compared with patients without RBBB. However, patients with RBBB more often had pulmonary comorbidity. A total of 84 patients died during follow-up. Kaplan–Meier analysis revealed that mortality at 720 days was significantly higher in patients with RBBB when compared with patients without RBBB (63% vs. 39%, P = 0.004). In Cox proportional hazard analysis, RBBB was associated with a two-fold increase in mortality (hazard ratio 2.18, 95% CI 1.26–3.66; P = 0.003). This association persisted after adjustment for age and comorbidity.

Conclusions.  RBBB is a powerful predictor of mortality in patients with ACHF. Early identification of this high-risk group may help to offer tailored treatment in order to improve outcome.


Introduction

  1. Top of page
  2. Abstract.
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusions
  8. Conflict of interest statement
  9. Acknowledgements
  10. References

The epidemic of heart failure (HF) is a major public health problem. HF is the most frequent cause of hospitalizations in patients more than 65 years of age and these hospitalizations contribute significantly to the enormous cost of the disease [1, 2]. In contrast to chronic HF, risk stratification and initial management is poorly validated in patients presenting with acute congestive heart failure (ACHF). Hence, current American College of Cardiology/American Heart Association (ACC/AHA) and European Society for Cardiology (ESC) initiatives call for more research targeting ACHF [1, 2].

The electrocardiogram (ECG) has been a cornerstone in clinical medicine for more than six decades. In contrast to current belief, additional diagnostic and prognostic applications continue to emerge each year [3, 4]. Twelve-lead ECG is an important tool in the diagnosis of ACHF, particularly in the identification of the cause of acute decompensation including tachyarrhythmia and myocardial infarction [1, 2]. It is unknown, whether electrocardiography also provides prognostic information in patients with ACHF. This would be very attractive, as electrocardiography is routinely performed, easy, safe and inexpensive. Whilst no data are available for ACHF, a large retrospective cohort study including patients with acute myocardial infarction reported that patients with right bundle brunch block (RBBB) had an increased risk of in-hospital death compared with patients with no BBB. RBBB seemed to predict in-hospital death at least as powerful as left bundle brunch block (LBBB) [5].

We hypothesized that RBBB may be a marker of pulmonary artery hypertension and/or right ventricular dysfunction [6] and may therefore be associated with increased mortality in patients with ACHF.

Methods

  1. Top of page
  2. Abstract.
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusions
  8. Conflict of interest statement
  9. Acknowledgements
  10. References

Setting and study population

This study specifically evaluated the prognostic utility of RBBB in patients with ACHF enrolled in the B-type natriuretic peptide for Acute Shortness of Breath Evaluation (BASEL) study [7]. The BASEL study was a prospective study conducted in the emergency department (ED) of the University Hospital Basel, Switzerland. The study was carried out according to the principles of the Declaration of Helsinki and approved by our local ethical committee. Written informed consent was obtained from all participating patients. A total of 452 patients were enrolled in the BASEL study, and 217 patients were diagnosed as ACHF according to current guidelines [1, 2]. The final discharge diagnosis of ACHF was based on clinical presentation and standard investigations, and adjudicated by an internal medicine specialist not involved in the ED care on the basis of all available medical records pertaining to the individual patient, including the response to therapy and autopsy data in those patients dying in-hospital. B-type natriuretic peptide (BNP) levels were measured and available for the final discharge diagnosis in 50% of patients. We excluded patients in whom the presence of RBBB could not be determined due to ventricular pacing, ventricular tachycardia, or missing ECG. Overall, 192 patients (88.5%) qualified for the current study.

ECG, RBBB and LBBB

At the time of presentation to the ED, resting 12-lead ECG was recorded at a paper speed of 25 mm s−1. The ECGs were interpreted by a core laboratory that classified the presence of RBBB and LBBB using standard criteria [8]. The core laboratory physician scoring the ECGs had no information regarding patient baseline characteristics or outcome.

Right bundle brunch block was defined by a QRS duration (QRSd) ≥ 120 ms, in association with the presence of rsR′, or rSR′ complexes in V1 or V2, delayed onset of the intrinsicoid deflection in V1 and V2 more than 50 ms, and wide, slurred S waves in leads I, V5, and V6. The ST-T-wave vectors are opposite in direction to the major QRS vector [8].

Left bundle brunch block was defined by a QRSd ≥ 120 ms, delayed onset of the intrinsicoid deflection in leads I, V5, V6 > 50 ms, the presence of a broad monophasic, often notched R-wave in leads I, V5 and V6, with rS or QS complexes in lead V1 and V2, and ST-T-wave vectors opposite in direction to the major QRS vector [8].

End-point and statistical analysis

All-cause mortality was the primary end-point of this study. Patients were contacted 6, 12 and 24 months after the initial presentation by telephone interview performed by a single trained researcher. In addition, referring physicians were contacted. The administrative databases of the respective hometowns were assessed to ascertain the vital status of those patients who could not be contacted by telephone. All information derived from contingent hospital readmission records or provided by the referring physician or by the outpatient clinic was reviewed and entered into the computer database. The statistical analyses were performed using the SPSS/PC (version 13.0; SPSS Inc., Chicago, IL, USA) software package. Com- parisons were made using the t-test, Mann–Whitney U-test, Fisher's exact test and chi-square test as appropriate. All hypothesis testing was two-tailed. The Kaplan–Meier method was used to analyse and compare survival in patients with or without RBBB. Cox proportional hazard analysis was used to identify predictors of death in univariate and multivariable analysis. Together with RBBB, all baseline, demographic, clinical and laboratory variables routinely available in the ED were entered in a univariate Cox regression analysis. Variables associated with long-term mortality in univariate analysis (P < 0.05) were entered into the multivariable models. To closely reflect clinical practice, three multivariate models were constructed. Model 1 adjusted for age and coronary artery disease (the well-established risk markers in HF patients). Model 2 adjusted for age, and all variables from patient history/comorbidity significantly associated with mortality in univariate analyses. Model 3 adjusted for all variables from history/comorbidity, vital signs, physical examination, laboratory tests routinely available in the ED, and discharge medication significantly associated with mortality in univariate analyses.

Results

  1. Top of page
  2. Abstract.
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusions
  8. Conflict of interest statement
  9. Acknowledgements
  10. References

This study included an elderly cohort (mean age 74 years) of ACHF patients. Nearly half of patients were women, and comorbidity including pulmonary disease was extensive (Table 1). RBBB was present in 27 patients (14%) and LBBB in 32 patients (17%). Baseline demographic, clinical, and laboratory characteristics including BNP levels and left ventricular ejection fraction (LVEF) were very similar in patients with RBBB when compared with patients without RBBB. In the BNP group, in those with RBBB no patient had a BNP < 100 pg mL−1 and 64% had a BNP > 500 pg mL−1. In those without RBBB, 5% had a BNP < 100 pg mL−1 and 66% had a BNP > 500 pg mL−1 (P = NS). Differences amongst groups were restricted to a higher incidence of pulmonary disease, tachypnea, and wheezing in patients with RBBB. In addition, concomitant left axis deviation with left anterior fascicular block was more frequent in patients with RBBB when compared with patients without RBBB (37% vs. 8%, P < 0.001). Initial management including hospitalization rate and admission to intensive care were similar amongst groups. Discharge medication was comparable in both groups with the exception of calcium channel blockers, which were prescribed more often to patients with RBBB (33% vs. 13%, P = 0.009). This difference was already present on admission.

Table 1.   Patient characteristics
 All patients (n = 192)RBBB (n = 27)No RBBB (n = 165)P value
  1. Data are presented as mean ± SD, median (IQR), or number of patients (%). The P-value is given for the comparison of patients with RBBB versus patients without RBBB. COPD, chronic obstructive pulmonary disease; JVP, jugular venous pressure. aIncluding interstitial lung disease, pneumothorax, and pleural effusion. bDetermined in 131 patients during hospitalization. cAmongst survivors (n = 181) at hospital discharge.

Age (years)74 ± 1176 ± 1174 ± 110.480
Female sex86 (45)9 (33)77 (47)0.197
History
 Coronary artery disease135 (70)20 (74)115 (70)0.644
 Arterial hypertension125 (65)18 (67)107 (65)0.854
 COPD43 (22)9 (33)34 (21)0.141
 Asthma4 (2)04 (2)1.000
 Previous pneumonia23 (12)6 (22)17 (10)0.077
 Previous pulmonary embolism6 (3)2 (7)4 (2)0.200
 Other pulmonary or pleural diseasea14 (7)5 (19)9 (6)0.031
 Any pulmonary disease77 (40)16 (59)61 (37)0.028
 Diabetes mellitus65 (34)12 (44)53 (32)0.210
 Chronic kidney disease75 (39)12 (44)63 (38)0.536
Symptoms
 Paroxysmal nocturnal dyspnoea93 (48)15 (56)78 (47)0.425
 Nycturia77 (40)15 (56)62 (38)0.077
 Weight gain32 (17)7 (26)25 (15)0.164
Vital status
 Systolic blood pressure (mmHg)148 ± 32149 ± 26148 ± 330.853
 Diastolic blood pressure (mmHg)88 ± 2286 ± 2189 ± 220.498
 Heart rate (per min)98 ± 6290 ± 17100 ± 270.091
 Temperature (°C)37.2 ± 0.937.3 ± 1.037.2 ± 0.90.796
Signs
 Tachypnoea (>20 per min)87 (45)17 (63)70 (42)0.047
 Elevated JVP41 (21)6 (22)35 (21)0.905
 Hepatojugular reflux30 (16)5 (19)25 (15)0.655
 Rales117 (61)16 (59)101 (61)0.835
 Wheezing26 (14)7 (26)19 (12)0.042
 Hyper-resonant percussion13 (7)3 (11)10 (6)0.399
 Lower-extremity oedema86 (45)11 (41)75 (46)0.648
Laboratory tests
 Creatinine clearance (mL min−1/1.73 m2)54 ± 2951 ± 2655 ± 290.545
 Haemoglobin (g dL−1)12.9 ± 2.412.4 ± 2.313.0 ± 2.40.201
 Serum albumin (g L−1)33 ± 632 ± 533 ± 60.461
 Troponin I (μg L−1)0.5 (0.3–2.4)1.0 (0.3–6.3)0.5 (0.3–2.3)0.380
 B-type natriuretic peptide (pg mL−1)840 (355–1300)847 (210–1300)840 (372–1300)0.545
 Left ventricular ejection fraction (%)b40 (30–55)40 (22–60)40 (30–53)0.810
Medication at admission
 ACE-inhibitor or angiotensin receptor blocker92 (47)16 (57)76 (45)0.221
 Beta-blocker71 (36)9 (32)62 (37)0.658
 Diuretics125 (63)19 (68)106 (62)0.576
 Nitroglycerin40 (20)8 (29)32 (19)0.234
 Digoxin27 (14)7 (25)20 (12)0.059
 Calcium channel blocker31 (16)9 (32)22 (13)0.010
 Aspirin89 (45)15 (54)74 (44)0.322
 Anticoagulation58 (29)13 (46)45 (27)0.032
 Oral steroids18 (9)7 (25)11 (7)0.002
 Inhaled bronchodilators18 (9)5 (18)13 (8)0.145
Medication at dischargec
 ACE-inhibitor or angiotensin receptor blocker143 (79)20 (83)123 (78)0.756
 Beta-blocker113 (62)14 (58)99 (63)0.656
 Diuretic158 (87)23 (96)135 (86)0.177
 Nitroglycerin66 (37)8 (33)58 (37)0.732
 Digoxin19 (11)3 (13)16 (10)0.722
 Calcium channel blocker28 (16)8 (33)20 (13)0.009
 Aspirin89 (49)13 (54)76 (48)0.599
 Anticoagulation90 (50)12 (50)78 (50)0.977
 Oral steroids15 (8)3 (13)12 (8)0.425
 Inhaled bronchodilators28 (16)5 (21)23 (15)0.543
Outcome
 Hospitalization171 (89)26 (96)145 (88)0.194
 Intensive care admission53 (28)8 (30)45 (27)0.800
 Time to discharge (days)11 (5–19)14 (7–19)10 (4–20)0.313
 30-day mortality (%)24 (13)7 (26)17 (10)0.023
 720-day mortality (%) 63.3 ± 9.438.6 ± 3.80.004

A total of 84 patients (44%) died during follow-up. Median duration of follow-up until patient death or last contact was 686 days. No patient was lost to follow-up within the first 12 months. Kaplan–Meier analysis (Fig. 1) revealed that mortality at 720 days was significantly higher in patients with RBBB when compared with patients without RBBB (63% vs. 39%, P = 0.004). In Cox proportional hazard analysis, RBBB was associated with a two-fold increase in mortality (hazard ratio 2.18, 95% CI 1.26–3.66; P = 0.003). As shown in Table 2, this association persisted after multivariable adjustment in several models. After adjusting for age, history/comorbidity, physical examination, vital signs, laboratory tests routinely available in the ED, and discharge medication, the predictive value of RBBB was no longer statistically significant (P = 0.090). In patients with RBBB, concomitant left ventricular systolic dysfunction (LVEF < 50%) did not further impact on the risk of death (P = 0.8).

image

Figure 1.  Survival rates in patients with right bundle branch block (RBBB) when compared with patients without RBBB.

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Table 2.   Univariate and multivariate analysis of right bundle brunch block (RBBB) as a predictor of all-cause mortality
  1. HR, hazard ratio. aAdjusting for age, and coronary artery disease (CAD). bAdjusting for age and patient history/comorbidity. Independent variables in the final model included age, CAD, arterial hypertension, and other pulmonary or pleural disease. cAdjusting for age, history/comorbidity, physical examination, vital signs, laboratory tests routinely available in the ED, and discharge medication. Independent variables in the final model included age (HR 1.05, P = 0.001), arterial hypertension (HR 0.53, P = 0.027), and oral steroids as discharge medication (HR 3.28, P = 0.003).

Univariate P0.003
HR (95% CI)2.18 (1.26–3.66)
Model 1a
 Multivariate P0.012
 HR (95% CI)1.96 (1.16–3.31)
Model 2b
 Multivariate P0.041
 HR (95% CI)1.82 (1.03–3.24)
Model 3c
 Multivariate P0.090
 HR (95% CI)1.79 (0.91–3.51)

In contrast to the findings regarding RBBB, mortality at 720 days was similar in patients with LBBB when compared with patients without LBBB (Fig. 2).

image

Figure 2.  Survival rates in patients with left bundle branch block (LBBB) when compared with patients without LBBB.

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Discussion

  1. Top of page
  2. Abstract.
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusions
  8. Conflict of interest statement
  9. Acknowledgements
  10. References

In patients presenting with ACHF to the ED, the ECG offers unique diagnostic and prognostic information. The major finding of this analysis was that RBBB – but not LBBB – is a powerful predictor of long-term mortality in unselected consecutive patients. This finding has important clinical implications. First, patients with ACHF have a very high mortality rate. Despite this, there are little data regarding long-term outcome of patients with ACHF [1, 2]. Therefore, risk stratification in patients with ACHF is by far less well validated than in patients with chronic HF. Secondly, RBBB can easily be assessed from the 12-lead ECG immediately on presentation. Thirdly, rapid initiation of intensive care and several specific therapeutic interventions possibly including levosimendan [9] or selective PDE5 inhibition [10] may particularly benefit high risk patients identified by RBBB [1, 2]. Fourthly, as the presence of RBBB not only increased 30-day mortality but also long-term mortality, patients with RBBB may benefit from more intense follow-up [1, 2]. Of note, the incidence of RBBB in ACHF was twice the incidence observed in patients with moderate to severe chronic HF [6].

This study complements and extends previous studies on the impact of RBBB in other patient settings. Go et al. [5] examined patients with acute myocardial infarction and found that patients with RBBB had an increased risk of in-hospital death when compared with patients without BBB. RBBB seemed to predict in-hospital death at least as powerful as LBBB. Wong et al. [11] confirmed this observation by showing that RBBB accompanying anterior acute myocardial infarction is an independent predictor of 30-day mortality [12, 13]. Similar findings were reported in patients referred for symptom-limited nuclear exercise testing. Complete RBBB and LBBB were independent predictors of all-cause mortality risk even after adjustment for exercise capacity, nuclear perfusion defects, and other risk factors [1]. Together with these reports, our data strongly contradict the dogma that RBBB heralds a much more favourable cardiovascular prognosis than LBBB [14]. Instead, our data highlight the fact that the prognostic impact of RBBB depends on the clinical setting in which it is recorded.

Why does RBBB predict mortality in ACHF?

By its observational design, our study can only partly elucidate the links between RBBB and mortality. RBBB may result from various disorders affecting the right heart including pulmonary comorbidity. RBBB indicates structural changes in the right ventricle and may highlight that pulmonary hypertension and/or right ventricular dysfunction has complicated the clinical course of the primarily left heart disease resulting in ACHF. In this regard, ACHF seems to have some pathophysiological details in common with acute anterior myocardial infarction [11, 13]. Both are disorders primarily involving the left ventricle where secondary pulmonary hypertension due to severe left ventricular dysfunction or confounding right ventricular disease may impact on outcome. Supporting this concept and data from Wong et al. [11], a large cohort study demonstrated that RBBB increased in-hospital and 1-year mortality rates in patients with acute anterior myocardial infarction [15]. Moreover, recent studies have shown that right ventricular systolic function as quantified by either echocardiography or right heart catheterization is an independent predictor of death in patients with chronic HF [4, 16–18]. In ACHF, RBBB may result from right ventricular pressure overload induced by the combination of passive transduction of increased left atrial pressure and hypoxia-triggered increase in pulmonary vascular resistance [1, 2]. Therefore, selective PDE5 inhibition might be a potential therapeutic strategy in ACHF patients with RBBB [10]. Obviously, further clinical studies are necessary to test this hypothesis. Concomitant left axis deviation with left anterior fascicular block was more frequent in patients with RBBB when compared with patients without RBBB. This finding is supported by previous studies and suggests the concept of ventricular dyssynchrony as reason for worse outcome [19–21]. Moreover, detailed investigations of the impact of RBBB on ventricular interdependence seem warranted [22].

How to detect right ventricular dysfunction in ACHF

Obviously, echocardiography and right heart catheterization provide more detailed information regarding right ventricular dysfunction than the ECG. However, logistic and practical considerations limit the use of echocardiography and right heart catheterization in patients presenting with ACHF to the ED. Respiratory distress, tachypnoea, inability to maintain the supine position are major limitations on the patient side. In addition, echocardiography and right heart catheterization require expertise and devices often not available on a 24-h basis in the ED. In contrast, the ECG is simple, inexpensive, readily available in an ED, and can be interpreted with high accuracy by emergency or internal medicine specialists working in the ED.

Why does LBBB not predict mortality in ACHF?

Left bundle brunch block indicates structural changes in the left ventricle and has consistently been shown to be a powerful predictor of cardiovascular disease and mortality in the general population [11, 12, 23]. In patients with acute myocardial infarction, LBBB identifies a high-risk group with increased comorbidity, less likely to receive therapy, and increased risk for in-hospital death [12]. Moreover, LBBB seems to be a predictor of mortality in stable outpatients with chronic HF [24]. Therefore, at first glance it is surprising that LBBB does not predict mortality in ACHF. The following consideration may explain this observation. By definition, the vast majority of patients with ACHF do have advanced cardiac disease involving the left ventricle that is severe enough to cause ACHF. Therefore, LBBB as an indicator of left ventricular disease does not provide additional prognostic information in a cohort of patients with severe left ventricular disease resulting in ACHF.

Our analysis has three particular strengths. First, it included a large contemporary cohort of consecutive patients. Secondly, the study population was highly representative of the elderly population of patients with ACHF in clinical practice [1, 2]. Thirdly, it is one of the first studies of patients with ACHF providing long-term follow-up data [2, 9].

Study limitations

Potential limitations of the present study merit consideration. First, this was a post-hoc analysis of a randomized controlled trial. However, as the BASEL study recruited consecutive patients, we are not aware of any bias potentially confounding our results. Secondly, echocardiography was performed during hospitalization in two-thirds of patients. However as common in clinical routine, this assessment did not include standardized measurement of right ventricular ejection fraction. Additional studies seem warranted to evaluate whether measurement of right ventricular ejection fraction provides additional prognostic information to that obtained by the simple identification of RBBB in the ECG of patients with ACHF. Thirdly, the onset of RBBB as well as potential disappearance during follow-up was unknown in our cohort. Systematic ECG follow-up might reveal whether patients have improved outcome once RBBB disappears.

Conclusions

  1. Top of page
  2. Abstract.
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusions
  8. Conflict of interest statement
  9. Acknowledgements
  10. References

Right bundle brunch block is a powerful predictor of mortality in patients with ACHF. Attention to this easy accessible parameter may improve patient management.

Acknowledgements

  1. Top of page
  2. Abstract.
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusions
  8. Conflict of interest statement
  9. Acknowledgements
  10. References

This study was supported by research grants from the Swiss National Science Foundation, the Swiss Heart Foundation, the Novartis Foundation, and the Krokus Foundation.

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  2. Abstract.
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusions
  8. Conflict of interest statement
  9. Acknowledgements
  10. References
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