Abstract
Background: Patients with right bundle branch block comprise 5–9% of all patients with acute myocardial infarction. In spite of this, limited data exist on early diagnosis or the usefulness of continuous electrocardiographic monitoring in these patients.
Methods: A prospective multicenter study with 14 Swedish coronary care units. Patients with right bundle branch block and suspicion of acute myocardial infarction with less than 6 hours symptom duration were included. All patients were monitored with continuous vectorcardiography for 12–24 hours.
Results: Seventy‐nine patients were included, 43% had acute myocardial infarction. Patients with acute myocardial infarction had significantly higher initial ST‐vector magnitude values (P = 0.0014) compared to patients without acute myocardial infarction. Patients with acute myocardial infarction also showed gradual regression of ST‐vector magnitude over time that was not seen for patients without acute myocardial infarction (P = 0.005). ST‐vector magnitude measured at the J‐point differentiated best between patients with and without acute myocardial infarction. A cutoff value of 125 μV for initial ST‐vector magnitude resulted in 55% sensitivity and 87% specificity for the diagnosis of acute myocardial infarction. Over time, patients with acute myocardial infarction showed greater changes in QRS‐vector difference compared to patients without acute myocardial infarction (P = 0.052).
Conclusion: Vectorcardiographic monitoring shows good diagnostic abilities for patients with right bundle branch block and clinical suspicion of acute myocardial infarction and could be useful for continuous monitoring of these patients.
Keywords: right bundle branch block, myocardial infarction, diagnosis, continuous vectorcardiography
Patients with right bundle branch block comprise about 5–9% of all patients with acute myocardial infarction. 1 , 2 , 3 , 4 , 5 In spite of this they have received surprisingly little attention regarding early diagnosis or continuous electrocardiographic monitoring.
Patients with narrow QRS complexes and suspicion of acute myocardial infarction benefit from thrombolytic treatment when ST elevation is present on 12‐lead ECG 6 and guidelines recommend the use of ST‐segment elevation criteria when deciding on reperfusion therapy. 7 , 8 No such criteria exist for right bundle branch block. Both patients with right and left bundle branch block benefit from thrombolytic treatment when acute myocardial infarction is suspected 6 and thrombolytic treatment is recommended by guidelines without differing between right or left bundle branch block or recommending the use of ECG criteria. 7 , 8 , 9 Treating all patients with suspicion of acute myocardial infarction may lead to over‐treatment, 10 stressing the need for criteria.
In right bundle branch block, pathological Q‐waves probably carry the same information as in the presence of narrow QRS complex, although this has been debated. 11 , 12 , 13 In the absence of ischemia, right bundle branch block causes secondary changes in the ST segment, 14 probably due to late and uneven depolarization and repolarization of the right ventricle. 15 Knowledge on how these secondary changes behave under ischemic circumstances or where in the ST segment changes should be measured is limited.
Patients with acute myocardial infarction show dynamic electrocardiographic changes and continuous electrocardiographic monitoring of patients with narrow QRS complexes, using vectorcardiography, 12‐lead ECG, or Holter, has been shown to be of value. 16 , 17 , 18 , 19 , 20 , 21 , 22 Analyses of trends for ST segment changes have shown that resolution of ST elevation predicts coronary artery patency, left ventricular function, and prognosis after acute myocardial infarction. 16 , 17 , 18 , 19 , 21 , 22 , 23 , 24 , 25 Likewise analyses of trends for changes in QRS morphology over time also predict outcome and coronary artery patency. 16 , 17 , 21
There is limited knowledge on the use of vectorcardiography in patients with right bundle branch block and suspicion of acute myocardial infarction. We know only of one small, retrospective study showing that vectorcardiographic ST‐segment analysis of patients with right bundle branch block might be useful for diagnosis and monitoring of patients with acute myocardial infarction. 26
The aims of this study were to investigate prospectively the usefulness of vectorcardiographic monitoring of patients with bundle branch block and acute myocardial infarction, the present report focuses on patients with right bundle branch block.
METHODS
The patients were included in the DAG VAG study (diagnosis of acute myocardial infarction with vectorcardiography in the presence of bundle branch block), a prospective multi‐centre study with 14 Swedish coronary care units. Consecutive patients from 11th March 1996 to 31st December 1997 were included.
Inclusion criteria were (1) bundle branch block on admission 12‐lead ECG; (2) chest pain with ≤6 hours duration; and (3) clinical suspicion of myocardial infarction. Exclusion criteria were (1) PQ interval ≤120 ms; (2) pacemaker; and (3) intermittent bundle branch block.
Inclusion was made at arrival to the coronary care unit. In the cases of multiple admissions, only the first admission meeting criteria led to inclusion. Informed consent in writing was gathered. The study was approved by all locally appointed ethics committees. The clinical experimental research laboratory at Sahlgrenska University Hospital/Östra served as a core‐laboratory for ECG and vectorcardiographic reading as well as coordinating the study.
Diagnosis of myocardial infarction was made with the following markers: CK‐MB mass concentration or CK‐B in combination with total CK. Local investigators made all diagnosis. In‐hospital complications were registered by local investigators as unstable angina pectoris after admission, congestive heart failure, or stroke.
12‐Lead ECG
Only patients with right bundle branch block on admission are reported here. A 12‐lead ECG was recorded on admission and was the base for inclusion. ECG calibration was 1 mV = 10 mm and paper speed was 50 mm/s. Right bundle branch block was defined as: (1) QRS duration ≥120 ms, (2) PQ interval >120 ms, (3) rSR´ in lead V1 or V2, and (4) S‐waves in lead I and either lead V5 or V6. Right bundle branch block was further classified according to the QRS axis as having concomitant left anterior hemiblock if the QRS axis was <−30° and concomitant left posterior hemiblock if the QRS axis was > + 90°.
All ECGs were read by all authors and classified as above. The authors were blinded to patient identity, diagnosis, and inclusion center. If authors disagreed on ECG classification of an ECG feature, a majority rule was adopted. If all three authors disagreed on a classification, that patient was excluded.
Vectorcardiography
All patients were monitored for at least 12–24 hours with computerized continuous on‐line vectorcardiography using a MIDA system (Ortivus Medical, Täby, Sweden/Hewlett Packard, Andover, MA, USA). The technique of computerized vectorcardiography has been described previously. 17 In short, the Frank lead system with eight unipolar leads is used to gather information forming three orthogonal leads (X, Y, and Z). 27 Signals are gathered for 1 minute and an average beat is formed. After accepting an initial average beat free from electric interference, which serves as a reference beat, all subsequent average beats are compared to it. Information for different parameters can be visualized on‐line as a trend curve. A derived 12‐lead ECG can also be visualized on‐line. The following vectorcardiographic parameters were analyzed: QRS‐vector difference, comparing the area of the initial QRS complex with the current one; ST‐vector magnitude, showing the sum of absolute ST‐segment deviation from the baseline; and STC‐vector magnitude, representing the change in ST vector of the current complex compared to the initial one. Both ST‐vector magnitude and STC‐vector magnitude were measured at the J‐point and 20, 40, 60, and 80 ms after the J‐point. Heart rate and QRS duration were also registered. When analyzing vectorcardiographic registrations, the above parameters were measured at the beginning of registration, after 90 minutes, 3, 6, 12, and 24 hours. Trends for the ST‐vector magnitude 20 ms after the J‐point were analyzed for 30, 50, and 70% decline from the maximal value during the first 90 minutes. Intermittent bundle branch block was diagnosed if QRS duration was 120 ms or less at any time and derived 12‐lead ECG did not show right bundle branch block.
A registration was excluded from analysis if it showed an interruption of more than 20 minutes for the first 90 minutes or more than 1 hour in conjunction to other time points of registration, if electric interference made analysis difficult, if registration was shorter than 12 hours. All registrations were analyzed by two experienced and independent observers, blinded to patient diagnosis.
Statistical Analysis
Statistical analysis was performed using Statview 4.5 for Macintosh. Contingency tables were compared with chi‐square tests or Fisher's exact test when appropriate. Mann‐Whitney U method was used to compare means. ANOVA methods were used to analyze repeated measurements. The ANOVA method requires a balanced model, all patients having registrations at all points. Not all patients had 24‐hour registrations, therefore ANOVA for repeated measurements was calculated for the first 12 hours. Spearmann´s rank correlation was used when analyzing correlation between continuous variables. P value < 0.05 was taken as significant.
Negative‐ and positive post‐test probabilities were calculated. The outcome of these calculations describes how an application of a diagnostic test revises the probability of disease up or down, given a positive or a negative test result. Post‐test probabilities are dependent on the prevalence of the disease (pretest probability). The formulas used were according to Schechter. 28
RESULTS
Seventy‐nine patients had vectorcardiographic registrations available for interpretation. Thirty‐one patients had isolated right bundle branch block, 40 had concomitant left anterior hemiblock, and 8 had concomitant left posterior hemiblock. Patient characteristics are shown in Table 1. The majority (86%) of patients who did not develop a myocardial infarction had unstable angina.
Table 1.
Patients Characteristics
| ALL | AMI | No AMI | |
|---|---|---|---|
| Number of patients (% of all) | 79 | 34 (43) | 45 (57) |
| Mean age in years (range) | 75 (45–93) | 74 (51–86) | 76 (45–93) |
| Age >75 years: n (%) | 46 (58) | 17 (50) | 29 (64) |
| Male: n (%) | 64 (81) | 27 (79) | 37 (82) |
| Previous MI: n (%) | 37 (47) | 13 (38) | 24 (53) |
| Diabetes: n (%) | 17 (22) | 7 (21) | 10 (22) |
| Heart rate on admission (bpm) | 75 | 77 | 74 |
| QRS duration on admission (ms) | 152 | 154 | 151 |
AMI = acute myocardial infarction; MI = myocardial infarction; bpm = beats per minute; ms = milliseconds.
All comparisons between AMI and no AMI nonsignificant.
Patients with acute myocardial infarction showed greater changes in QRS‐vector difference over time compared to those without acute myocardial infarction (Fig. 1). QRS‐vector difference values at 12 and 24 hours correlated positively with maximal CK‐MB (P = 0.0122 and P = 0.032, respectively). QRS‐vector difference trends did not differ between patients with acute myocardial infarction treated with thrombolytics or not.
Figure 1.
Changes in QRS‐vector difference over time. Patients with and without acute myocardial infarction compared. Points show mean QRS‐vector difference, vertical bars indicate 95% confidence interval. P = 0.023 for overall difference between AMI and no AMI. P = 0.052 for difference between trends. AMI, acute myocardial infarction; μV, microvolts; QRS‐VD, QRS‐vector difference.
ST‐vector magnitude was measured at different points of the ST‐segment, at J + 0, J + 20, J + 40, J + 60, and J + 80 ms. Patients with acute myocardial infarction had significantly higher initial ST‐vector magnitude values compared to patients without acute myocardial infarction and showed greater changes over time. This was true for all points of measurement of the ST segment. ST‐vector magnitude at J + 0 ms discerned best between those with and without acute myocardial infarction with smaller differences for measurements farther away from the J‐point. ST‐vector magnitude changes over time for measurement at J + 0 and J + 60 ms are shown in Figure 2. Initial ST‐vector magnitude value and maximal CK‐MB value correlated positively (P = 0.0004). There was no significant difference of initial values of ST‐vector magnitude for isolated right bundle branch or concomitant left anterior or left posterior hemiblock, this was true for measurement at all the predefined points of the ST segment. More patients with acute myocardial infarction reached 30, 50, and 70% decline in ST‐vector magnitude compared to those without, 71% versus 88% (P = 0.066), 44% versus 71% (P = 0.025), and 31% versus 59% (P = 0.0136), respectively.
Figure 2.
Changes over time in ST‐vector magnitude at J + 0 and J + 60 ms point. Patients with and without acute myocardial infarction compared. Points show mean ST‐vector magnitude, vertical bars indicate 95% confidence interval. Difference between trends for AMI and no AMI: P = 0.005 and P = 0.0007 for ST‐VM at J + 0 and J + 60 ms, respectively. Trend for no AMI: P = 0.55 and P = 0.0096 for J + 0 and J + 60 ms, respectively. Trend for AMI: P < 0.0001 for J + 0 and J + 60 ms. AMI, acute myocardial infarction; μV, microvolts; ST‐VM, ST‐vector magnitude.
Thrombolytic treatment of patients with acute myocardial infarction did not shorten the time to, or increase the number of patients reaching 30%, 50%, or 70% decline in ST‐vector magnitude.
STC‐vector magnitude at J + 0, J + 20, J + 40, J + 60, and J + 80 ms showed similar trends over time with significant increase for patients with acute myocardial infarction compared to those without, Figure 3 shows STC‐vector magnitude for J + 0 ms as an example.
Figure 3.
Changes in STC‐vector magnitude at J + 0 ms, comparison of patients with and without acute myocardial infarction. Points show mean STC‐vector magnitude, vertical bars indicate 95% confidence interval. P = 0.019 for difference between AMI and no AMI. AMI, acute myocardial infarction. μV, microvolts; STC‐VM, STC‐vector magnitude.
A receiver operating characteristics curve for different levels of initial ST‐vector magnitude values for J + 0 ms was drawn to see what value best discriminated between those with and without acute myocardial infarction (Fig. 4). A ST‐vector magnitude value of 125 μV was closest to the upper left corner and using that as a cutoff value for diagnosis of acute myocardial infarction, gives a sensitivity of 55% (95% confidence interval 39–79%) and specificity of 87% (95% confidence interval 79–96%). Given the pretest probability of 0.43 for acute myocardial infarction, this resulted in a positive post‐test probability of 0.76 and negative post‐test probability of 0.28. A previously proposed cutoff value of 200 μV or ST‐vector magnitude at J + 20 ms 26 resulted in a sensitivity of 30% and specificity of 93%.
Figure 4.
Receiver operating characteristic curve for initial ST‐vector magnitude at J + 0 ms. Points show sensitivity and specficity in steps of 5 μV from 50 to 220 μV. μV, microvolts; ST‐VM, ST‐vector magnitude.
DISCUSSION
Our study is the only prospective study we know of that investigates patients with right bundle branch block and suspected acute myocardial infarction, considering early diagnosis and continuous electrocardiographic monitoring of any kind. We found differences between patients with and without acute myocardial infarction in QRS parameters and more pronounced differences in ST parameters. In order to get a more objective view of changes in different parameters, we chose to look at actual values for different parameters over time rather than use predefined patterns as has been done earlier. 17 , 29
QRS‐vector difference for patients with acute myocardial infarction increased more with time, compared to those without acute myocardial infarction. The same pattern is seen for patients with narrow QRS complexes and might reflect the evolution of myocardial necrosis. 16 , 17 , 21 Both patients with and without acute myocardial infarction showed QRS‐vector changes, this might be explained by that most of the patients without myocardial infarction had ischemic heart disease and therefore most likely exhibit QRS‐vector difference changes of transient ischemic nature. 30 , 31 Thrombolytic treatment in patients with narrow QRS complexes results in less pronounced QRS‐vector changes. 16 , 17 , 21 The reason that we do not see this in our study might be that the study is too small to detect such differences or that the patients treated with thrombolytics might have had more “myocardium at risk” before decision on thrombolytic treatment was made.
ST‐vector magnitude analyses showed clear difference between patients with and without acute myocardial infarction. Patients with acute myocardial infarction showed decline of ST‐vector magnitude with time and gradually reaching a level similar to those without acute myocardial infarction. This is the same pattern seen for patients with narrow QRS complexes and in agreement with previous findings. 17 , 29 ST‐vector magnitude trends were different depending on where in the ST‐segment measurements were made. As an example, trends for ST‐vector magnitude at J + 0 ms remained unchanged for patients without acute myocardial infarction, while trends for ST‐vector at J + 60 ms declined significantly for patients with as well as for those without acute myocardial infarction. Higher ST‐vector magnitude values further away from the J‐point might be explained by the secondary STT changes normally apparent in the right bundle branch block. 14 The fact that the ST‐vector magnitude trends for measurements farther away from the J‐point show regression for both patients with and without acute myocardial infarction might be due to the fact that the majority of patients without acute myocardial infarction had unstable angina. Patients with unstable angina might have had down sloping ST‐segment depression that would produce greater ST‐vector magnitude changes when measured farther away from the J‐point. Thus, ST measurements at J + 0 ms may be more sensitive for detection of transmural myocardial ischemia than measurements obtained further away from the J‐point. Thrombolytic treatment of patients with narrow QRS complex and acute myocardial results in greater ST‐vector magnitude regression and in shorter time. 17 , 18 We saw no significant change in that direction. The reason for this could be the same as discussed above for the effect of thrombolytic treatment on QRS‐vector difference.
Vectorcardiographic monitoring of ST changes in patients with right bundle branch block and suspicion of acute myocardial infarction seems useful. After 3 hours, ST‐vector magnitude changes for patients with acute myocardial infarction had regressed to the same value as that of patients without myocardial infarction. Thus, recurrent increase in ST‐vector magnitude would most likely reflect myocardial ischemia and indicate a risk for progression to reinfarction. Indeed, patients with right bundle branch block undergoing percutaneous coronary angioplasty exhibit an increase in ST‐vector magnitude during coronary artery occlusion. 32
The diagnostic abilities of initial ST‐vector magnitude value with a sensitivity of 55% and specificity of 87% may be considered good and is comparable to the diagnostic abilities of the 12‐lead ECG for narrow QRS complexes. 33 , 34 An initial ST‐vector magnitude of ≥125 μV gave the best diagnostic abilities. In small study of 23 patients with right bundle branch block and suspected acute myocardial infarction, a cutoff value of ≥200 μV for ST‐vector magnitude at J + 20 ms, sometime during the first 4 hours gave 64% sensitivity and 100% specificity. 26 Using that cutoff value for initial value in this study gave a sensitivity of only 30% and specificity of 93%.
CONCLUSION
It is feasible to use vectorcardiography for monitoring patients with right bundle branch block and suspicion of acute myocardial infarction both for early diagnosis and subsequent on‐line monitoring during the first 12–24 hours after admission.
Acknowledgments
Acknowledgments: This work was supported by a grant from the Swedish Heart and Lung Foundation. The authors would like to thank research nurses Gerd Kallstrom, Ann‐Marie Svensson, Monica Eriksson, Jenny Rossberg, and Helena Svensson for their invaluable assistance. We also thank all the participating centres: Sahlgrenska University Hospital/Östra, Sahlgrenska University Hospital/Mölndal, Sahlgrenska University Hospital/Sahlgrenska, Linköping University Hospital, Danderyd University Hospital, Örebro Hospital, Västerås Hospital, Gävle Hospital, Västervik Hospital, Bollnäs Hospital, Köping Hospital, Kungälv Hospital, Säffle Hospital, Skene Hospital.
Parts of these results have been submitted in abstract form to the XXIII Congress of the European Society of Cardiology. This work was supported by a grant from the Swedish Heart and Lung Foundation.
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