Significance of an isolated new right bundle branch block in a patient with chest pain

Abstract

Chest pain is a common presenting symptom in emergency departments, and a typical manifestation of acute myocardial infarction (AMI). Recognition of ECG changes in AMI is essential for timely diagnosis and treatment. Right bundle branch block (RBBB) may be an isolated sign of AMI, and was previously considered as a criterion for fibrinolytic therapy. Since the most recent European Society of Cardiology and American Heart Association guidelines in 2013, RBBB alone is no longer considered a diagnostic criterion of AMI, even if it occurs in the context of acute chest pain, as RBBB does not usually interfere with the interpretation of ST-segment alteration. Our case illustrates an acute septal myocardial infarction with an isolated RBBB, and thus the importance of recognising this pattern in order to permit timely diagnosis and treatment.

Background

The prevalence of a right bundle branch block (RBBB) in the general population is 1% in the absence of structural heart disease; its prevalence increases with age, suggestive of a degenerative process of the conduction system.¹ It is also associated with several structural heart diseases (myocarditis, hypertension, congenital heart disease) or right ventricular overload (cor pulmonale, pulmonary embolism). On the other hand, RBBB is reported in 5–11% of acute myocardial infarctions (AMI),^{2 3} and can be an isolated ECG sign of AMI, without ST segment elevation. Compared to a left bundle branch block, the significance of a RBBB may be underestimated. Knowledge of this ECG pattern permits timely diagnosis and treatment of AMI.

Case presentation

A middle-aged man presented to an urgent care clinic 15 min after a sudden onset of chest pain triggered by coughing. The pain started in the lower chest and migrated to the upper chest without being worsened by movement or deep respiration. The patient had type II diabetes on oral treatment and had no other cardiovascular risk factors. On admission, he was in acute distress, diaphoretic with a pain intensity rated as 8/10. He was without fever, the blood pressure was 160/102 mm Hg in the right arm and 160/120 mm Hg in the left, the heart rate 72/min, and oxygen saturation 99% on room air. Lung and heart auscultation was normal, as was abdominal examination. Peripheral pulses were symmetric.

Investigations

The admission electrocardiogram showed no acute ischaemic changes (figure 1) and the first troponin I level was within normal limits. A chest CT angiogram ruled out both an aortic dissection and a large pulmonary embolism. As severe pain persisted, however, the patient was referred and admitted to the emergency department of our university hospital for further investigations. A repeat ECG, performed on arrival and 3 h after the beginning of symptoms, showed a RBBB (figure 2). Pain gradually subsided over 30 min.

Figure 1.

First ECG.

Figure 2.

Second ECG, 3 h after the onset of chest pain.

Outcome and follow-up

The high-sensitivity troponin T level increased to 127 ng/L (N<14 ng/L). An acute coronary syndrome was diagnosed, and the patient underwent coronary angiography. A long 50–70% stenosis of the proximal left anterior descending (LAD) coronary artery was found with a subocclusive stenosis of the first major septal branch (figure 3). No angioplasty was performed. A cardiac MR scan for ischaemia and viability assessment demonstrated a non-dilated left ventricle with a normal ejection fraction of 58% despite localised akinesia of the basal to mid-septal segments. Subendocardial late gadolinium enhancement with a small core of microvascular obstruction was seen in these segments, indicating a recent acute myocardial infarction in the territory of the first septal branch of the LAD (figure 4). Adenosine stress perfusion sequences demonstrated inducible ischaemia in the territory of the LAD coronary artery and an angioplasty of this vessel was subsequently performed. On discharge ECG, the RBBB had resolved.

Figure 3.

Long 50–70% stenosis of the left anterior descending artery (white thin arrow) and a very tight stenosis of the first septal branch (short thick arrow).

Figure 4.

Late gadolinium enhancement sequence in a 3-chamber orientation with cardiac MR showing a localised subendocardial infarction in the basal to mid-subendocardial segments. The area of necrosis appears as a hyperintense signal (thin arrow) while normal myocardium is black. Note the presence of a small core of microvascular obstruction within the area of necrosis (thick arrow). LV, left ventricle; RV, right ventricle; Ao, aorta; LA, left atrium.

Discussion

In 1999, the guidelines of the American Heart Association (AHA) recommended that a ‘bundle branch block associated with history suggesting AMI’ be considered as a criterion for fibrinolytic therapy, a statement also made by the American College of Emergency Physicians clinical policy in 2006.² However, the most recent European Society of Cardiology and AHA guidelines for the management of ST-segment elevation myocardial infarction consider that RBBB does not usually interfere with the interpretation of ST-segment elevation.^4 5 Therefore, according to international guidelines, the diagnostic criteria for AMI are no different in patients with RBBB and in patients with no conduction abnormalities. Furthermore, unlike LBBB, RBBB alone is not considered as a diagnostic criterion for AMI even if it occurs in the context of acute chest pain.⁶ Conversely, some authors report that AMI occurs without ST segment elevation. In a recent retrospective study, nearly 50% of 427 AMIs with RBBB had no ST elevation,³ despite the fact that the infarct-related artery was more frequently completely occluded at the time of coronary angiography.^3 7 The LAD artery is most commonly involved,^{7 8} and left main stem occlusion may present in 26–37% with RBBB without ST elevation.^{3 9} Septal perforator arteries of the LAD perfuse the right bundle branch and the anterior fascicle of the left bundle branch in 90%, and their occlusion leads to a RBBB. Although alcohol septal ablation, a procedure used in the treatment of hypertrophic cardiomyopathy, is a well-known cause of a controlled septal infarction and RBBB,¹⁰ spontaneous isolated occlusion such as in our case has rarely been reported. One recent case report presented a similar case of AMI with an isolated RBBB in an Indian woman with atypical chest pain, and diagnosed with an occlusion of a septal artery without significant disease of the LAD coronary artery.¹¹ As there is a paucity of data concerning the efficacy and safety of septal branch interventions, these branches are usually ignored as potential targets for revascularisation.¹²

From a prognostic point of view, AMI with a new RBBB is associated with higher short-term mortality, particularly when RBBB persists after hospital discharge.^{3 7 8} This higher mortality is linked to a higher percentage of anterior AMI, larger size of infarction and acute heart failure or cardiogenic shock.^{3 7 8 10} Since ST elevation may be absent in a significant proportion of RBBB-AMIs and since recent guidelines do not list RBBB as an AMI criterion, this subset of patients with AMI may experience delayed diagnosis. In line with other authors,³ this case would support an aggressive and early invasive approach in any case of a new onset RBBB occurring with acute chest pain, as is currently recommended for new onset LBBB.

Learning points.

• Right bundle branch block (RBBB) does not usually interfere with the interpretation of ST-segment elevation in acute myocardial infarction (AMI).

• However, RBBB may be the only ECG sign of an AMI.

• Where a new RBBB is found in a clinical context suggestive of an acute coronary syndrome, clinicians must consider AMI in their differential diagnosis and initiate reperfusion therapy without delay once the diagnosis is confirmed.