Chest pain and left bundle branch block

D. Luke Glancy, MD, and Bahij Khuri, MD

From the Section of Cardiology, Department of Medicine, Louisiana State University Health Sciences Center and the Medical Center of Louisiana, New Orleans, Louisiana.

Corresponding author: D. Luke Glancy, MD, Section of Cardiology, Department of Medicine, Louisiana State University Health Sciences Center, 1542 Tulane Avenue, Room 441, New Orleans, Louisiana 70112.

A 64-year-old hypertensive, diabetic woman came to the emergency department complaining of intermittent chest and left arm pain for 6 days. An electrocardiogram (ECG) showed left bundle branch block (LBBB) that was atypical because T waves in the limb leads were concordant in direction with the QRS complexes instead of being discordant (Figure 1). Thus, the T-wave changes were not secondary to the conduction disturbance but were primary and suggested inferior ischemia or injury. When chest pain recurred 2 hours later, LBBB with concordant T waves and QRS complexes in the limb leads persisted, and new ST-segment elevation and Q waves appeared in leads III and aVF (Figure 2).

Less than an hour later the pain intensified, and the patient became diaphoretic, pale, and hypotensive. A rhythm strip showed sinus bradycardia, with a rate of 41 beats per minute. After intravenous administration of atropine, the heart rate and blood pressure increased, but the rhythm became irregular. An ECG demonstrated second-degree atrioventricular block of the Wenckebach type and striking ST-segment elevation in leads II, III, and aVF, with reciprocal changes in leads I and aVL (Figure 3).

Although atrioventricular Wenckebach occasionally occurs infra-His, which is suggested by the LBBB, in the presence of fresh inferior myocardial infarction, the block is almost certainly at atrioventricular nodal level. ST-segment elevation in lead III greatly exceeds that in lead II, suggesting right coronary occlusion with right ventricular infarction, and this is confirmed by an ECG with right-sided precordial leads (Figure 4) and by angiography (Figure 5).

Because LBBB may both obscure the ECG features of acute myocardial infarction and increase its mortality (1), current American College of Cardiology/American Heart Association guidelines recommend reperfusion therapy for all patients with LBBB whose history suggests acute myocardial infarction (2). Unfortunately, only a minority of such patients are so treated either in the USA or in the United Kingdom (3, 4). Although diagnosing acute myocardial infarction from an ECG showing LBBB may prove daunting, the GUSTO-1 trial has provided 3 ECG signs that subsequently have been validated (5, 6). In order of decreasing predictive value, these are ST elevation >=1 mm in leads with a positive QRS, ST depression >=1 mm in leads V1 to V3, and ST elevation >=5 mm in leads with a negative QRS. The ECGs in Figures 3 and 4 meet the first of these criteria, and after the fourth ECG, the patient received tissue plasminogen activator. The total creatine kinase, 107 U/L, was normal at the time but rose to 2599 the next morning.

Right bundle branch block usually does not obscure the ECG features of acute myocardial infarction, and at times the diagnosis of myocardial infarction can be made from the ECGs of patients with other conditions causing a wide QRS complex, such as ventricular tachycardia and right ventricular pacing (7, 8). Hopefully, improved recognition of patterns of myocardial infarction in the presence of wide QRS complexes, especially LBBB, will result in more widespread and prompt use of reperfusion therapy (6). (BUMC Proceedings 2001;14:452-454)