Mori Quartet Part 4

This 33 year old woman was seen in the Emergency Department 12 days ago with epigastric discomfort at rest that resolved after treatment with morphine and antacids. The ECG taken at that time is shown in Figure 1, and an enlarged view of Leads aVF and V3 in Figure 2. Her serum troponin concentration was normal, and she was sent home.

Figure 1

Figure 2

+ What are the main findings in this ECG?

The rhythm is sinus with a ventricular rate of about 88 beats per minute (computer report), a normal frontal plane QRS axis and normal QRS width. Tall QRS voltages in some leads (e.g. Lead I, Lead aVR and Lead V1) raise the possibility of left ventricular hypertrophy (LVH), but voltage criteria for LVH are unreliable in persons below the age of 40 years.

Lead V2 has a elevated J point with 1 mm of ST segment elevation.

The upstroke of the R wave in Lead V3 (and in Lead aVF) has a slight initial concave shape that hints at the presence of a delta wave. The PR interval is at the upper limit of normal, which argues against the presence of an accessory pathway. The shape of the upstroke is thus due to an increased intrinsicoid deflection.

Final diagnosis: Within normal limits

The patient returned with a history of 60 minutes of mild epigastric discomfort associated with slight discomfort in her throat and numbness in the inner aspect of her left upper arm. The discomfort came on while she was driving her car, and had almost resolved after she had been treated by paramedics with morphine, aspirin and GTN.

Her blood pressure was normal, and there were no abnormalities on examination.

The initial ECG is shown in Figure 3

Figure 3

+ What are the main findings in this ECG?

This tracing shows sinus rhythm with a ventricular rate of about 94 beats per minute (computer report), a normal axis and a left bundle branch block (LBBB). In most cases when we see a ECG with LBBB we do not have a previous ECG , so all we can say is that the current LBBB is "not old". Here we have a previous normal ECG, which confirms that this tracing is a new onset LBBB.

This new onset LBBB is present in a young woman with (atypical) epigastric/throat/left arm symptoms that have now resolved. The patient is haemodynamically stable. The main diagnostic issues are:

  1. Could an acute coronary syndrome (ACS) be the cause of the LBBB ?
  2. How does the presence of a LBBB affect the ECG changes produced by a ST elevation myocardial infarction (STEMI) ?
  3. What are other likely non-ACS causes of LBBB in this case ?

The following issues are relevant to the issue of LBBB in persons with possible ACS:

  1. Individuals with LBBB represent approximately two percent of all persons who present with suspected ACS. These persons are more likely to be older, to be female, and to have a history of pre-existing cardiovascular disease, hypertension, and congestive heart failure than non-bundle branch block patients with ACS. Persons with LBBB also have a greater likelihood of major adverse cardiac events and an increased rate of revascularization over long-term follow-up compared with patients without bundle branch block.
  2. The prevalence of chronic LBBB likely is increasing, despite a general decline in overall incidence of ST elevation myocardial infarction (STEMI). This suggests that chronic LBBB (not due to ACS) has become more common.
  3. In LBBB septal Q waves due to acute myocardial infarction are absent, and secondary ST-T wave abnormalities obscure the ST-T changes caused by ischaemia and infarction. Because of this there has been a widespread belief (myth) that it is impossible to diagnose a acute STEMI in the presence of LBBB.
  4. The initial outcome in studies of fibrinolysis in patients with suspected acute myocardial infarction (AMI) found that subjects with bundle branch block (BBB) treated with early fibrinolysis had lower mortality than those treated with placebo. This resulted in guidelines that recommended that new (or presumably new) LBBB in a person with suspected ACS should be regarded as a STEMI equivalent, and that these patient should be transferred urgently for angiography and if needed angioplasty.
  5. Less than half of all patients with suspected ACS and LBBB who are taken urgently to the cardiac catheterisation laboratory are found to have a AMI. Moreover, a significant proportion of patients with AMI do not have an occluded culprit artery at catheterization, and thus have had a non ST segment elevation myocardial infarction (NSTEMI), unstable angina, or non-ACS presentation.
  6. The Sgarbossa criteria were developed to diagnose AMI in the presence of LBBB in persons with possible ACS. The Sgarbossa criteria include ST-segment elevation of 1 mm or more concordant with the QRS complex in any lead; ST-segment depression of 1 mm or more in lead V1, V2, or V3; and ST-segment elevation of 5 mm or more discordant with the QRS complex in any lead. The Sgarbossa criteria were originally based on a rise and fall of cardiac biomarkers, and not angiography (in other words the Sgarbossa criteria combined STEMI and NSTEMI cases). A limitation of the original Sgarbossa criteria is a sensitivity of only 20 percent, so the original criteria have been modified to improve the sensitivity.

+ What are your management options?

The current approach to the LBBB in a person with a possible ACS has moved on from an emphasis on early coronary angiography to an integrated approach based on the patient's haemodynamic stability, Sgarbossa criteria and serial troponin measurements, supplemented if needed by echocardiography (Figure 4)

In this case:

  • The patient is young and has no risk factors for coronary artery disease.
  • Her vital signs are normal, and her initial serum troponin level is normal
  • The ECG taken at 1916 does not have Sgarbossa criteria consistent with an AMI (the T wave in Lead V4 is discordant [i.e. upright] but the ST segment is not elevated)

A second ECG taken two hours after arrival is shown in Figure 5.

Figure 5

+ What are the main changes in the third ECG (figure 5)?

In this tracing taken at 2112 sinus rhythm with LBBB is seen in most of the leads. In the rhythm strip there are three sinus beats where the QRS complexes suddenly narrow and resemble the complexes seen in the initial tracing two weeks ago. The LBBB pattern then reappears in the last three sinus beats in the rhythm strip.

The rhythm strips from each tracing are compared in Figure 6.

The rhythm strips can be summarised thus:

  • A: Sinus rhythm and normal QRS morphology, with a ventricular rate of about 80 beats per minute and an average R-R interval of 693 msec
  • B: Sinus rhythm and LBBB QRS morphology, with a ventricular rate of about 100 beats per minute and an average R-R interval of 656 msec
  • C: Complexes 1 to 6: Sinus rhythm and LBBB QRS morphology, with a average R-R interval of 664 msec
  • C: Complexes 6 to 9: Sinus rhythm and LBBB QRS morphology, with a average R-R interval of 733 msec
  • C: Complexes 9 to 11: Sinus rhythm with normal QRS morphology

Important Points:

  • Assessment of chest pain in persons with an ECG that shows LBBB
  • Sgarbossa criteria
  • Acceleration dependent LBBB

Sources:

  1. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Uti lization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med 1996; 334: 481-487
  2. Neeland IJ, Kontos MC, Lemos JA. ,Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol 2012; 60:96–105
  3. Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce PA. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med. 2012;60:766-776
  4. Denes P, Pick A, Miller RH, Pietras RJ, Rosen KM. A characteristic precordial repolarization abnormality with intermittent left bundle-branch block. Ann Intern Med 1978; 89: 55-57.
  5. Engel TR, Shah R, De Podesta LA, Frankl WS, Krause RL. T-wave abnormalities of intermittent left bundle-branch block. Ann Intern Med 1978; 89: 204-206.
  6. Virtanen K, Heikkila J, Kala R et al. Chest pain and rate dependent left bundle branch block in patients with normal coronary arteriograms. Chest 1982; 81: 326-31.
  7. Surawicz B. Transient T wave abnormalities in intermittent bundle branch block. Amer J Cardiol 1982; 50: 363-364.
  8. Wayne V, Bishop R, Cook L et al. Exercise-induced bundle branch block. Am J Cardiol 1983; 52:283-286.
  9. Vasey C, O’ Donnel J, Morris S et al. Exercise induced left bundle branch block and its relation to coronary artery disease. Am J Cardiol 1985; 56: 892-895.
  10. Malozzi C, Wenzel G, Karumbaiah K, Courtney M, Omar B. Chest pain associated with rate-related left bundle branch block and cardiac memory mimicking ischemia. Journal of Cardiology Cases 9 (2014) 87–90