International Journal of Cardiology 179 (2015) 36–37

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Letter to the editor

Managing LBBB: Extracting full electrocardiographic information Cheuk-Kit Wong ⁎ Department of Cardiology, Dunedin School of Medicine, University of Otago, Dunedin Public Hospital, Dunedin, New Zealand

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Article history: Received 13 October 2014 Accepted 20 October 2014 Available online xxxx Keywords: LBBB Electrocardiographic information

LBBB is increasingly seen in today's practice and patients often present with symptoms of ischemia or heart failure. Table 1 summarizes a management path. In those with acute ischemic symptoms, the use of the 2 major Sgarbossa criteria (concordant ST elevation ≥ 1 mm and V1–3 ST depression ≥ 1 mm) in diagnosing “STEMI equivalent” has been reviewed summarizing observational findings from large-scale STEMI trials [1]. To increase the diagnostic utility, recent proposal has been made in modifying the third (minor) Sgarbossa criterion from ≥5 mm discordant V1–3 ST elevation to ST elevation ≥ 25% of the absolute magnitude of the preceding S wave [2]. The rationale for emphasizing ST elevation during LBBB, whether concordant or discordant, is that the current of injury of a STEMI should produce new ST elevation in the recording leads facing the ongoing infarction. It is often hard to confidently exclude “STEMI equivalents”, resulting in many “false” primary PCI cath lab activations [3]. Nonetheless, the angiographic information is useful in those with ongoing myocardial damage (raised troponin levels) and in those with ventricular impairment. LBBB is common and prognostically relevant amongst patients with cardiomyopathy. In the Italian Network on Congestive Heart Failure Registry of unselected outpatients with heart failure in the 1990's [4], 1-year outcome was reported for 5517 patients (45.6% with ischemic heart disease, 36% with dilated cardiomyopathy, 12.9% with hypertensive heart disease and 5.5% with other causes). LBBB (25.2% of the cohort) was associated with a 70% increase in mortality and 58% increase in sudden death, independent of age, underlying cardiac disease, heart failure severity and the use of ACE-inhibitors and beta-blockers. ⁎ Corresponding author at: Department of Cardiology, Dunedin School of Medicine, University of Otago, Dunedin Hospital, Dunedin, New Zealand. E-mail address: [email protected] 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.

Cardiac resynchronization therapy (CRT) is recommended for LBBB with severe left ventricular systolic dysfunction. The good recovery in many responders suggests that LBBB has reversibly worsened left ventricular function through asynchronous activation. Animal studies have provided mechanistic insights. Vernooy et al. induced LBBB by radiofrequency ablation of the left bundle system in 8 dogs and serially evaluated them [5]. Fortnightly echocardiography showed progressive left ventricular remodeling. Over 16 weeks, left ventricular end-diastolic volume increased by 25 ± 19%. Left ventricular wall mass increased by 17 ± 16%, but the septal-to-lateral wall mass ratio decreased by 6 ± 9%. Overall, global left ventricular ejection fraction decreased by 23 ± 14%. Acutely after LBBB, myocardial blood flow (measured using fluorescent microsphere injected into the left ventricle) decreased in the septum, but increased in the left ventricular lateral wall. Systolic circumferential shortening (calculated off-line from tagged MRI short-axis cross sections) also decreased in the septum but increased in the lateral wall. There was no further change over 16 weeks. The findings suggested that the asynchronous ventricular activation from LBBB led immediately to redistribution of circumferential shortening (dyssynchrony) and myocardial blood flow, followed by left ventricular remodeling. In a related experiment [6], the same investigators found that biventricular pacing for 8 weeks largely reversed all abnormalities induced by LBBB. Clinically, a third of LBBB patients with left ventricular dysfunction do not respond to CRT with biventricular pacing. The general explanation varies from bad left ventricular lead positioning to irreversible myocardial damage with scars. Evaluating further, LBBB in humans is perhaps more heterogeneous than the animal model of left bundle ablation. Auricchio et al. [7] studied left ventricular activation sequence in 24 LBBB patients with heart failure and found a binary distribution of transseptal activation times. Nine had normal transseptal activation time and slightly prolonged left ventricular endocardial activation time. They also had a longer distance from the first left ventricular activation (breakthrough) site to the line of conduction block indicating that the main bulk of the left ventricle is activated early with late activation of a smaller posterolateral part. These 9 patients had ~ 40 ms shorter QRS duration than the remaining 15 patients. It follows that the conventional ECG criteria for LBBB may have included patients with slightly longer left ventricular activation time with relatively normal pattern (ie, having less dyssynchrony). To help distinguish them from others with abnormal and prolonged left ventricular activation from “genuine” LBBB, the QRS complex may contain useful information from its duration and morphology.

C.-K. Wong / International Journal of Cardiology 179 (2015) 36–37


Table 1 Management steps for LBBB patients with chest discomfort and dyspnea. Step Diagnosis 1 2 3 4 a



STEMI equivalents Non-STEMI equivalents and /or ongoing ischemia

Sgarbossa ECG criteria; acute angiography Serial troponin levels; angiography; imaging tests for ischemia Sustained left ventricular dysfunction not due to acute Echocardiogram or other imaging modalities reversible insults Left ventricular failure amendable to CRT, or clinical QRS duration during LBBB; A–V conduction delay and heart need for pacing block (often more prevalent after beta-blockers)a

Primary PCI Early revascularization Evidence based anti-failure drug +/− defibrillator therapies CRT with bi-ventricular pacing

CRT often allows beta-blockers to be titrated towards higher dose.

Table 2 Maximizing electrocardiographic information from LBBB morphology. Suspected diagnosis Acute coronary syndrome particularly STEMI equivalents

Left ventricular systolic failure with dyssynchrony amendable to CRT a


Major diagnostic features

Other helpful clues

1. ≥1 mm concordant ST elevation 2. ≥1 mm V1–3 ST depression

Discordant ST elevation ≥ 5 mm or ≥25% of the preceding S wave in V1–3

QRS duration ≥ 150 ms in males and ≥130 ms in females

Mid QRS notching or slurring

Interpretation of ST segment changes is enhanced by serial ECG comparison and comparison with old tracings.

In a pooled patient-level data analysis (4076 patients) from 3 randomized trials (CRT-defibrillator versus defibrillator alone), LBBB patients with a broader QRS duration have been found more responsive to resynchronization [8]. Women respond better than men, perhaps reflecting that with the same LBBB criteria women have relative broader QRS duration after correction for their smaller body (heart) size. The main difference was with QRS duration of 130–149 ms, where women had 76% reduction in combined heart failure or death and 76% reduction in death alone. In contrast, there was no significant benefit in men for both endpoints. Neither women nor men with LBBB benefited from CRT at QRS duration b 130 ms, while both benefited at QRS duration ≥ 150 ms. Using “strict” LBBB criteria incorporating different cut-points according to gender: QRS duration ≥ 140 ms (men) or ≥ 130 ms (women), QS or rS in leads V1 and V2, and specifically mid-QRS notching or slurring in ≥2 of the leads V1, V2, V5, V6, I and aVL, a cardiac MRI myocardial tagging study [9] evaluated 64 heart failure patients. The 31 with “strict” LBBB had a longer time delay between septal and lateral LV peak circumferential wall strain than the 19 who satisfied conventional but not the “strict” LBBB criteria (210 ± 137 ms vs 122 ± 102 ms, P = 0.045), and the latter patients did not differ from the non-LBBB patients (122 ± 102 ms vs 100 ± 86 ms, P = 0.51). In another 67 LBBB patients studied by 2-dimensional strain echocardiography, about two-thirds satisfied the strain-echo criteria: early termination of contraction in the septal wall with the opposing posterolateral wall exhibiting initial pre-stretch and late contraction. There was a close concordance between those who satisfied the above strain-echo criteria and those who satisfied the “strict” LBBB criteria including mid QRS notching. Both criteria correctly identified CRT responders [10]. While interpretations of myocardial strain can be subjective, strain imaging comparing septal versus lateral/posterolateral wall mechanistically focuses on the “LBBB dyssynchrony” from abnormal left ventricular activation. Table 2 summarizes the electrocardiographic clues during LBBB.

References [1] C.K. Wong, H.D. White, The HERO-2 ECG sub-studies in patients with ST elevation myocardial infarction: implications for clinical practice, Int. J. Cardiol. 170 (2013) 17–23. [2] Q. Cai, N. Mehta, E.B. Sgarbossa, S.L. Pinski, G.S. Wagner, R.M. Califf, A. Barbagelata, The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am. Heart J. 166 (2013) 409–413. [3] C.K. Wong, Minimizing false activation of cath lab for STEMI — a realistic goal? Int. J. Cardiol. 172 (2014) e91–e93. [4] S. Baldasseroni, C. Opasich, M. Gorini, D. Lucci, N. Marchionni, M. Marini, C. Campana, G. Perini, A. Deorsola, G. Masotti, L. Tavazzi, A.P. Maggioni, Italian Network on Congestive Heart Failure Investigators. Left bundle-branch block is associated with increased 1-year sudden and total mortality rate in 5517 outpatients with congestive heart failure: a report from the Italian network on congestive heart failure, Am. Heart J. 143 (2002) 398–405. [5] K. Vernooy, X.A. Verbeek, M. Peschar, H.J. Crijns, T. Arts, R.N. Cornelussen, F.W. Prinzen, Left bundle branch block induces ventricular remodelling and functional septal hypoperfusion, Eur. Heart J. 26 (2005) 91–98. [6] K. Vernooy, R.N. Cornelussen, X.A. Verbeek, W.Y. Vanagt, A. van Hunnik, M. Kuiper, T. Arts, H.J. Crijns, F.W. Prinzen, Cardiac resynchronisation therapy cures dyssynchronopathy in canine left bundle-branch block hearts, Eur. Heart J. 28 (2007) 2148–2155. [7] A. Auricchio, C. Fantoni, F. Regoli, C. Carbucicchio, A. Goette, C. Geller, M. Kloss, H. Klein, Characterization of left ventricular activation in patients with heart failure and left bundle-branch block, Circulation 109 (2004) 1133–1139. [8] R. Zusterzeel, K.A. Selzman, W.E. Sanders, D.A. Caños, K.M. O'Callaghan, J.L. Carpenter, I.L. Piña, D.G. Strauss, Cardiac resynchronization therapy in women: US Food and Drug Administration meta-analysis of patient-level data, JAMA Int. Med. 174 (2014) 1340–1348. [9] L.G. Andersson, K.C. Wu, B. Wieslander, Z. Loring, T.F. Frank, C. Maynard, G. Gerstenblith, G.F. Tomaselli, R.G. Weiss, G.S. Wagner, M. Ugander, D.G. Strauss, Left ventricular mechanical dyssynchrony by cardiac magnetic resonance is greater in patients with strict vs nonstrict electrocardiogram criteria for left bundle-branch block, Am. Heart J. 165 (2013) 956–963. [10] N. Risum, D. Strauss, P. Sogaard, Z. Loring, T.F. Hansen, N.E. Bruun, G. Wagner, J. Kisslo, Left bundle-branch block: the relationship between electrocardiogram electrical activation and echocardiography mechanical contraction, Am. Heart J. 166 (2013) 340–348.

Managing LBBB: Extracting full electrocardiographic information.

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