LBBB

Left Bundle branch Block
LBBB and ACS
Pathogenesis of ventricular dysynchrony
CRT indications

1. LBBB DR. ASWIN R. M.

2. ANATOMY

3. BLOOD SUPPLY HIS BUNDLE – LAD + AV NODAL ARTERY PROXIMAL RBBB – LAD + AV NODAL ARTERY DISTAL RBBB – LAD LAF – LAD LPF – DUAL SUPPLY IN MOST CASES RCA+LCX

4. BUNDLE BRANCH BLOCKS Intrinsic impairment of conduction in the left or right bundle branches or its branches Can be chronic or intermittent Can be rate dependent Can be present without cardiac disease Most often due to CAD or HTN causing ischemic or degenerative changes

5. LBBB Considered as Bifascicular block Complete LBBB Disease in main LBB ( predivisional ) Or in both of its fascicles ( postdivisional ).

6. LBBB EPIDEMIOLOGY ~ 1 % (0.2 to 1.1 % in different populations) Incidence Increases with age Etiology Structural and functional Structural CAD ACS Cardiomyopathy SHTN Aortic valve disease Post cardiac surgery esp aortic root surgeries Functional Rate dependent BBB

7. LBBB QRS duration greater than or equal to 120 ms in adults, greater than 100 ms in children 4 to 16 years of age, and greater than 90 ms in children less than 4 years of age. Broad notched or slurred R wave in leads I, aVL , V5, and V6 and an occasional RS pattern in V5 and V6 Absent q waves in leads I, V5, and V6, but in the lead aVL , a narrow q wave may be present in the absence of myocardial pathology. R peak time greater than 60 ms in leads V5 and V6 but normal in leads V1, V2, and V3, when small initial r waves can be discerned in the above leads. ST and T waves usually opposite in direction to QRS. Positive T wave in leads with upright QRS may be normal (positive concordance). Depressed ST segment and/or negative T wave in leads with negative QRS (negative concordance) are abnormal The appearance of LBBB may change the mean QRS axis in the frontal plane to the right, to the left, or to a superior, in some cases in a rate-dependent manner. AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram

8. STRICT CRITERIA QRS ≥ 140  ms for men and ≥130 ms for women QS or rS in V1-V2 M id-QRS notching or slurring in ≥2 contiguous leads

9. INCOMPLETE LBBB QRS duration between 110 and 119 ms in adults, between 90 and 100 ms in children 8 to 16 years of age, and between 80 and 90 ms in children less than 8 years of age. R peak time greater than 60 ms in leads V4, V5, and V6. Absence of q wave in leads I, V5, and V6 . MECHANISM Slowed conduction through the LBBB Enlargement of the left ventricle – prolongation of the QRS complex that mimics incomplete LBBB ( LBB has multiple fascicles, involvement of few major fascicles but not all. AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram

10. NONSPECIFIC OR UNSPECIFIED INTRA VENTRICULAR CONDUCTION DISTURBANCE QRS duration greater than 110 ms in adults 90 ms in children 8 to 16 years of age 80 ms inchildren less than 8 years of age without criteria for RBBB or LBBB. RBBB criteria in the precordial leads and LBBB criteria in the limb leads, and vice versa.

11. ECG CAHNGES MECHANISM Block in conduction system myocardial spread of electrical activity (cell to cell conduction ) Ventricles depolarized successively rather than simultaneously

12. SECONDARY ST T WAVE CHANGES

13. RATE DEPENDENT BUNDLE BRANCH BLOCK Tachycardia or Bradycardia dependent BBB HR at which BBB manifests-critical HR Reproducible each time Tachycardia dependent BBB Phase 3 aberrancy When impulses are transmitted at a faster rate than the ability to repolarize from prior impulse in that part of conducting system. Bradycardia dependent BBB Phase 4 aberrancy Due to gradual loss in transmemebrane resting potential from prolonged diastole ( subsequent excitation from a much negative potential)

14. ASHMAN PHENOMENON Gouaux and Ashman in 1947 A berrant ventricular conduction due to a change in QRS cycle length More often affects RBB(longer RP) In AF, when a relatively long cycle is followed by a relatively short cycle, the beat with a short cycle often has bundle-branch block morphology . Refractory period proportionate to R-R interval Will be diagnosed as VPC

15. EXERCISE INDUCED LBBB 0.4 %-0.5% of patients undergoing exercise tests. May not specifically indiates underlying CAD But many studies observed higher rates of mortality in such patients.

16. LBBB CLINICAL EXAMINATION Narrow or paradoxical splitting of 2 nd heart sound

17. LBBB ECHO ABNORMAL SEPTAL MOTION Early systolic movement of IVS towards the center of LV followed by movement away from the center of LV (paradoxical movement) Mimics RWMA BASAL & MID SEGMENTS APEX-ROCKING MOVEMENT PRESERVED THICKNESS USUALLY TEMPORAL DYSSYNCHRONY NORMAL LV GEOMETRY EARLY SYSTOLIC BEAKINIG OF IVS IN M MODE

18. LBBB ECHO

19. LBBB ECHO M-mode echo - early systolic downward motion of the ventricular septum Seen just after the peak R wave on ECG or just at the closing of mitral valve.

20. TISSUE DOPPLER Septal flash

21. LBBB ECHO ISCHEMIC RWMA LBBB RV PACED MAXIMAL LOCATION DISTAL SEPTUM, APEX , ANTERIOR WALL, PROXIMAL /MID ANTERIOR SEPTUM DISTAL SEPTUM OFTEN INFERIOR THICKNESS THINNING PARTIALLY PRESERVED PARTILLY PRESERVED ABNORMAL GEOMETRY COMMON UNCOMMON UNCOMMON TEMPORAL DYSYNCHRONY NO YES YES

22. LBBB & MI

23. LBBB & MI 2% of all patients who present with a suspected ACS Unique diagnostic and therapeutic challenge ECG changes of LBBB can mask & mimics acute MI changes Not all new onset or presumed new onset LBBB is due to coronary artery disease More likely to be older, female, and have a history of pre-existing cardiovascular disease, hypertension, and congestive heart failure than non-BBB patients with ACS These patients are at increased risk of adverse outcomes – Not due to LBBB but by underlying ischemic and structural heart disease that has contributed to LBBB

24. HOW TO APPROACH 2004 ACC/AHA STEMI guidelines - New or presumed new onset LBBB is considered STEMI equivalent LBB more diffuse structure than RBB – LBBB as part of MI indicates extensive myocardial damage ( very rarely discrete lesion in proximal conduction system). Newer studies has shown that Transmural MI as a cause of LBBB is uncommon 2013 ACC/AHA STEMI guidelines – Has to be considered as STEMI equivalent. But not in isolation as new or presumed new onset STEMI are infrequent Sgarbossa criteria should be also considered ESC 2017 – ECG diagnosis of STEMI difficult with LBBB. Concordant ST elevation best indicator of ongoing ischemia Clinical suspicion of ongoing Ischemia LBBB should be managed similar to STEMI patients

25. SGARBOSSA CRITERIA Proposed in 1996 To diagnose AMI in the setting of a known chronic LBBB. Current data shows usefulness in new or indeterminate-age LBBB also Score of ≥ 3 has specificity for AMI greater than 95% and is associated with higher 30-day mortality compared with LBBB patients with discordant ST-segment elevation alone  Sensitivity of a Sgarbossa score of ≥ 3 is only approximately 20 %

26. SGARBOSSA POSITIVE

27. MODIFIED SGARBOSSA CRITERIA ≥ 1 lead with ≥1 mm of concordant STelevation ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave. Any of above three is STEMI equivalent I mproved sensitivity but with reduced specificity compared with the original Sgarbossa criteria (90 vs. 98%)

28. OTHER SIGNS OF MI IN LBBB The presence of QR complexes in leads I, V5, or V6 or in II, III, and avf with LBBB strongly suggests underlying infarction Prominent notching of the ascending part of a wide S wave in the midprecordial leads (V3 V4) - Cabrera's sign Prominent notching in ascending limb of a wide R wave in lead I, aVL , V5 , or V6 - Chapman's sign

29. CABRERA'S SIGN prominent (0.05 sec) notching in the ascending limb of the S wave in leads V3 and V4;

30. CHAPMAN'S SIGN Prominent notching in ascending limb of a wide R wave in lead I, aVL , V5, or V6

31. PROPOSED NEW CRITERIA Cai et al

32. RADIONUCLEOTIDE MYOCARDIAL PERFUSION IMAGING Stress ECG not usefull in LBBB For evaluation of underlying CAD Both Excersise & Pharmacologic Excersise testing High incidence of false positive results in septal & anteroseptal More apparent with tachycardia associated with excersise Perfusion defects in the inferior and lateral zones are not LBBB-related – signifies LCX or RCA disease

33. PHARMACOLOGIC STRESS TESTING Preferred over exercise testing Dobutamine testing has same disadvantage as exercise testing Should preferentially undergo Vasodilator ( dipyridamole or adenosine) radionuclide imaging ACC/AHA/ASNC Guidelines for the Clinical Use of Cardiac Radionuclide Imaging

34. IMPACT ON LV FUNCTION N ormal heart , closely tuned electrical function – results in a cordinated sequence of mechanical function results in efficient B iventricular filling, contraction Relaxation & pump function LBBB – Dysynchronous mechanical activity of different part of heart

35. AV DYSYNCHRONY There is a delay between atrial and ventricular contraction Reduced LV filling shortened ventricular filling time superimposition of atrial contraction on early passive filling, The ratio between LV diastolic filling time and duration of a complete cardiac cycle (A LV filling time of < 40% cardiac cycle is indicative of A-V dys .) It can also be associated with late diastolic (presystolic ) mitral regurgitation (MR).

36. INTERVENTRICULAR DYSSYNCHRONY Delay between RV and LV activation. RV contraction will precede LV contraction abnormal septal motion and a decreased LV Function

37. INTERVENTRICULAR DYSSYNCHRONY Normal ventricular activation sequence is disrupted, resulting in Dis cordinated contraction of the LV segments. T hose LV wall segments, which contract early (ex septum), do not contribute to the LV output, Late contracting segments do so at a higher wall stress – are hypercontractile stretches the early contracting segments Asymmetric hypertrophy and assymetric LV dilatation MR worsens LV remodeling P resystolic regurgitation delayed contraction of papillary muscle rootattachments .

38. LV FUNCTION AND LBBB

39. INTRAVENTRICULAR DYSYNCHRONY Inter-ventricular mechanical delay(IVMD) &LV PEF

40. Inter-ventricular mechanical delay(IVMD) values of > 40 ms LV PEP of > 140 ms are considered pathological Pulse tissue Doppler for IVMD The time from QRS onset to the peak myocardial systolic velocities ( Sm ) of the RV free wall (tricuspid annulus) versus the same time of LV lateral mitral annulus (apical 4-chamber view)

41. INTRAVENTRICULAR DYSYNCHRONY Septal -to-posterior wall motion delay SPWMD D ifference in timing of septal and posterior wall contraction M-mode in PLAX SPWMD is the difference between the time from the onset of ECGderived Q wave to the initial peak posterior displacement of the septum , and the time from the onset of QRS to the peak systolic displacement of posterior wall

42. SPWMD> 130 ms was considered pathological

43. Lateral wall post-systolic displacement LWPSD Difference of QRS onset to maximal systolic displacement of the basal LV lateral wall(assessed by M-mode in the apical 4-chamberview) QRS onset to the beginning of transmitral E velocity ( assessed by pulsed Doppler of mitral inflow) P ositive LWPSD, i.e. a longer interval -severe post systolic contraction I ndependent predictor of CRT response

44. Pulsed Tissue Doppler – used to measure time interval between the onset of ECG derived QRS and the Sm peak (= time to Sm peak) time interval between the onset of QRS and the onset of Sm (= time to Sm onset ), which correspond to LV PEP Intra-ventricular mechanical delay has been defined for differences of > 65 ms of time to Sm Peak between LV segments

45. 3-D Echocardiography allows intraventricular dyssynchrony to be evaluated by analyzing LV wall motion in multiple apical planes during the same cardiac cycle . It also offers better spatial resolution thana single plane.

46. CRT IN LBBB CRT or biventricular pacing aims at eliminating the electrical dysynchrony

47. CRT INDICATIONS IN WIDE QRS LVEF NYHA LBBB or Not ECG ACC/AHA ESC <35 II III IV(ambulatory) LBBB SR QRS >150 Class I Class I <35 II III IV(ambulatory) LBBB SR QRS 120-149 ms Class IIa Class I III IV(ambulatory Non LBBB SR QRS >150 Class IIa (NYHA II also) <35 II Non LBBB SR QRS >150 Class IIb Class IIa III IV(ambulatory) SR QRS 120-149 ms Class IIb (NYHA II also) <30 I – Ischemic cause of heart failure LBBB SR QRS >150

48. PACING IN LBBB Patient with syncope 2013 ESCGuidelines on cardiac pacing and cardiac resynchronization therapy

49. PACING Class I LBBB + unexplained syncope and abnormal EPS HV interval ≥ 70 ms . Second- or third-degree His-Purkinje block demonstrated during incremental atrial pacing or with pharmacological challenge. Alternating BBB Class IIb BBB + unexplained syncope & non diagnostic investigations. Pacing may be considered in selected patients Class III Asymptomatic BBB

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