Clinical importance of LBBB

Clinical importance of LBBB

Left bundle branch block (LBBB) is usually associated with structural heart disease, unlike right bundle branch block which may be seen without associated heart disease. LBBB is one cause for paradoxical splitting of second heart sound. Normal split closes in expiration. In paradoxical splitting, split is audible in expiration and closes in inspiration.

In normal conduction sequence, left bundle branch is activated first. Hence a left bundle branch block can affect the initial vector in the ECG. This leads to errors in interpretation of Q waves in myocardial infarction. Secondary ST segment and T wave abnormalities common with LBBB makes assessment of myocardial ischemia difficult, both at rest and during exercise testing. Various criteria have been proposed for diagnosis of myocardial infarction in the presence of LBBB, of which Sgarbossa criteria is most popular [1]. Other criteria described are Selvester 10% RS criteria and Smith 25% S-wave criteria.

LBBB has great significance in the setting of left ventricular dysfunction. Dyssynchrony of left ventricular contraction characteristic of LBBB can worsen heart failure. That is why cardiac resynchronization therapy aims at reducing the dyssynchrony in those with symptomatic heart failure. Benefits of cardiac resynchronization therapy in heart failure is largely restricted to those with LBBB and QRS width of 150 ms or more, suggesting the role of left ventricular dyssynchrony in heart failure progression. Responders to cardiac resynchronization therapy which constitutes about two third of the patients, exhibit left ventricular reverse remodeling. They also show reduction in QRS width on resynchronization. All cause mortality was significantly lower in responders [2].

Both His bundle pacing and left bundle branch pacing have been used for correction of dyssynchrony. This results in normal QRS and left ventricular synchronization [3]. His bundle pacing helps by pacing the fibres destined to the left bundle branch within the His bundle. It is known that the fibres segregate before the actual division into left and right bundle branches.

LBBB can interfere with echocardiographic interpretation due to the associated abnormalities in left ventricular wall motion. In LBBB there is pre-ejection contraction with leftward movement of the septum, followed by immediate rebound stretch and subsequent paradoxical rightward movement [4]. This has also been called as septal flash. Please note that septal flash is different from the respirophasic ventricular septal shift known as septal bounce in constrictive pericarditis. Septal flash is early systolic while septal bounce is early diastolic.

LBBB often causes septal perfusion defects in radionuclide myocardial perfusion imaging during exercise test. But this is rare with vasodilator stress. A study comparing 10 patients with LBBB, 10 age matched controls and 10 pacemaker patients with right ventricular pacing off and on has been reported. They concluded that the apparent septal perfusion defect in LBBB is mainly due relative lateral hypoperfusion rather than an absolute decrease in septal flow. Switching pacemaker on during exercise decreased the ratio of septal/lateral myocardial blood flow by 17% [5].

Septal perfusion defect is partly due to the heterogeneity in blood flow between left anterior descending and left circumflex coronary arteries due to the delayed septal relaxation. It may be noted that myocardial blood flow is better in diastole when the myocardium relaxes as the systolic contraction reduces blood flow in systole into the intramyocardial vessels. There may be a reduced oxygen demand due to the late septal contraction which occurs when the wall stress is less.

References

  1. Cai Q, Mehta N, Sgarbossa EB, Pinski SL, Wagner GS, Califf RM, Barbagelata A. 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. 2013 Sep;166(3):409-13.
  2. Yu CM, Bleeker GB, Fung JW, Schalij MJ, Zhang Q, van der Wall EE, Chan YS, Kong SL, Bax JJ. Left ventricular reverse remodeling but not clinical improvement predicts long-term survival after cardiac resynchronization therapy. Circulation. 2005 Sep 13;112(11):1580-6.
  3. Lin J, Dai Y, Wang H, Li Y, Chen K, Zhang S. A comparison of left bundle branch pacing with His bundle pacing in a patient with heart failure and left bundle branch block. Heart Rhythm Case Rep. 2019 Oct 18;6(6):293-296.
  4. Aalen JM, Remme EW, Larsen CK, Andersen OS, Krogh M, Duchenne J, Hopp E, Ross S, Beela AS, Kongsgaard E, Bergsland J, Odland HH, Skulstad H, Opdahl A, Voigt JU, Smiseth OA. Mechanism of Abnormal Septal Motion in Left Bundle Branch Block: Role of Left Ventricular Wall Interactions and Myocardial Scar. JACC Cardiovasc Imaging. 2019 Dec;12(12):2402-2413.
  5. Koepfli P, Wyss CA, Gaemperli O, Siegrist PT, Klainguti M, Schepis T, Namdar M, Bechir M, Hoefflinghaus T, Duru F, Kaufmann PA. Left bundle branch block causes relative but not absolute septal underperfusion during exercise. Eur Heart J. 2009 Dec;30(24):2993-9.