Introduction:
Approximately, one third of patients with heart failure and reduced
ejection fraction (EF) have left bundle branch block
(LBBB)4. Clark et al5 have shown
that this proportion increased from 34.0% at baseline to 36.7%, 37.7%
and 42.3% at 1, 2 and 3 years follow up, respectively. Baseline LBBB
was associated with a worse outcome and development of new LBBB was an
independent adverse prognostic feature. CRT with BiVP plays an important
role in the management of HF patient with LBBB. By reestablishing
synchrony between the left and right ventricle, BIV pacing improves
clinical parameters (NYHA class, 6‐minute walk test, quality‐of‐life,
and hospitalization rate) and echocardiographic indicators such as LVEF,
LV end diastolic and diastolic volumes6. Importantly,
CRT with BIV pacing trials with7 or without
ICD8 decreases hospitalization and mortality.
Furthermore, patients with narrowing of the QRS on ECG with BIV pacing
had a better survival rate and rapidly recovering left ventricular
systolic function9. New pacing modalities for CRT are
being assessed in clinical trials. HBP pacing has been shown to
circumvent proximal LBBB and restore electrical resynchronization in
patients with HF. LVSP has emerged as an alternative method for
delivering CRT particularly in patients with infranodal atrioventricular
block and LBBB. In this review article, we will discuss the options of
CRT in HF and LBBB with BiVP, HBP and LVSP.
In LBBB, the onset of electrical activation occurs in the RV and then
slowly propagates through the interventricular septum towards the
lateral wall of the LV10. In patients with HF and
LBBB, LV endocardial breakthrough is heterogenous and may occur at
different septal regions11,12. . Auricchio et al have
demonstrated that patients with LBBB morphology have a specific
“U-shaped” activation sequence that turns around the apex and inferior
wall of the LV. This activation pattern is generated by a functional
line of block that is oriented from the base toward the apex of the
LV11. The altered electrical activation of the
ventricles results in a significant delay between the onset of LV and RV
contraction13. This dyssynchrony results in reduction
of LVEF and is associated with decrease in cardiac output and mean
arterial pressure14,15. In addition, LBBB induced
dyssynchrony causes redistribution of circumferential shortening and
myocardial blood flow and that leads to LV
remodeling16.
CRT restores coordinated contraction and improves net systolic
performance within one beat17, and increases ejection.
Interestingly, this is achieved without a rise in myocardial oxygen
consumption18,19. Moreover, Kyriacou et al. have shown
that CRT improves coronary blood flow and flow velocity predominantly by
increasing the dominant diastolic backward decompression (suction)
wave20.
Clinical trials in CRT :
To date, more than 4000 patients have been enrolled in randomized
controlled trials for CRT. Benefits have been demonstrated for patients
with New York Heart Association (NYHA) class III HF, in particular, and,
to some degree, for those with class IV HF. These trials have
demonstrated consistent improvements in quality of life, functional
status, exercise capacity and mortality, with the weight of evidence
supporting current practice and guideline
recommendations21.