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.