Cardiomyopathy induced by LBBB
Approximately one third of patients with heart failure (HF) present with conduction disturbances that result in a QRS of greater than 120 ms. Most commonly (in approximately 25% of HF patients) this is exhibited as a left bundle branch block (LBBB) pattern This percentage is significantly higher than the estimated 1.5% prevalence ofLBBB in the general patient population .
A left bundle branch block (LBBB) does not usually cause symptoms, but it can diminish cardiac performance in a healthy heart. A LBBB causes the ventricles to be activated sequentially rather than simultaneously; this leads to wall-motion abnormalities. When the two papillary muscles are not simultaneously activated, mitral regurgitation can result. The significance of these abnormalities may not be apparent in the patient with adequate left ventricular systolic function, but they can make systolic dysfunction more pronounced.
LBBB deteriorates both diastolic and systolic left ventricular (LV) functions and constitutes a risk factor for the development and progression of cardiovascular diseases (CVD). As with other conduction defects, LBBB appears to be irreversible despite pharmacological treatment, but can be mitigated by cardiac resynchronisation therapy (CRT) in patients with moderate to severe HF and deteriorated LV systolic function. It is unknown whether CRT could slow or prevent emergent remodelling in non-HF patients presenting with LBBB.
Pathophysiology and treatment of LBBB
The reduced cardiac function and/or poor clinical status observed in patients presenting with abnormal ventricularconduction patterns may support a possible cause-and-effect relationship between LBBB and HF.
In LBBB there is delays in LV systolicand diastolic events . The delays were associated with a shortening of LV diastole, abnormal septal motion with an associated decrease in regional ejection fraction and an overall reduction in global ejection fraction in the LBBB . researches confirmed the prolongation of pre-ejection and relaxation times that directly impairs diastolic function by shortening LV filling time to an extent likely to limit stroke volume. This effect has been quantified by Zhou et al. who showed that the LBBB-dependent activation abnormalities have a dominant effect, over the presence of cardiomyopathy, on the deterioration of LV function.
Although LBBB is a complex electrical disease resulting from conduction delays located at several anatomic levels of the activation sequence, most patients with HF and LBBB have a specific ‘‘U-shaped’’ activation sequence that turns around the apex of the LV.
Intra-left ventricular asynchrony, observed in the majority of patients with LBBB, is an independent predictor of severe cardiac events in HF patients. This has been shown in patients with non-ischaemic cardiomyopathy either by tissue Doppler imaging .
Some patients have a cardiomyopathy induced by left bundle branch block in the absence of structural heart disease that can be resolved with cardiac resynchronization therapy (CRT). The prevalence of left bundle branch block in humans is about 1%, and the condition is generally associated with structural heart disease. The conduction abnormality can be isolated, however, in the absence of structural defects.
Datas strongly suggest that patients with left bundle branch block but initially normal hearts may develop a progressive disorder in which dyssynchrony induces reduced left ventricular performance, cardiac remodeling, and eventually the manifestation of clinical heart failure.
The following characteristics, define an left bundle branch block-induced cardiomyopathy:
-History of typical left bundle branch block for more than 5 years and normal sinus rhythm
-Left ventricular ejection fraction greater than 50% when diagnosed with left bundle branch block
-Decrease in left ventricular ejection fraction to 40% or less, left ventricular end-diastolic diameter of 55 mm or greater, and development of NYHA functional class II to IV heart failure over several years
-Major left heart mechanical dyssynchrony
-Lack of other identifiable cause of cardiomyopathy
-Indication for and super-response to CRT, defined as a left ventricular ejection fraction of 45% or greater and a decrease in NYHA functional class at 1 year .
Even if the distinct improvement after introduction of CRT strongly suggests a causal effect of dyssynchrony, we do not know to which extent reverse remodeling would persist without support by angiotensin-converting enzyme inhibitors and beta-blockers.