Heart Failure is the result of heterogeneous structural heart diseases, especially ischemic disease, and is becoming increasingly common in all Western countries.Many patients continue to be symptomatic in spite of progress in pharmacological therapy, and the risk of mortality remains high in the most advanced functional classes. Cardiac resynchronization therapy can be used as a therapeutic strategy for alleviating symptoms and reducing mortality in selected patients with heart failure.Cardiac resynchronization therapy provides both immediate and medium/long-term results. The immediate results are the reduced QRS duration, the synchrony restoration between the ventricles and between the lateral and septal walls of the left ventricle, the reduced mitral regurgitation and the increased stroke volume. In the medium/long term, left ventricular reverse remodeling occurs and left ventricular ejection fraction is increased.Several trials have documented both increased functional capacity and improvements in quality of life and New York Heart Association class. Moreover, cardiac resynchronization therapy has been seen to reduce HF hospitalizations and mortality and the total number of days of hospitalization.In order to reduce the percentage of non-responders to cardiac resynchronization therapy, it is necessary to optimize the prognostic stratification of candidates for implantation through multi-parameter evaluations and to ensure correct device programming with periodic updates which are widely recommended but not so often performed.Whether indications should be extended will need to be evaluated in view of the known complications mainly associated with lead implantation.
RationaleIt is well known that QRS duration is inversely correlated with survival in HF patients in functional classes II-IV, and patients with QRS ≥200 ms have a 5-fold higher risk of death than those with a narrow QRS [7]. In particular, left bundle branch block (LBBB) usually delays activation of the posterior/lateral wall of the left ventricle, leading to asynchronous contraction between the septum and posterior-lateral wall and reducing the left ventricular ejection fraction (LVEF).CRT can correct this asynchronous contraction through the preexcitation of the posterior-lateral wall of the left ventricle, thereby improving systolic function [8,9]. Indeed, the dyssynchrony due to prolonged QRS duration involves the heterogeneous propagation of electrical activity in the ventricle, which determines various degrees of impaired coordination in filling and contraction [10]. Consequently the contractile efficiency of the heart is compromised and the myocardial oxygen consumption increases, worsening the clinical course of HF.