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Cardiac resynchronisation therapy (CRT) is a pacing treatment for heart failure. It was first proposed in the 1990s for selected patients with drug refractory heart failure, on the basis of a series of pioneering experiences performed in France.1 ,2
The pathophysiological background for CRT is the presence, in a substantial subset of heart failure patients, of a left intraventricular conduction delay (wide QRS at 12 lead ECG) with associated left ventricular mechanical dyssynchrony. Stimulation of the left ventricle through an electrode, inserted into the venous system until its tip reaches a posterolateral or lateral branch of the coronary sinus, is able to correct the electrical dyssynchrony, thus improving haemodynamics, exercise performance and the patient's symptoms.
In patients with symptomatic improvement, the correction of electrical dyssynchrony (ie, resynchronisation) is usually associated with a reduction in left ventricular volumes (‘reverse remodelling’), a reduction of mitral regurgitation and an improvement in left ventricular ejection fraction.3
Evidence supporting the clinical value of CRT
Following the first pilot experiences, CRT has now been the subject of a series of randomised controlled trials (RCTs) and the evidence in support of CRT is based on more than 9000 patients.4 Initially, RCTs were focused on patients with heart failure in New York Heart Association (NYHA) functional class III-IV despite optimised medical treatment and wide QRS (>120 ms); >4500 patients were enrolled in trials that provided solid evidence in favour of CRT, both on the basis of individual studies and meta-analysis.4 Meta-analysis showed that appropriate use of CRT in NYHA class III-IV patients has the potential to reduce all cause mortality by 22% (95% CI 9% to 33%) and hospitalisations by 35% (95% CI 14% to 50%).4
More recently, the role of CRT in reducing mortality and morbidity has also been tested in patients with wide QRS in the setting …