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Cardiac resynchronisation therapy: when the drugs don’t work.
  1. R A Bleasdale1,
  2. M P Frenneaux2
  1. 1Department of Cardiology, Royal Glamorgan Hospital, Llantrisant, UK
  2. 2Department of Cardiovascular Medicine, University of Birmingham, Birmingham, UK
  1. Correspondence to:
    Dr R A Bleasdale
    Department of Cardiology, Royal Glamorgan Hospital, Ynysmaerdy, Llantrisant, CF72 8XR;

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Heart failure effects 1–2% of the population1 and accounts for approximately 5% of all medical admissions2; despite the undoubted improvements in treatment over the past two decades, the outcome remains poor. One third of those patients admitted with decompensated heart failure die within one year of their first hospitalisation3 and up to 50% will be readmitted within the first six months after the initial hospitalisation.4 There appears little scope for further advances aimed at blocking neurohumoral maladaptive mechanisms, and other strategies, including cytokine blockade, have been disappointing. While cellular transplantation holds out considerable promise in the longer term, medically refractory heart failure remains a huge (and growing) clinical problem. Over the past decade an emerging body of evidence has suggested that biventricular and/or left ventricular pacing may provide effective palliation in some of these patients.

Initial attention regarding the potential use of pacing therapy in heart failure focused on short atrioventricular (AV) delay right sided pacing to reduce pre-systolic mitral regurgitation. This phenomenon is most pronounced in patients with long AV delays, especially when left ventricular end diastolic pressure is notably raised. Despite impressive improvements in acute haemodynamic measurements in selected patients,5–7 long term results were disappointing.8,9 The next target for pacing therapy was the dysynchronous contraction associated with the presence of left bundle branch block in patients with heart failure. Overall, approximately one third of patients with heart failure have a left bundle branch block pattern,10 although this figure rises in patients with more severe left ventricular dysfunction.11 By causing a dysynchronous left ventricular activation sequence, left bundle branch block impairs left ventricular contractile performance.12 It is not surprising, therefore, that the presence of left bundle branch block is associated with more severe symptoms and greater mortality …

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  • The British Heart Foundation supports Professor Frenneaux