Resynchronisation therapy in heart failure: searching for predictors

Cardiac resynchronisation therapy (CRT) has been gaining clinical application. However, prospective identification of responders or non-responders to this therapy is still challenging. Over the past decade, significant progress has been made in understanding the deleterious effects of ventricular dysynchrony in patients with congestive heart failure (CHF). Randomised controlled clinical trials have demonstrated that CRT improves clinical symptoms and left ventricular (LV) function, and reduces morbidity and mortality in patients with moderate to severe CHF (New York Heart Association Functional Class III-IV).1–4 However, up to one-third of patients may not respond fully to CRT. Synchrony of heart contraction is important because it is effective and energetically efficient. Left bundle branch block, a common form of “electrophysiological abnormality” in heart failure, can result in three mechanical problems: 1) abnormal left atrioventricular timing, 2) delayed intraventricular timing, and 3) delayed interventricular timing. The net result is a decline in systolic function with reduced cardiac output, increased end-systolic volume and wall stress, and delayed relaxation. Atrial-ventricular delay can result in suboptimal chamber filling and contribute to diastolic mitral regurgitation. Prolongation of isometric contraction time (pre-ejection time) caused by desynchronisation is associated with an acute drop of systolic pressure in animal models.5 The delay in LV contraction shortens filling time, which may cause or exacerbate restrictive filling.6 Abnormal timing of intraventricular contraction worsens the underlying systolic and diastolic performance and increases …