Cardiac resynchronization therapy is certainly cardiac therapy, but how much resynchronization and how much atrioventricular delay optimization?

Heart Fail Rev. 2012 Nov;17(6):727-36. doi: 10.1007/s10741-011-9271-1.

Abstract

Cardiac resynchronization therapy has become a standard therapy for patients who are refractory to optimal medical therapy and fulfill the criteria of QRS >120 ms, ejection fraction <35% and NYHA class II, III or IV. Unless there is some other heretofore unrecognized effect of pacing, the benefits of atrio-biventricular pacing on hard outcomes observed in randomized trials can only be attributed to the physiological changes it induces such as increases in cardiac output and/or reduction in myocardial oxygen consumption leading to an improvement in cardiac function efficiency. The term "Cardiac Resynchronization Therapy" for biventricular pacing presupposes that restoration of synchrony (simultaneity of timing) between left and right ventricles and/or between walls of the left ventricle is the mechanism of benefit. But could a substantial proportion of these benefits arise not from ventricular resynchronization but from favorable shortening of AV delay ("AV optimization") which cannot be termed "resynchronization" unless the meaning of the word is stretched to cover any change in timing, thus, rendering the word almost meaningless. Here, we examine the evidence on the relative balance of resynchronization and AV delay shortening as contributors to the undoubted clinical efficacy of CRT.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cardiac Resynchronization Therapy*
  • Heart Atria / physiopathology
  • Heart Failure / physiopathology
  • Heart Failure / therapy*
  • Heart Rate*
  • Heart Ventricles / physiopathology
  • Humans
  • Treatment Outcome