Article Text

Download PDFPDF
  1. Derek G Gibson1,
  2. Darrel P Francis2
  1. 1Department of Echocardiography, Royal Brompton Hospital, London, UK
  2. 2Heart Function Unit, Royal Brompton Hospital, London, UK
  1. Correspondence to:
    Dr Derek Gibson, Department of Echocardiography, Royal Brompton Hospital, London SW3 6NP, UK;

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Diastolic left ventricular disease is being increasingly incriminated as a cause of limitation of exercise tolerance, whether or not ejection fraction is normal,1,2 though the mechanisms by which it does so are far from clear. Indeed, it has been suggested that no diastolic abnormality at all need be demonstrated for a diagnosis of possible or probable diastolic heart failure to be made.3


Measurements can be made during diastole with many techniques, old or new, but can there be said to be as many impaired “functions” as there are abnormal measurements? Surely, the term “diastolic function” applies only to a small number of more basic mechanisms whose nature must be elucidated independently of the method used to detect them and whose number depends on rigorous use of Occam's razor. Difficulties in defining diastolic heart failure strongly suggest that agreement in this field has still to be achieved. Indeed, no simple definition of diastolic disease itself has emerged. “Increased resistance to filling” has been suggested. While the resistance of a valve orifice or circulation can readily be defined in terms of pressure drop and flow, resistance to filling involves neither and so is poorly defined. This lack of gold standards by which discrete mechanisms can be assessed in individual patients is a major impediment to identifying and quantifying disturbances in disease.


Left ventricular diastole is traditionally defined as the period in the cardiac cycle from the end of aortic ejection until the onset of ventricular tension development of the succeeding beat.4 Even in the normal subject, several mechanisms are involved:

  • Decline of the myocardial active state following systole.

  • Passive effects of connective tissue. Compression or extension of connective tissue may store potential energy from systole and release it in early diastole. In late diastole, the properties of connective …

View Full Text

Linked Articles

  • Miscellanea
    BMJ Publishing Group Ltd and British Cardiovascular Society
  • Miscellanea
    BMJ Publishing Group Ltd and British Cardiovascular Society
  • Miscellanea
    BMJ Publishing Group Ltd and British Cardiovascular Society