European Society of Cardiology
Skip navigation links
Home
About the ESC
Membership
Communities
Congresses
Education
Guidelines & Surveys
Journals
Initiatives
Welcome to the European Society of Cardiology. Our mission: to reduce the burden of cardiovascular disease in Europe
 
07 Dec 2012

Heart failure: preserved vs depressed ejection fraction 

Joint with Heart Failure Association

Professor Frank Arnold Flachskampf 

Professor Frank Arnold Flachskampf
Topics: Heart Failure (HF)
Session number: 117
Session title: Heart failure: preserved vs depressed ejection fraction
Authors: Professor Frank Arnold Flachskampf



This session organized jointly by the EACVI and the Heart Failure Association reviewed diagnosis and management of heart failure with “preserved” (HFPEF) and reduced ejection fraction (HFREF). 

The first speaker, Burkert Pieske from Graz, Austria, reviewed current diagnostic concepts in particular for HFPEF. This condition has been defined somewhat differently by different guidelines and represents a common pathophysiological pathway for several diseases, most prominently hypertension, diabetes, coronary artery disease, and others. In the recently published, large (n=4128)  I-PRESERVE study, which included patients with symptomatic heart failure and preserved ejection fraction, only 59% of patients showed remodeling or hypertrophy, one third had normal atrial size, and only two thirds had signs of diastolic dysfunction on echocardiography. This emphasizes the heterogenous and difficult-to-define nature of HFPEF.

Nevertheless, a number of parameters, mainly echocardiographic parameters of increased left ventricular filling pressures and natriuretic peptides, allow the identification of HFPEF with some confidence. Burkert Pieske pointed out the increasing role of several recent refinements in the diagnosis: the diastolic stress test, lower longitudinal (but initially not circumferential!) left ventricular strain, elevated pulmonary arterial pressures, decreased apical rotation of the left ventricle, and atrial enlargement and functional impairment (measured by strain or strain rate), which make it possible to diagnose diastolic dysfunction with increasing accuracy.

Antonello D’Andrea from Naples, Italy, discussed the existing approaches to identification of myocardial “scars” or “fibrosis”, which may make it possible to identify the reversibility of myocardial dysfunction in HFREF. This is a field in which many modalities, from echocardiography to positron emission tomography, can be employed. D’Andrea underlined that it is less the theoretical accuracy of these methods that is critical for their use, but rather the local expertise and availability.
 
Alexandra Frogoudaki from Athens beautifully illustrated in two instructive cases the striking role of diastolic dysfunction for the clinical picture of heart failure:

1) A patient with sarcoidosis with no overt symptoms, but a massively impaired ejection fraction of 28%; however, only very mild echocardiographic signs of diastolic dysfunction.

2) A patient with renal failure and coronary artery disease, who had a normal ejection fraction, but advanced diastolic dysfunction (E/e’ = 26), who was admitted to hospital with pulmonary oedema.

After these two characteristic examples, she reviewed current knowledge on prognosis of HFPEF and HFREF, showing that while HFREF does have a worse prognosis than HFPEF, both entail substantial adverse event rates. In HFPEF patients die more often of co-morbidities than of heart disease proper, but some patients originally diagnosed with HFPEF over time convert to HFREF, e.g. after myocardial infarction. Further, as Burkert Pieske pointed out in a comment, high natriuretic peptide levels are clear indicators of increased mortality in HFPEF.
 
In the last talk of the session, Philip Cokkinos from Athens showed data and echocardiographic images from a patient with severe heart failure, left bundle branch block, and an ejection fraction of 31%, who was treated by cardiac resynchronization therapy and improved optimally his ejection fraction to 50%, with smaller volumes, higher longitudinal strain, a decrease in mitral regurgitation, and a narrower QRS complex. He “runs and hunts” again, Dr. Cokkinos remarked, and then went on to comprehensively review the literature and current guidelines on cardiac resynchronization therapy. The case and the history of cardiac resynchronization therapy shows vividly that, for some patients at least, heart failure is not an unchangeable fate.


The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.