Heart failure is primarily a disease of the elderly, with approximately half of these cases
occurring in patients aged ≥75 years. Heart failure is the leading cause of hospitalization
in the elderly. Moreover, it worsens cognition, physical function and quality of life,
increases health care costs and leads to higher mortality. Nearly half of the patients with
heart failure have preserved ejection fraction (HFPEF), and the prevalence appears to be
rising. Although patterns of morbidity and functional decline are similar in patients with
HFPEF to those with heart failure and reduced ejection fraction (HFREF), HFPEF represents a
particular challenge since there is no proven treatment. Therapies that are effective in
HFREF, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and
beta blockers, have so far been unsuccessful in HFPEF. This differential response to therapy
combined with distinct patterns of structural remodeling suggests that HFPEF and HFREF are
two discrete entities with fundamentally different pathophysiologies. A recently proposed
mechanism for HFPEF development identifies a systemic pro-inflammatory state induced by
comorbidities as the primary cause of HFPEF. Therefore, progress in managing HFPEF requires
improved understanding of HFPEF pathogenesis with a focus on the impact of comorbidities.
Hypothesis: HFPEF in the elderly is dominated by multiple comorbidity which are not a
complicating factor in HFPEF, but a major part of the syndrome, contribute to the HFPEF.
Therefore, to make comorbidity as attractive therapeutic target will promote a paradigm shift
toward individualized optimal care in elderly patients with HFPEF.
Main purpose: To promote a paradigm shift toward individualized optimal care in elderly
patients with HFPEF by effective treatment of the comorbidities.
Specific aim: To determine if systematic screening and optimal management of comorbidities
associated with HFPEF will improve outcome in patients with HFPEF
Work plan: The investigators' intervention study will use a multi-centre, prospective,
randomized, open procedure but blinded end-point (PROBE) design. Patients (n=220) are
randomized 1:1 to either usual care (n=110) or intervention (n=110). Inclusion criteria are
HFPEF >60 years. In the Intervention arm, all patients will be subject to systematic
screening and optimal treatment of 12 most frequently seen co-morbidity. Endpoints will be
collected by Independent Endpoint Committee once a year during 2 years.
Significance and clinical relevance : The present study focuses on an important issue in the
investigators' society, namely HFPEF in the elderly population. This health problem has been
largely ignored despite the fact that there is no recommended therapy. The investigators'
proposed study represents a paradigm shift in therapy. It is based on a new concept focusing
on comorbidities that are considered to be predisposing factors to HFPEF in contrast to
available trials that target only the heart. The investigators' study therefore challenges
the current clinical practice and may fill the knowledge gap in HFPEF.
