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Heart failure with preserved ejection fraction; from pathophysiology to therapy"

Session presentations
  • Pathophysiology - what is new and clinically relevant? Presented by M Volpe (Rome, IT) See the slides
  • Diagnosis - is it really heart failure? Presented by B Pieske (Graz, AT) See the slides
  • Biomarkers and imaging - can they establish the diagnosis? Presented by S Solomon (Boston, US) See the slides
  • Current and future management. Presented by G Hasenfuss (Goettingen, DE) See the slides
Heart Failure (HF)


Heart failure with preserved ejection fraction (HFPEF) is a complex cardiovascular syndrome, often complicated by co-morbidities. The pathophysiological background of HFPEF has been related to a wide range of alterations of the heart and the vasculature ranging from myocardial fibrosis and increased cardiomyocyte passive stiffness to microcirculatory dysfunction.

According to the 2012 ESC guidelines for the management of heart failure, the diagnosis of HFPEF requires: symptoms and signs typical of HF, normal or mildly reduced LVEF without LV dilation, and relevant structural/functional heart disease (LV hypertrophy/LA enlargement and/or diastolic dysfunction). Invasive hemodynamic indices, Doppler tissue imaging and biomarkers (e.g. BNP or NT-proBNP) are very important in this context. Moreover, new echocardiographic techniques (e.g. speckle-tracking) and exercise testing will soon also enhance the diagnosis of HFPEF. The management of HFPEF is problematic, as no therapies have been shown to improve its clinical outcomes. However, recent clinical studies on the effects of exercise training in HFPEF suggested improvements in LV diastolic function and exercise capacity.

Interestingly, results of the Aldo-DHF study indicated that pharmacological inhibition of the pro-fibrotic mineralocorticoid receptors by spironolactone also improved LV diastolic function, but without alterations in exercise capacity. Moreover, data of the PARAMOUNT study suggested that combined inhibition of angiotensin-receptors and the enzyme responsible for breakdown of natriuretic peptides (by LCZ696) might be an effective approach for treating HFPEF.

Finally, experimental evidence implicates modulators of the autonomic nervous system or cardiomyocyte ionic homeostasis (e.g. through ryanodine-receptor stabilization or inhibition of the late sodium current) may also hold promises for future pharmacological management in HFPEF.

References


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SessionTitle:

"Heart failure with preserved ejection fraction; from pathophysiology to therapy"

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.