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Pathophysiology of heart failure with preserved ejection fraction

  • Myocyte alterations, presented by Z Papp (Debrecen, HU) - Slides
  • Extracellular matrix, presented by J Diez Martinez (Pamplona, ES) - Slides
  • Vascular remodelling and pulmonary hypertension, presented by C S P Lam (Singapore, SG) - Slides
  • Atrial dysfunction and chronotropic incompetence, presented by V Melenovsky (Prague 4, CZ) - Slides
Heart Failure (HF)

Myocyte alterations

In the first talk of this translational symposium, Dr. Papp from Debrecen, Hungary presented an overview on the role of post-translational modifications of titin and other sarcomeric proteins in left ventricular diastolic dysfunction and diabetes.

Extracellular matrix

This was followed by the presentation of Dr. Diez from Pamplona, Spain who talked about extracellular matrix. Besides the amount of collagen and its distribution (collagen I vs. III) also the type of collagen (soluble vs. insoluble) seems to play a role for HFpEF. One important protein altering collagen homeostastis is lysyl oxidase (LOX). In a clinical approach, torasemide seems to decrease LOX and results in favorable effects on diastolic function in contrast to furosemide.

Vascular remodelling and pulmonary hypertension

Dr. Lam from Singapore elegantly presented a case of a woman with pulmonary hypertension most likely due to diastolic heart failure pointing to the role of vascular remodeling in HFpEF. In contrast to nitroglycerin, sodium nitroprusside improved haemodynamic parameters in the patient. An innovative clinical approach seems to be phosphodiesterase inhibition using sildenafil where a clinical trial is (RELAX) is currently performed.

Atrial dysfunction and chronotropic incompetence

Finally, Dr. Melenovsky from Prague convincingly showed that atrial dysfunction and chronotropic incompetence of the atria contribute significantly to the clinical phenotype of HFpEF. Although the Frank-Starling mechansim can be also found in the atria, increased fibrotic tissue which, interestingly, is unevenly distributed throughout the atria and older age are important contributors to altered atrial function.




Pathophysiology of heart failure with preserved ejection fraction

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.