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Chronic heart failure: Not everyone affected is equally responsive to ACE inhibitors

Chronic heart failure: Not everyone affected is equally responsive to ACE inhibitors

A cross-sectional study by MedUni Vienna in patients with chronic heart failure was able to show that the patients respond individually and very differently to the ACE inhibitors administered for the basic therapy. Perhaps in the subgroups different endogenous overactivated systems dominate the clinical picture. For the first time, this provides an explanation why not all patients benefit equally from an ACE inhibitor. The findings of the study support the efforts in the development of a targeted individualized therapy (precision medicine) in heart failure. At the end of May 2018, Vienna will be the meeting place for international cardiologists with two cardiology congresses.

Chronic heart failure (cardiac insufficiency) is becoming increasingly challenging in western society due to its frequency, mortality and hospitalization. It is associated with a long course of illness, high suffering and poor prognosis for those affected.

The basic therapy for chronic heart failure has been the ACE inhibitor (angiotensin-converting enzyme inhibitor) for 25 years. It affects the renin-angiotensin system, which regulates volume balance and blood pressure. The overactivation of this hormone system is believed to be an essential mechanism that favors the progression of the disease. The use of ACE inhibitors not only improves patient discomfort or performance, it also prevents hospitalization and prolongs survival. So far, the recommendation is to prescribe an ACE inhibitor to anyone with heart failure. At the same time, you know that you can not help every patient with it. Apparently, there are different phenotypes in heart failure, which consequently affect the response to therapy.

The cross-sectional study was conducted by Noemi Pavo at the Cardiac Insufficiency Outpatient Clinic of the Clinical Department of Cardiology of the MedUni Vienna / AKH Vienna and for the first time examined the entire renin-angiotensin system in patients with chronic systolic heart failure with ACE inhibitors. This was possible with a novel elaborate mass spectrometric analysis, which shows the hormone system holistically. Despite comparable drug types and dosages, and regardless of the severity of heart failure, the patients showed an individually extremely different response to therapy at the molecular level of the renin-angiotensin system.

In addition, it could be shown that the activation of the crucial peptides can be estimated directly by means of the easily determinable renin, so that future investigations can also be carried out on large patient numbers. Significant in this context is the new realization that in many patients with heart failure mentioned above renin-angiotensin system is apparently not or only slightly activated. For the first time, this gives an explanation why not all patients benefit from an ACE inhibitor. Here, other body-own overactivated systems may dominate the clinical picture. On the other hand, there are many patients with excessive activation of the renin-angiotensin system, who may need a more aggressive therapy.

Precision medicine for heart failure

The findings of the study support efforts in the development of a targeted individualized therapy in heart failure with the possibility of a therapy adjustment according to the existing phenotype with already known drugs. At the same time, they open up further questions concerning the regulation of the renin-angiotensin system with potential development of new approaches to heart failure therapy.

Chronic heart failure (cardiac insufficiency) is an increasing challenge in Western society. This is why heart failure is already the most prevalent in the European Society of Cardiology. In May this year, more than 5,000 cardiologists are expected in Vienna for a specialist congress.


Pavo N, Goliasch G, Wurm R, Novak J, Strunk G, Gyöngyösi M, Poglitsch M, Säemann MD, Hülsmann M. Low- and High-renin Heart Failure Phenotypes with Clinical implications. Clin Chem. 2017 Nov 14. pii: clinchem.2017.278705. doi: 10.1373 / clinchem.2017.278705.

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