In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

We use cookies to optimise the design of this website and make continuous improvement. By continuing your visit, you consent to the use of cookies. Learn more

Heart failure therapies: latest evidence

Session presentations
Heart Failure (HF)

The aim of this session was to propose an overview of all the therapies proposed in the care of patients with heart failure.

Martin Cowie spoke about patient monitoring, first stressing that in the present system, we get long periods without any medical contact, so that it is not astonishing that there remains room for improvement of care for outpatients. The ideal approach is proposed in the guidelines, and is very dense, and can be consulted on the website of the ESC. Regarding monitoring, “possibly” is the term proposed, and 2 lines are all that are devoted to this technique. On top of the absence of clear data, we have to take into account the absence of extra finance available from our health systems.
Different monitoring types can be evoked:

  • BNP monitoring: data is conflicting, with a meta-analysis indicating decreased mortality, but probably an effect depending on the population studied. The aim of such monitoring would be to be more strict with the application of the guidelines, which could be done without BNP, said M Cowie.
  • Telephone support: the meta-analysis indicates a slight and non significant effect on mortality, but a strong effect on hospitalisation rate. This telemonitoring is incorporated in most heart failure care programs.
  • Remote monitoring: not supported by the latest HF guidelines from the ESC. There is great heterogeneity in the different systems proposed, the different parameters monitored and the way to use them to adapt therapy for the patient.
    A meta-analysis indicated no benefit on mortality and hospitalisation; which appeared astonishing to Dr Cowie. The TeleHF Trial, using telephone monitoring, also did not report a benefit, but 15% of the population did not even call once, and the monitoring was very limited. Time HF, including 710 patients, demonstrated no effect on mortality or hospitalisation, but the population included may have been too stable, with a low event rate, so that it would have been difficult to demonstrate a benefit. The key question here is what is the optimal population to target? A recent study performed by the English government suggests that such a program could decrease visits to GPs by 15%, and visits to the emergency department by 20%. More data are obviously needed.
  • The last monitoring technique is based on use of implanted devices: lung fluid (impedance) in DOT-HF was associated with an increased hospitalisation rate, whereas CHAMPION, based on pulmonary artery pressure monitoring indicated a decreased hospitalisation rate. Monitoring of LA pressure should also be soon possible. Heart rate variability may also emerge as an important parameter to monitor.

More than trying to find “THE” perfect parameter, it may be wise to determine which combination of parameters is most informative and useful. Lastly, another aspect of the telemonitoring problem is the organisation beyond indicators: How are these parameters going to be used by the telemonitoring system, who is participating in the system and making the decisions (doctors, nurses, specific protocol to be applied by the patient...).

John Teerlink then reviewed medical therapy, starting with neurohormonal antagonism and minerallocorticoid antagonists (MRA). The recently reported Emphasis study filled the gap in the range of heart failure for which this should be indicated (now post MI, severe and less severe heart failure with LVEF<35%). Aldo DHF was presented during the hotline session and reported that LV filling pressure decreased (E/E’) whereas VO2 remained unchanged. LV mass was also decreased, as were sBP, and Nt ProBNP. Some increase in potassium and alteration in renal function was observed.

BAY 94-8862 is a non steroidal antagonist that has been showing promising results in animal models, and is being evaluated in the ARTS studies, dealing with patients with systolic dysfunction (EF<40%) and eGFR 60-90, vs placebo (ARTS1) or vs spironolactone (ARTSB). No increase in potassium is expected and the question of whether this is a beneficial factor (no hyperkaliemia) or not (antiarrhythmic protection of high potassium) remains. Some biased ligands to AT1 receptors are being developed which, when attached to the receptor, stimulate myocardial contractility but do not induce vasoconstriction. It seems also that potentiation of furosemide effects is observed. First human data will be presented at the AHA. Direct renin inhibitors are being tested in the Atmosphere and Astronaut studies dealing with chronic and acute heart failure.
LCZ results were presented in the hotline session (PARAMOUNT) and published in the Lancet, in patients with preserved EF and high BNP, showing a decrease in NtBNP and an improvement in the NYHA class. Paradigm, including 8000 patients, is ongoing with class II-IV patients with increased BNP, and compared with enalapril. Some molecules derived from the natriuretic peptides are also in the process of evaluation. An activator of the cGMP had to stop its development because of the excess of hypotension even at low doses (BAY58-26627). Relaxin is being tested in the RELAX study, which completed its enrolment and will complete its follow up before the end of the year (relaxin is the hormone liberated by women during pregnancy, and is tested here in acute heart failure).

Some new inotropes are also in development, including some myosin activators. Lastly, ivabradine is the latest approved drug in systolic heart failure, decreasing hospitalisation, and more effective when the heart rate is higher.

K. Dickstein reviewed the latest guidelines, and stressed the fact that guidelines are meant to be a rope to help go forward on rocky ground, and should not mean that clinical experience is null, and that medical doctors should not keep searching for new ways.

Lastly, Dr Pitris reviewed the assist devices, introducing the importance of the problem by stressing the number of patients with advanced heart failure (100,000 at least in the USA) compared to the population receiving a VAD today (3,000), the plateau obtained in transplantation for numerous years.

Much improvement has been achieved with continuous flow pumps, which show improved survival compared to pulsatile pumps (83% at 1 year, 75% at 2 years), acceptable for long term assistance in patients without cardiogenic shock and patients with renal failure. The number of patients has been multiplied by 10 since the FDA approved these devices, while the number of patients implanted as bridge to transplantation remained stable, indicating that a new population is benefiting from the use of these devices.

The main problem today is to define the appropriate population: not the most severe (Class 1 intermacs, “crash and burn”), who should be stabilized with other techniques before being implanted, but all the intermacs patients from 2 to 5 are potential candidates. A trial is ongoing for patients in profile 4. Today, cardiogenic shock, diabetes, age, BUN, natremia, and necessity for BIVAD remain risk factors. Adverse events remain a problem with these devices, predominantly stroke (1/10 patients year). The rate of infection has decreased and this improvement should continue, but bleeding remains a problem because of angiodysplasia resulting from continuous flow. In the presence of RV dysfunction requiring assistance, transplantation is the right option, and VAD is not. Progress is foreseen with smaller pumps, which should allow endovascular implantation, totally implanted devices, and restoration of some pulsatility with magnetic devices (such as Heart Mate 3), which allow rapid acceleration and deceleration. This could be of importance to prevent angiodysplasia.




Heart failure therapies: latest evidence

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.