Heart failure: new drug can save lives
All content is checked by medical journalists.MunichA new active ingredient for the treatment of heart failure is causing a stir. The as yet unnamed substance worked so well in the clinical study that experts are already calling for the new drug to replace the previous treatment.
It happens again and again that comparative drug studies have to be ended earlier than planned. There are two main reasons for this: Either the new active ingredient has so little effect or is so poorly tolerated that the patient has to be given the tried-and-tested therapy again in order not to endanger them unnecessarily. Or the newly developed drug turns out to be so much better that it can no longer be withheld from the sick.
A "little sensation"
As happened recently when an international research group led by the US cardiologist Prof. Milton Packer decided after an interim analysis to end a large-scale drug comparison study (PARADIGM HF) prematurely after a little more than two years. They examined differences in the effectiveness of the ACE inhibitor enalapril and the newly developed active ingredient LCZ696.
In view of the results now published in the renowned New England Medical Journal, some experts speak of a "small sensation": In a total of almost 8,500 patients with cardiac insufficiency who were treated with either enalapril or LCZ696, the numbers for hospital admissions as well as for heart fell - Circulatory deaths from LCZ696 by one fifth. At the same time, the quality of life of these patients improved significantly. Study leader Packer is already calling for consequences of the study results: "LCZ696 must replace ACE inhibitors and pure angiotensin receptor blockers (ARB) in the treatment of chronic heart failure."
Gold standard is losing its luster
Treatment with enalapril has so far been considered the golden standard in the treatment of heart failure. The active ingredient inhibits a specific enzyme (angiotensin converting enzyme, ACE). As a result, less angiotensin II is formed - a messenger substance that increases blood pressure in the kidneys and blood vessels via various mechanisms. To put it simply, less angiotensin II means lower blood pressure and thus relief for the weakened heart muscle.
LCZ696 can do that too. But this drug has two active components. It not only blocks the angiotensin-II docking sites in the kidney and artery walls. At the same time, another section of its molecule also inhibits a certain enzyme (neprilysin). As a result, it improves the excretion of sodium and water by the kidneys and lowers the tension in the arterial walls. LCZ696 facilitates the work of the weakened heart muscle via two mechanisms.
Heart muscle in distress
In people with a pumping weakness of the heart (systolic heart failure), the heart muscle can only continue to pump a small part of the blood flowing into the heart chambers. His strength is no longer sufficient. The ejection rate can be measured, for example, using ultrasound. In the case of pronounced heart failure, it is often well below 50 percent, which means that more than half of the amount of blood remains in the chamber after the "heartbeat".
Symptoms of severe systolic heart failure include shortness of breath even with the slightest physical exertion or even at rest, which is particularly agonizing at night, as well as fluid accumulation in the extremities (edema) and sometimes in the lungs (pulmonary edema). (jr)
Source: McMurray, Packer et al .: Angiotensin – Neprilysin Inhibition versus Enalapril in Heart Failure (PARADIGM-HF study), New England Medical Journal (online), August 30, 2014
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