Solving the mystery of the off-beat heart
Modern medicine has come a long way, but the mere thought of having a heart defect can still rattle us to our very core. The heart is a human body's engine room. Each time its beat propels blood through our bodies, it is a reassuring affirmation of our existence.
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Unfortunately, for far too many people suffering from electrical heart disease, that beat can sound like a countdown towards the end. Or even worse, in the case of sudden cardiac death (SCD), the end can come unexpectedly. Children with genetic defects have died from SCD in the course of normal exertion, such as a school race or exam; adults have met their end following the shock of something as innocuous as a ringing morning alarm clock.
The project EUTrigTreat aims to improve this situation. It received €12 million in EU funding to examine causes of electrical heart disease and improve predictions of therapy success. EUTrigTreat’s starting point is molecular causes of heart irregularities. Current treatments fail to consider these, which may contribute to these treatments being precisely that: a treatment rather than a cure.
In a healthy heart, electrical pulses propagate regularly across its muscle mass, causing the heart’s ventricles and atria to contract and relax at regular intervals. When these electrical pulses become irregular, heartbeat becomes erratic and blood is no longer pumped properly.
These disturbances in heartbeat are known as arrhythmias. “The conundrum is that the population with increased risk for cardiac disease and dangerous arrhythmias is growing, but we still have insufficient understanding of what exactly triggers cardiac arrhythmias and therefore cannot predict how and when electrical heart disease might occur in different people,” says Professor Stephan Lehnart from the University Medical Center Goettingen, who has been coordinating EUTrigTreat, since 2009.
Indeed, serious arrhythmias mean devastating health problems and significantly increased SCD risk. Patients suffering from arrhythmia may need a defibrillator implanted. These devices send a strong electric current across the heart, setting chaotic electric pulses straight again. However, the treatment is far from perfect. Lehnart explains that “because our ability to predict the risk of SCD is weak and unspecific, many patients – who are thought to be at increased risk for arrhythmia induced death – will have this very expensive and invasive technology inserted. But they may never actually benefit from it and may experience potentially serious side effects.” These can include excruciating pain (patient testimonies have compared defibrillators to being electrocuted) and perforations of the heart.
“Currently we cannot say how likely it is someone will have a potentially dangerous defect or predict how that individual will react to a specific therapy. Solving these problems would be a watershed development.” According to Lehnart, the multi-disciplinary EUTrigTreat consortium’s potential to answer at least some of these questions is substantial.
“We are developing a new method of modelling human arrhythmia activity using the small worm, C. elegans,” Lehnart says. These worms only take a week to develop – much less than other model systems – and can be easily genetically manipulated to model genetic determinants of arrhythmia. “We can envisage that these model approaches could eventually be used to assess an individual patient’s genetic defect. This would lead to a whole range of advantages, such as identifying which drug compounds would have the least side effects.”
To treat ventricular fibrillation, the most aggressive form of arrhythmia that typically causes SCD, the 15-partner consortium developed an alternative strategy to the oftentimes-painful conventional defibrillators, called LEAP (Low-Energy Anti-fibrillation Pacing).
Unlike a classic defibrillator, which uses a very strong electric current to simultaneously excite all of the organ’s cells – effectively jump-starting the heart – LEAP uses several low-energy pulses to sequentially synchronise the tissue. “Our breakthrough realisation was that these really dangerous electric irregularities are functionally associated with intrinsic structures of the heart. This allowed us to exploit the heart’s microanatomy to devise a less aggressive electro-therapy,” Lehnart explains. So far LEAP has used at least 50 percent less energy than classical defibrillators in test trials. This reduction in energy reduction opens the door to innovative, more cost effective design, as implanted defibrillators could last twice as long.
Currently 17.3 million people die globally from cardiovascular disease each year and a staggering €310 billion are spent annually fighting the heart’s failures . High as these figures are, the increase in populations at risk means they are set to rise further, making the work of the EUTrigTreat team ever more valuable for the future.
“We were fortunate to get EU funding for this project, because it allows us to go beyond national borders and really pick the best experts and researchers from different fields to tackle these problems,” Lehnart says. “I am confident the project’s broad focus is really going to move our understanding and treatment possibilities of arrhythmia forward.”
- Project acronym: EUTrigTreat
- Participants: Germany (Coordinator), Belgium, France, Greece, Italy, Netherlands, Switzerland, United Kingdom, United States
- Project FP7 241526
- Total costs: €15 857 600
- EU contribution: €12 000 000
- Duration: October 2009 - September 2014
Project web site
Project information on CORDIS