What are heart rhythm disorders?
Your heart has an electrical system controlling how it beats and pumps blood around the body. If you’re diagnosed with a heart rhythm disorder, also known as an arrhythmia, this could mean your heart is beating too fast, too slow or with an irregular rhythm.
Over a million people in the UK have a heart rhythm problem. But these conditions can be difficult to diagnose, and are often picked up late – after they cause symptoms or complications, or have even proved fatal. Our research helps identify people with heart rhythm disorders, and gives them the best chance of living longer, healthier lives.
Find out more about the causes and symptoms of heart rhythm problems.
Understanding atrial fibrillation
Atrial fibrillation (AF) occurs when electrical impulses fire in a disorganised way in the atria - the top chambers of the heart. It’s one of the most common types of abnormal heart rhythm - around 1.3 million people in the UK have been diagnosed with AF, and it’s thought another half a million people have AF but have not yet been diagnosed.
AF can increase the risk of a blood clot forming inside the heart. If the clot is swept up out of the heart and into the blood vessels of the brain, it can cause a stroke.
BHF Professor Barbara Casadei combines her role as a heart doctor at the John Radcliffe Hospital in Oxford with pioneering research to improve our understanding of AF. Her team at the University of Oxford has found that changes in the heart muscle of the atria start before AF occurs, and could be a cause of it. AF tends to come and go before it becomes persistent. The team has found that in cases where AF is persistent, the atria have lower levels of two proteins – ‘dystrophin’ and ‘neuronal nitric oxide synthase’. Professor Casadei is studying whether these changes can be prevented or reversed to stop AF from occurring and becoming persistent.
By improving our understanding of AF and finding new ways to treat it, fewer people will be at risk of heartbreak from a stroke.
Ending heartbreak from SADS
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare inherited heart rhythm problem, which usually affects young people and children. The most common symptoms of CPVT are blackouts, palpitations and dizziness, often brought on by strenuous exercise or stress. People with CPVT can develop severely abnormal heart rhythms, which can lead to a cardiac arrest and sudden cardiac death (called Sudden Arrhythmic Death Syndrome, or SADS).
CPVT is caused by a rise in calcium inside the cells of the heart. BHF Professor Alan Williams at the University of Swansea is researching proteins in the heart called ryanodine receptors, or RyR2. These proteins control the movement of calcium into heart cells from a large calcium store inside the cell. Faults in RyR2 can lead to heart rhythm disorders like CPVT. By understanding how changes in proteins affect the movement of calcium in and out of cells, Professor Williams’ work could reveal new ways to treat people with life-threatening arrhythmias.
Does our nervous system play a part?
Long QT syndrome (LQTS) is a heart rhythm disorder where the QT interval (part of the heartbeat cycle) is lengthened. In LQTS, strenuous exercise or severe exertion can trigger a dangerous abnormal heart rhythm, called torsade de pointes, which if persistent, leads to cardiac arrest and SADS. LQTS affects around 1 in 2,000 people. It can be inherited, but can also be caused by medications taken for other conditions.
In most cases of LQTS, the flow of potassium out of heart muscle cells is delayed, which delays electrical impulses as they travel through the heart. In rarer cases, the sodium channels are affected, and too many sodium ions enter the cells. This also delays the electrical impulse, which shows up on an ECG scan as a lengthened QT interval.
Dr James Winter at King’s College London is looking at how the autonomic nervous system (which is responsible for ‘unconscious’ bodily functions, like breathing, your heartbeat and digestive functions) has a role in sudden death in people with ‘acquired’ (not inherited) LQTS. His team will find out whether stimulating autonomic nerves triggers torsades de pointes, increasing the risk of sudden cardiac death.
The difference we’ve already made
Since our foundation in 1961, we’ve come a long way in improving the lives of people with abnormal heart rhythms. From understanding the electrical pathways in the heart to improving treatments, we have much to be proud of. But the job is not done. We’re working hard to build on this work and protect more people from sudden cardiac death.
Find out more about our successes in arrhythmia research