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Aaron pulled his stethoscope out of his ears. He was tall and always wore a hooded sweatshirt and headphones, which made his neck look fat from behind. “What can you hear?” the cardiology professor asked. “Lub-dub-dubcha-dubcha-bup-cha-CH-BUP-ch-cha-ch-CH,” Aaron said, weaving his head as the sounds shot out of his mouth. “Exactly so,” Professor C said. It was the only time I have ever heard atrial fibrillation performed in human beatbox. It has never sounded clearer.

In atrial fibrillation (AF), the top two chambers of the heart quiver chaotically rather than squeezing and relaxing in a co-ordinated fashion. This “dithering” – as the professor described it – has a disruptive effect on the heart sounds and the pulse. Instead of the metronomic regularity of “lub-dub, lub-dub” you get a kind of jazz solo made up of skipped, merged and mangled beats. The heart rate often speeds up, too, as the ventricles (which are regulated by electrical signals from the atria) try to keep pace.

AF is the commonest cardiac arrhythmia, affecting up to 9 per cent of people in their eighties; 3 to 6 per cent of patients admitted to hospital in Britain have been found to be in AF. It can be dangerous in itself, especially if the heart rate goes too high, but the main reason we want to know if someone is in AF is the threat it poses to a different organ altogether.

In AF the flow of blood through the heart is altered. Instead of pouring smoothly, it churns and eddies. You can see the physics in action if you lower a probe into the gullet and do a trans-oesophageal echocardiogram. The reduced flow rate means that, instead of racing freely alongside each other, the red blood cells start to cling together. The clumps they form create characteristic echo shadows: “dynamic clouds of echoes curling up slowly in a circular shape”, in one researcher’s poetic description.

This phenomenon, which cardiologists call “smoke”, is a sign of stasis in the atria, and a predictor for thrombus formation. Red cells that have started to clump like this are at risk of aggregating into clots. If a clot does form, and breaks off, it is potentially lethal. It will be pumped out through the left ventricle of the heart into the aorta and from there into the arteries supplying the body. If it reaches the small arteries of the brain it is liable to get stuck, blocking the vessel and depriving all the tissues beyond it of nutrition and oxygen. This is a stroke.

AF is not the only cause of the clots that can lead to a stroke (you can also get a stroke from bleeding into the brain, rather than from a blockage, though this is much less common). But the strokes caused by AF are more likely to be fatal and, if you survive, you have a higher chance of being severely disabled.

Fibrillating atria provide a relatively sheltered environment for a growing blood clot (a small rough-walled pouch in the left atrium called the left atrial appendage is especially favourable). Clots have time to grow to a greater size before they shear off, which makes them more damaging when they eventually get stuck. The bigger the clot, the more fibrin cross-links it will contain (fibrin is a string-bag-like protein that holds clots together), making them harder for the body to dissolve. It can be difficult to explain to someone why their randomly syncopated pulse (which they may be completely unaware of: AF is often asymptomatic) means they should take blood-thinning medication for life. This is why.

Sophie Harrison is a hospital doctor in South Yorkshire. This column appears fortnightly

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