AF reduces the heart's pumping capacity. Although the atria are small chambers with relatively weak muscles, they still contribute a "kick" or boost to the larger, more powerful ventricles. In addition, the rapid heart rate of AF reduces the efficiency of each beat. In all, AF reduces the heart's pumping capacity by 10% to 30%. People whose hearts are otherwise healthy can compensate for this impairment, but those with damaged heart muscles or valves cannot. As a result, they experience the fatigue, breathlessness, exercise intolerance, and swelling of the feet and legs that are so characteristic of heart failure. AF can also trigger the chest pain of angina or a heart attack in patients with coronary artery disease.
The other major complication of AF is stroke. Although doctors have studied AF for over 100 years, the risk of stroke was not fully appreciated until the 1980s, when the Framingham Heart Study reported that 24% of its stroke patients were also in AF, and that the abnormal heart rhythm developed within the six months preceding the stroke in about a third of these participants. AF quintuples the risk of stroke. It accounts for about 15% of all strokes and for nearly a quarter of all strokes in people ages 80 to 89.
How does a cardiac abnormality cause brain damage? Since fibrillating atria don't contract, they contain relatively stagnant pools of blood. Clots (thrombi) form in these areas, then break off and travel to the brain, where they block small arteries, depriving the brain of its vital oxygen and causing tissue damage and death. It's a devastating sequence of events, but it can be prevented by anticoagulants, medications that fight blood clots. In fact, the use of anticoagulants is one of the key priorities in the management of patients with AF. The others are slowing the heart rate and, in some patients, restoring a normal heart rhythm.