In a recent animal study, researchers from the Division of Cardiology at Cedars-Sinai Medical Center, in collaboration with the University of California, Los Angeles, have found that over time, the absorption of nicotine after myocardial infarction (MI) significantly increases the incidence of cardiac fibrosis in canine hearts. This reaction promotes a kind of rapid heart rhythm that has many similarities to typical human atrial flutter, a potentially life-threatening condition that affects approximately a quarter million Americans each year.
In an article published online in the January issue of the American Journal of Physiology: Heart and Circulatory Physiology, researchers report a study that tested the effects of nicotine on hearts with healed myocardial infarction. Numerous studies have shown that smoking promotes coronary heart disease and myocardial infarction and is a major cause of chronic obstructive pulmonary disease, an independent predictor of atrial flutter. These findings have raised the possibility that a causal link might exist between nicotine and atrial flutter in patients with myocardial infarction.
Atrial flutter is a type of rapid heart rate caused by the upper chambers of the heart (the right and left atria). The resulting rhythm is so rapid (about 400 beats/min) that the atria are not able to fully empty their contents into the ventricles, and the "left behind" blood stagnates, increasing the risk of thromboembolism and stroke. Fibrosis is an abnormal condition in which fibrous connective tissue spreads over or replaces smooth muscle; it is most common in the heart, lung, peritoneum and kidney.
Sandra Van | EurekAlert!
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