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Articles in PresS, published online ahead of print January 31, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00825.2001
Submitted on September 19, 2001
Accepted on January 18, 2002
1 Cardiology, Northwestern University Medical School, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: j-goldberger{at}northwestern.edu.
Depressed parasympathetic tone is associated with an increased risk of sudden cardiac death. Exercise and the post-exercise recovery period, which are associated with parasympathetic withdrawal, are high risk periods for sudden death. However, parasympathetic effects on cardiac electrophysiology during exercise and recovery have not been described. Electrophysiology studies were performed using non-invasive programmed stimulation (NIPS) in 9 subjects (age 59 ± 18 years) with implanted dual chamber devices and normal left ventricular function during multiple bicycle exercise sessions. NIPS was performed at rest, during exercise, and in the early recovery period both before and after parasympathetic blockade with atropine. Parasympathetic effect was defined as the value of the parameter of interest in the absence of atropine minus the value of the parameter in the presence of atropine. During exercise, sinus cycle length, AV block cycle length, AV interval, and ventricular effective refractory period shortened; in recovery the values were intermediate between the rest and exercise values (p<0.0001 by ANOVA). Parasympathetic effects on sinus cycle length, AV block cycle length, AV interval, and ventricular effective refractory period were 247 ± 140 ms, 58 ± 20 ms, 76 ± 20 ms, and 8.6 ± 7.5 ms at rest, 106 ± 20 ms, 37 ± 14 ms, 24 ± 13 ms, and 2.6 ± 7.8 ms during exercise, and 209 ± 114 ms, 50 ± 23 ms, 35 ± 21 ms, and 9.5 ± 11.8 ms during recovery, respectively. There was poor correlation among the parasympathetic effects noted at the sinus node, AV node, and ventricle. Further work evaluating parasympathetic effects on cardiac electrophysiology during exercise and recovery in patients with heart disease is required to elucidate its role in modulating the risk of sudden cardiac death noted at these times.
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