. Pronounced HR variability after exercise in inferior ischemia: evidence that the cardioinhibitory vagal reflex is invoked by exercise-induced inferior ischemia. Am J Physiol Heart Circ Physiol 288: H1179 -H1185, 2005. First published October 21, 2004; doi:10.1152/ajpheart.00045.2004.-Potent cardioinhibitory vagal reflex resulting in bradycardia and hypotension has been observed under particular conditions of transmural inferior ischemia and its reperfusion, such as those observed with acute infarction. However, whether exercise-induced ischemia with ST depressions that is subendocardial and that might be recurrently experienced in daily activities can evoke this reflex remains unknown. In patients with exercise-induced ST depressions due to either inferior [right coronary artery stenosis (RCA), n ϭ 52] or anterior ischemia [left anterior descending artery stenosis (LAD), n ϭ 51], we evaluated postexercise vagal activity (from 0 to 6 min) by the time constant of heart rate (HR) decay and HR variability by 30-s averages of the absolute values of successive RR interval differences (⌬RR). Exercise parameters were similar between groups. The time constant was slightly but significantly shorter in RCA than LAD patients (79 Ϯ 24 vs. 93 Ϯ 29 s, P Ͻ 0.01). More significantly, ⌬RR early after exercise (0.5-2.5 min) was approximately twofold greater in RCA than LAD patients (from ϩ76 to ϩ118%, P Ͻ 0.001), indicating pronounced vagal activity stimulated by inferior ischemia. Revascularization prolonged the time constant (P Ͻ 0.05) and attenuated recovery ⌬RR in RCA patients (P Ͻ 0.05, n ϭ 10) but did not change both parameters in LAD patients (n ϭ 12). As well as acute inferior infarction, exercise-induced inferior subendocardial ischemia, which might recurrently occur in daily activities, activates the cardioinhibitory reflex. These new findings must be taken into account in interpreting vagal activity in patients with coronary artery disease.heart rate variability; vagus nerve; coronary artery disease EXPERIMENTAL STUDIES in animals have demonstrated that excitation of vagal sensory nerve endings from myocardial ischemia involving the inferoposterior wall of the left ventricle activates potent cardioinhibitory reflex resulting in bradycardia and hypotension (7,24). In humans, similar observations have been made under particular conditions of severe transmural inferior ischemia and its reperfusion, such as those that occur with myocardial infarction, vasospastic angina, or angioplasty of the right coronary artery (12,15,21,22,28). For example, in the first hour of the onset of acute myocardial infarction, patients with inferior infarction often (ϳ75%) show sinus bradycardia and/or hypotension, which generally responds to intravenous administration of atropine. This observation contrasts with that in patients with anterior infarction, about 50% of whom show sinus tachycardia and/or hypertension (15).Despite these well-recognized clinical observations, little attention has been paid to the question as to whether this refle...
