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(Circulation. 2007;115:430-431.)
© 2007 American Heart Association, Inc.

Editorial

Should Early Acceleration of Heart Rate During Exercise Be Used to Risk Stratify Patients With Suspected or Established Coronary Artery Disease?

Bernard R. Chaitman, MD

From the Division of Cardiology, Department of Medicine, St Louis University School of Medicine, St Louis, Mo.

Correspondence to Bernard R. Chaitman, MD, St. Louis University School of Medicine, 1034 S Brentwood Blvd, Ste 1550, St. Louis, MO 63117. E-mail chaitman@slu.edu

Key Words: Editorials • exercise • heart rate • prognosis • vagus nerve

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Exercise is one of the most common noninvasive stressors used to risk stratify patients with suspected or established coronary disease. Functional capacity, time to onset of demand-induced ischemic ST-segment shifts or angina, complex ventricular arrhythmias, a progressive fall in systolic blood pressure during exercise, and abnormal heart rate (HR) responses either during or after exercise are all well-established independent predictors of long-term outcome and, when used in combination, have the potential to identify prognostic high-risk patients who may be candidates for coronary angiography and coronary revascularization.¹ Among HR variables tested that are predictive of mortality, the most common include the ability to augment HR to age-predicted maximum (chronotropic response), the HR recovery response in the immediate postexercise phase, and the ST-segment response corrected for HR.^2,3

Article p 468

A normal increase in HR during exercise and the ability to slow HR in the immediate postexercise phase are dependent on the autonomic nervous system and the ability of the cardiac conduction tissue to normally propagate the electrical impulse. The vasomotor center, located in the reticular substance of the medulla and pons, has the capability to transmit parasympathetic impulses through the vagus nerves to the heart that slow HR and can modulate excitatory impulses through the sympathetic nervous system that increase HR and contractility.⁴ Regulation of the vasomotor center is affected by higher nervous centers that can excite or inhibit the center, as well as by circulatory reflexes initiated by aortic arch and carotid sinus baroreceptors that stimulate the vagal parasympathetic center. . . . [Full Text of this Article]

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