Author + information
- Received August 3, 1992
- Revision received February 9, 1993
- Accepted March 2, 1993
- Published online September 1, 1993.
- Masaki Hashimoto, MDa,∗,
- Mitsunori Okamoto, MDa,
- Togo Yamagata, MDa,∗,
- Tetsuya Yamane, MDa,∗,
- Mitsumasa Watanabe, MDa,∗,
- Yukiko Tsuchioka, MDa,∗,
- Hideo Matsuura, MDa,∗ and
- Goro Kajiyama, MDa,∗
- ↵∗Address for correspondence: Masaki Hashimoto, MD, Department of Cardiology, Hiroshima Prefectural Hiroshima Hospital, 1-5-54 Ujinakanda, Minami-ku, Hiroshima City, Japan 734.
Objectives. This study was conducted to clarify the mechanisms of the abnormal systolic blood pressure response after exercise in patients with angina pectoris.
Background. An abnormal systolic blood pressure response in patients with angina pectoris has been observed not only during exercise but also during the recovery period after exercise. However, the mechanisms of this abnormal response during recovery have not been elucidated.
Methods. Thirty-five patients with angina pectoris and 17 control subjects underwent bicycle ergometric studies after insertion of a Swan-Ganz catheter.
Results. In control subjects, all hemodynamic variables decreased rapidly after exercise. In 7 of the 35 patients, systolic blood pressure increased after exercise. The patients with angina were classified into two groups. In group I (17 patients), changes in systolic blood pressure during recovery were smaller than those in control subjects. In group II (18 patients) recovery of systolic blood pressure was normal. Changes in stroke index from rest to peak exercise were smaller in group I than in group II. Stroke index in both patient groups increased paradoxically during recovery. The increase in systemic vascular resistance index during recovery and the ratio of plasma norepinephrine concen tration to cumulative work load were greater in group I than in group II.
Conclusions. An abnormal systolic blood pressure response after physical exercise in patients with angina pectoris is indicative of severe myocardial ischemia during exercise and may be caused by an increase in stroke volume due to recovery from myocardial ischemia and increased systemic vascular resistance secondary to exaggerated sympathetic nervous activity.
- Received August 3, 1992.
- Revision received February 9, 1993.
- Accepted March 2, 1993.