Author + information
- Received December 30, 1988
- Revision received March 29, 1989
- Accepted April 21, 1989
- Published online September 1, 1989.
- Takashi Irie, MD,
- Tsutomu Imaizumi, MD, FACC∗,
- Takeyuki Matuguchi, MD,
- Samon Koyanagi, MD,
- Hideo Kanaide, MD,
- Akira Takeshita, MD, FACC and
- Motoomi Nakamura, MD
- ↵∗Address for reprints: Tsutomu Imaizumi, MD. Research Institute of Angiocardiology and Cardiovascular Clinic. Faculty of Medicine. Kyushu University, 3-1-1 Maidashi, Higashi-Ku. Fukuoka 812, Japan.
It is not known whether coronary vasospasm is associated with coronary thrombosis. In this study, plasma levels of fibrinopeptide A during anginal attacks in 24 patients with variant angina were examined. A hyperventilation test was used to induce angina. Hyperventilation induced angina and ST segment elevation (ΔST: 0.32 ± 0.14 mV, p < 0.01) in eight patients with variant angina. Fibrinopeptide A increased from 0.75 ± 0.27 at control to 7.8 ± 4.4 ng/ml (p < 0.01) during anginal attacks in these eight patients. In addition, four patients had spontaneous attacks of angina; they also had elevated levels of fibrinopeptide A during attacks (from 2.0 ± 1.2 at control to 21.9 ± 18.0 ng/ml (p < 0.01) during attacks). Hyperventilation did not induce either angina or ST segment elevation in 12 of the patients with variant angina. Fibrinopeptide A levels did not change with hyperventilation in these patients.
To determine whether elevated plasma levels of fibrinopeptide A were associated with angina, the plasma levels of fibrinopeptide A were examined during exercise-induced angina in seven additional patients with stable effort angina. They all developed angina with treadmill exercise; however, plasma fibrinopeptide A did not change. Therefore, only the patients with variant angina demonstrated elevated levels of fibrinopeptide A during anginal attacks. These findings suggest that coronary vasospasm associated with myocardial ischemia may induce stasis of blood, resulting in fibrinogen-fibrin conversion in the coronary vessels.
- Received December 30, 1988.
- Revision received March 29, 1989.
- Accepted April 21, 1989.