Abstract
Background. Microvascular angina can occur during exercise and at rest. Reduced vasodilator capacity of the coronary microvessels is implicated as a cause of angina during exercise, but the mechanism of angina at rest is not known. Our aim was to test the hypothesis that primary hyperconstriction (spasm) of coronary microvessels causes myocardial ischaemia at rest. Methods. Acetylcholine induces coronary artery spasm in patients with variant angina. We tested the effects of intracoronary acetylcholine at graded doses in 117 consecutive patients with chest pain (at rest, during exertion, or both) and no flow-limiting (> 50%) organic stenosis in the large epicardial coronary arteries. We also assessed the metabolism of myocardial lactate during acetylcholine administration in 36 of the patients by measurement of lactate in paired blood samples from the coronary artery and coronary sinus vein. Findings. Of the 117 patients, 63 (54%) had large-artery spasm, 29 (25%) had microvascular spasm, and 25 (21%) had atypical chest pain. The 29 patients with microvascular spasm developed angina-like chest pain, ischaemic electrocardiogram (ECG) changes, or both spontaneously (two patients) or after administration of acetylcholine (27 patients) without spasm of the large epicardial coronary arteries. Testing of paired samples of arterial and coronary sinus venous blood showed that lactate was produced during angina attack in nine of 11 patients with microvascular spasm. There was more women (p < 0.01) and fewer coronary risk factors (p < 0.01) in patients with microvascular spasm than in those with large-artery spasm. Interpretation. Coronary microvascular spasm and resultant myocardial ischaemia may be the cause of chest pain in a subgroup of patients with microvascular angina.
| Original language | English |
|---|---|
| Pages (from-to) | 1165-1169 |
| Number of pages | 5 |
| Journal | Lancet |
| Volume | 351 |
| Issue number | 9110 |
| DOIs | |
| Publication status | Published - Apr 18 1998 |
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- Medicine(all)
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Angina pectoris caused by coronary microvascular spasm. / Mohri, Masahiro; Koyanagi, Masamichi; Egashira, Kensuke; Tagawa, Hirofumi; Ichiki, Toshihiro; Shimokawa, Hiroaki; Takeshita, Akira.
In: Lancet, Vol. 351, No. 9110, 18.04.1998, p. 1165-1169.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Angina pectoris caused by coronary microvascular spasm
AU - Mohri, Masahiro
AU - Koyanagi, Masamichi
AU - Egashira, Kensuke
AU - Tagawa, Hirofumi
AU - Ichiki, Toshihiro
AU - Shimokawa, Hiroaki
AU - Takeshita, Akira
PY - 1998/4/18
Y1 - 1998/4/18
N2 - Background. Microvascular angina can occur during exercise and at rest. Reduced vasodilator capacity of the coronary microvessels is implicated as a cause of angina during exercise, but the mechanism of angina at rest is not known. Our aim was to test the hypothesis that primary hyperconstriction (spasm) of coronary microvessels causes myocardial ischaemia at rest. Methods. Acetylcholine induces coronary artery spasm in patients with variant angina. We tested the effects of intracoronary acetylcholine at graded doses in 117 consecutive patients with chest pain (at rest, during exertion, or both) and no flow-limiting (> 50%) organic stenosis in the large epicardial coronary arteries. We also assessed the metabolism of myocardial lactate during acetylcholine administration in 36 of the patients by measurement of lactate in paired blood samples from the coronary artery and coronary sinus vein. Findings. Of the 117 patients, 63 (54%) had large-artery spasm, 29 (25%) had microvascular spasm, and 25 (21%) had atypical chest pain. The 29 patients with microvascular spasm developed angina-like chest pain, ischaemic electrocardiogram (ECG) changes, or both spontaneously (two patients) or after administration of acetylcholine (27 patients) without spasm of the large epicardial coronary arteries. Testing of paired samples of arterial and coronary sinus venous blood showed that lactate was produced during angina attack in nine of 11 patients with microvascular spasm. There was more women (p < 0.01) and fewer coronary risk factors (p < 0.01) in patients with microvascular spasm than in those with large-artery spasm. Interpretation. Coronary microvascular spasm and resultant myocardial ischaemia may be the cause of chest pain in a subgroup of patients with microvascular angina.
AB - Background. Microvascular angina can occur during exercise and at rest. Reduced vasodilator capacity of the coronary microvessels is implicated as a cause of angina during exercise, but the mechanism of angina at rest is not known. Our aim was to test the hypothesis that primary hyperconstriction (spasm) of coronary microvessels causes myocardial ischaemia at rest. Methods. Acetylcholine induces coronary artery spasm in patients with variant angina. We tested the effects of intracoronary acetylcholine at graded doses in 117 consecutive patients with chest pain (at rest, during exertion, or both) and no flow-limiting (> 50%) organic stenosis in the large epicardial coronary arteries. We also assessed the metabolism of myocardial lactate during acetylcholine administration in 36 of the patients by measurement of lactate in paired blood samples from the coronary artery and coronary sinus vein. Findings. Of the 117 patients, 63 (54%) had large-artery spasm, 29 (25%) had microvascular spasm, and 25 (21%) had atypical chest pain. The 29 patients with microvascular spasm developed angina-like chest pain, ischaemic electrocardiogram (ECG) changes, or both spontaneously (two patients) or after administration of acetylcholine (27 patients) without spasm of the large epicardial coronary arteries. Testing of paired samples of arterial and coronary sinus venous blood showed that lactate was produced during angina attack in nine of 11 patients with microvascular spasm. There was more women (p < 0.01) and fewer coronary risk factors (p < 0.01) in patients with microvascular spasm than in those with large-artery spasm. Interpretation. Coronary microvascular spasm and resultant myocardial ischaemia may be the cause of chest pain in a subgroup of patients with microvascular angina.
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U2 - 10.1016/S0140-6736(97)07329-7
DO - 10.1016/S0140-6736(97)07329-7
M3 - Article
C2 - 9643687
AN - SCOPUS:0032542882
VL - 351
SP - 1165
EP - 1169
JO - The Lancet
JF - The Lancet
SN - 0140-6736
IS - 9110
ER -