Abstract

BackgroundReverse redistribution (RR) is one of the features on myocardial perfusion scintigraphy (MPS) in patients with coronary artery spasm (CAS). This study was aimed to explore the mechanism of RR in patients with suspicion for CAS. Methods and ResultsThirty patients with RR and suspicion for CAS but without coronary artery stenosis (RR group) and 32 control patients without RR (control group) underwent coronary angiography before and after a dipyridamole administration. Coronary blood flow velocity and myocardial perfusion, as determined by corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC) and TIMI myocardial perfusion grade (TMPG), were measured. Coronary angiography showed significantly slower blood flow velocity [CTFC (37 ± 6) frame vs (29 ± 7) frame, P < .01] and lower myocardial perfusion [TMPG (2.08 ± 0.38) grade vs (2.55 ± 0.33) grade, P < .05] in RR-related arteries than in RR-unrelated arteries in the RR group. But, there was no significant difference among different coronary artery branches in the control group. After the injection of dipyridamole, CTFC decreased and TMPG increased in the RR group. The decline in CTFC and the increase in TMPG in RR-related arteries were more significant than those in RR-unrelated ones (28% vs 14% and 45% vs 16%, respectively; both P < .01). The endothelin-1/nitric oxide (NO) ratio was significantly higher in the RR group than in the control group before the injection of dipyridamole (2.79 ± 0.37 vs 1.70 ± 0.19, P < .01). After the injection of dipyridamole, the ratio went down in both groups, but the decline was statistically significant in the RR group (2.42 ± 0.33, P < .05) but not in the control group (1.42 ± 0.19, P < .05). Pearson correlation analysis showed that there was a positive correlation between summed rest scores on MPS and the endothelin-1/NO ratio (r = 0.853, P = .000) as well as CTFC (r = 0.808, P = .000) before the injection of dipyridamole in the RR group. ConclusionPatients with suspicion for CAS may exhibit a mild spasm of RR-related arteries and corresponding microvasculature and a significant imbalance of coronary blood flow velocity and myocardial perfusion at rest between RR-related and RR-unrelated areas. This is overcome by stress-induced hyperemic flow increases and which may account for RR on MPS.

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