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Decreased resting coronary flow and impaired endothelial function in patients with vasospastic angina

Saito, Yuichi; Kitahara, Hideki; Nishi, Takeshi; Fujimoto, Yoshihide; Kobayashi, Yoshio

doi: 10.1097/MCA.0000000000000721
Coronary Vasospasm

Objectives Coronary endothelial and circulatory dysfunction plays important roles in the pathogenesis of vasospastic angina (VSA). However, a complete understanding of the entire coronary circulation including microvasculature in patients with VSA is lacking.

Patients and methods A total of 32 patients without obstructive coronary artery disease in the left descending coronary artery, who underwent an intracoronary acetylcholine (ACh) provocation test for diagnosis of VSA, were enrolled prospectively. A positive diagnosis of the ACh test was defined as total/subtotal coronary artery narrowing accompanied by chest pain and/or ischemic ECG changes. Angina frequency and severity at baseline, and 1 and 3 months were recorded. Coronary circulation was evaluated invasively using a thermodilution method by obtaining the mean transit time (Tmn) at rest and hyperemia, coronary flow reserve, and index of microcirculatory resistance. Systemic endothelial function was assessed by the reactive hyperemia index.

Results There were 14 (44%) and 18 (56%) patients with and without a positive ACh provocation test. The baseline characteristics did not differ significantly between the two groups. Patients with VSA had a significantly lower reactive hyperemia index compared with those without VSA (1.70±0.33 vs. 2.12±0.53, P=0.02). Coronary flow reserve, index of microcirculatory resistance, and hyperemic Tmn were not different between the two groups, whereas resting Tmn was significantly longer in patients with VSA (1.20±0.44 vs. 0.71±0.37, P=0.002). Although the frequency and severity of angina improved from baseline to 1 and 3 months in patients with both positive and negative ACh tests, there was no difference between the two groups.

Conclusion Patients with VSA had decreased resting coronary flow and impaired endothelial function.

Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine, Chiba, Japan

Correspondence to Yuichi Saito, MD, Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8677, Japan Tel/fax: +81 432 262 340; e-mail:

Received September 19, 2018

Received in revised form January 14, 2019

Accepted January 14, 2019

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