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Updated: May 12, 2026

Measurement of Myocardial Lactate Production for Diagnosis of Coronary Microvascular Spasm
Published on: September 17, 2021
Higher serum uric acid and lipoprotein(a) are correlated with coronary spasm
Masami Nishino1, Naoki Mori, Takahiro Yoshimura
1Division of Cardiology, Osaka Rosai Hospital, 1179-3 Nagasone-cho, Sakai, Osaka, 591-8025, Japan, mnishino@orh.go.jp.
Insights
Serum uric acid and lipoprotein(a) are significantly elevated in patients with vasospastic angina (VSA). These markers are independently correlated with VSA, suggesting potential therapeutic targets for managing this condition.
Area of Science:
- Cardiology
- Biochemistry
Background:
- Endothelial dysfunction is a primary cause of vasospastic angina (VSA).
- Serum uric acid and lipoprotein(a) have been linked to endothelial dysfunction.
Purpose of the Study:
- To investigate the correlation between serum uric acid, lipoprotein(a), and VSA.
- To identify potential biomarkers for VSA diagnosis and management.
Main Methods:
- A cohort of 441 patients with suspected VSA underwent acetylcholine provocation testing.
- Serum levels of uric acid, lipoprotein(a), hs-CRP, and other markers were compared between VSA and atypical chest pain (ACP) groups.
- Multivariate analyses were performed to identify independent predictors of VSA.
Main Results:
- Uric acid, hs-CRP, and lipoprotein(a) levels were significantly higher in the VSA group compared to the ACP group.
- Multivariate analysis confirmed uric acid and lipoprotein(a) as significant independent markers for VSA.
- No significant differences were observed in other tested parameters between the groups.
Conclusions:
- Serum uric acid and lipoprotein(a) are correlated with VSA.
- Lowering uric acid and lipoprotein(a) may be a potential therapeutic strategy for VSA management.
Abstract:
It has been reported that a major cause of coronary vasospastic angina (VSA) is endothelial dysfunction of the coronary artery. On the other hand, some studies showed that serum uric acid and lipoprotein(a) are correlated with endothelial dysfunction. Thus, we examined whether uric acid and lipoprotein(a), are correlated with VSA. Four hundred forty-one patients with suspected VSA who underwent a coronary angiogram with acetylcholine provocation (ACh test) during an 8-year period were enrolled. We divided them into a VSA group, who showed coronary spasm by the ACh test, and an atypical chest pain (ACP) group, who showed negative ACh test. We compared serum markers between the two groups, including low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, high-sensitivity C-reactive protein (hs-CRP), lipoprotein(a), fibrinogen, total plasminogen activator inhibitor-1, and uric acid. Uric acid, hs-CRP, and lipoprotein(a) were significantly higher in the VSA group than in the ACP group (all P < 0.05) while there were no significant differences in the other parameters. Multivariate analyses identified uric acid and lipoprotein(a) as significant independent markers for VSA. Uric acid and lipoprotein(a) are correlated with VSA, and medical intervention to decrease uric acid and lipoprotein(a) might be effective in controlling VSA.
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