Microvascular angina. The possible role of inflammation, uric acid, and endothelial dysfunction

Abstract

Microvascular angina is a condition characterized by angina-like chest pain and normal coronary angiography. Endothelial dysfunction and systemic inflammation with elevated serum high-sensitive C-reactive protein (hsCRP) levels play a role in its pathogenesis. This study aimed to explore the possible relation between CRP, brachial flow-mediated dilatation (FMD), and microvascular angina. We included 21 patients with attacks of chest pain diagnosed as microvascular angina (study group) and 10 normal asymptomatic subjects (control group). Patients and controls were thoroughly examined clinically and by echocardiography, electrocardiography, and brachial FMD (using external brachial ultrasonography). Serum hsCRP and uric acid levels were assessed in all subjects. A significantly higher mean hsCRP level was found in the study group compared to controls (11.5 ± 3.8 versus 3.34 ± 1.5 mg/L; P < 0.001). FMD of the brachial artery showed significant impairment in patients with microvascular angina compared to controls (0.16 ± 0.06 versus 0.76 ± 0.09 mm; P < 0.001). There were significantly higher total cholesterol (196.1 ± 44.4 versus 150.8 ± 14.5 mg/dL; P = 0.018) and triglyceride levels (185.0 ± 103.2 versus 113.0 ± 17.6 mg/dL; P = 0.038) in the patients compared to controls; but there was a statistically insignificant difference in mean serum uric acid levels between these two groups. There were no significant correlations between the brachial FMD and any of the clinical variables studied (apart from ankle/brachial index). Microvascular angina may have an inflammatory element (reflected as a higher serum hsCRP level), together with a contribution by endothelial dysfunction (reflected as impaired brachial artery FMD); while serum uric acid is possibly not associated with microvascular angina.