Abstract
BackgroundPatients with metabolic syndrome (MetS) are at increased risk of asymptomatic hyperuricemia (i.e., elevated serum uric acid (SUA) level without gout) and cardiovascular disease. We conducted a cross-sectional study to examine associations between SUA levels and coronary flow reserve and urate deposits in carotid arteries in patients with asymptomatic hyperuricemia and MetS.MethodsAdults aged ≥40 years with MetS and SUA levels ≥6.5 mg/dl, but no gout, were eligible. Using a stress myocardial perfusion positron emission tomography (PET), we assessed myocardial blood flow (MBF) at rest and stress and calculated coronary flow reserve (CFR). CFR < 2.0 is considered abnormal and associated with increased cardiovascular risk. We also measured insulin resistance by homeostatic model assessment (HOMA-IR) method and urate deposits using dual-energy CT (DECT) of the neck for the carotid arteries.ResultsForty-four patients with the median age of 63.5 years underwent a blood test, cardiac PET and neck DECT scans. Median (IQR) SUA was 7.8 (7.1–8.4) mg/dL. The median (IQR) CFR was abnormally low at 1.9 (1.7–2.4) and the median (IQR) stress MBF was 1.7 (1.3–2.2) ml/min/g. None had urate deposits in the carotid arteries detected by DECT. In multivariable linear regression analyses, SUA had no association with CFR (β = − 0.12, p = 0.78) or stress MBF (β = − 0.52, p = 0.28). Among non-diabetic patients (n = 25), SUA was not associated with HOMA-IR (β = 2.08, p = 0.10).ConclusionsAmong MetS patients with asymptomatic hyperuricemia, we found no relationship between SUA and CFR, stress MBF, and insulin resistance. No patients had any DECT detectable subclinical urate deposition in the carotid arteries.
Highlights
Patients with metabolic syndrome (MetS) are at increased risk of asymptomatic hyperuricemia (i.e., elevated serum uric acid (SUA) level without gout) and cardiovascular disease
A reduced coronary flow reserve (CFR) can be a sign of flowlimiting coronary artery disease (CAD) [14] and presence of coronary vascular dysfunction involving smaller vessels, which increases the severity of inducible myocardial ischemia and sub-clinical myocardial injury beyond the effects of
Study population For this cross-sectional study, eligible patients were men and women aged 40 years or older who had asymptomatic hyperuricemia defined as SUA ≥6.5 mg/dL and metabolic syndrome defined by the presence of at least 3 out of 5 traits in the National Cholesterol Education Program – Adult Treatment Panel III (NCEP-ATP III) criteria [i.e., obesity with body mass index (BMI) > 29.4 kg/m2, high triglyceride level, low high-density lipoprotein level, hypertension, or hyperglycemia] [24]
Summary
Patients with metabolic syndrome (MetS) are at increased risk of asymptomatic hyperuricemia (i.e., elevated serum uric acid (SUA) level without gout) and cardiovascular disease. We conducted a cross-sectional study to examine associations between SUA levels and coronary flow reserve and urate deposits in carotid arteries in patients with asymptomatic hyperuricemia and MetS. Debate persists as to whether serum uric acid (SUA) has a causal role in the development of Positron emission tomography (PET)-measured coronary flow reserve (CFR) - the ratio of peak hyperemic myocardial blood flow (MBF) over that at rest as– is shown to be a reliable imaging marker of clinical cardiovascular risk [12, 13]. While in some studies up to 24% had DECT-positive urate deposits in the joints of asymptomatic hyperuricemic patients [22, 23], no data is available whether urate crystals exist and/or can be detected in the vasculature using DECT scans
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