**Background:** There is growing interest in establishing normal and stable glucose levels in patients with coronary artery disease (CAD). Hyperglycemia is a well-known risk factor for developing CAD in both diabetic and non-diabetic populations. Abnormal glycemic levels can cause both chronic and acute events such as acute coronary syndrome or stroke. Standard markers like HbA1c reflect glucose levels over 2-3 months, while fructosamine covers 2-4 weeks. Neither adequately captures short-term glucose fluctuations, particularly postprandial hyperglycemia, which may be significant in triggering cardiovascular events through endothelial dysfunction, inflammatory reactions, and oxidative stress. 1,5-anhydroglucitol (1,5-AG) is a candidate marker that reflects postprandial glycemia over the last 24-48 hours.
**Methods:** This is a narrative review summarizing the existing literature on 1,5-AG as a marker of acute hyperglycemia and its usefulness in cardiovascular disease. The review covers the structure, history, dietary sources, metabolism, assessment methods, and clinical utility of 1,5-AG. 1,5-AG is a 6-carbon monosaccharide (polyol) similar to D-glucose, first isolated from Polygala senega in 1888. It occurs naturally in human plasma, with the human body containing an estimated 500-1000 mg. Daily intake is about 4.5 mg/day. In healthy subjects, serum levels range from 12-40 μg/ml, with higher levels in males than females. The main dietary source is soya. 1,5-AG is absorbed in the intestine and excreted in the kidney, where it is 99.9% reabsorbed by active sodium-glucose co-transporter SGLT4. Its half-life is estimated at about 1-2 weeks. When serum glucose exceeds the renal threshold (typically >180 mg/dl), tubular reabsorption of 1,5-AG is blocked, causing increased urinary loss and reduced serum concentration. 1,5-AG can be measured in serum, plasma, cerebrospinal fluid, or urine using enzymatic kits, gas chromatography mass spectrometry (GC/MS), or high-performance liquid chromatography (HPLC). The reference method is HPLC. The GlycoMark test has a reference range of 10-31 μg/ml.
**Key Results:** Multiple studies are summarized. Ito et al. showed that 1,5-AG levels were significantly lower in non-diabetic patients with acute coronary syndrome (ACS) than those with effort angina pectoris. Fujiwara et al. found that lower 1,5-AG is associated with CAD even in controlled diabetic and non-diabetic patients, and that 1,5-AG was an even better marker of CAD than HbA1c or glycated albumin. Selvin et al. reported that low values of 1,5-AG (<6 μg/ml) were strongly associated with CAD, ischemic stroke, heart failure, and death compared with subjects with >6 μg/ml. Ouchi et al. discovered that low levels of 1,5-AG predict long-term cardiac mortality (70 months) in ACS patients with HbA1c levels <7%, with a cut-off point at the median level of 18.5 μg/ml. Wada et al. showed that low 1,5-AG was associated with more severe plaque calcification detected by intravascular ultrasound. Torimoto et al. found that vascular endothelial function correlated robustly with 1,5-AG in patients with HbA1c <8%. Ishida et al. demonstrated that low plasma 1,5-AG was closely associated with the extent of severely injured myocardium and systolic and diastolic function at first month after acute myocardial infarction. The DECODE study showed that postprandial hyperglycemia was a better predictor of mortality than fasting glucose. Watanabe et al. found that lower serum 1,5-AG levels are useful to detect men at higher risk of cardiovascular disease regardless of diabetes status, but no significant relationship was observed in women.
**Clinical Implications:** 1,5-AG is a sensitive marker of postprandial hyperglycemia and may be complementary to HbA1c and fructosamine in glycemic control assessment. It may be helpful in monitoring short-term glycemic changes in preoperation, preconception, pregnancy, and after glycemia-related therapeutic changes. Low levels of 1,5-AG are associated with increased risk of macrovascular complications such as CAD, severe coronary calcification, cardiovascular events, and death. However, there is no clear recommendation for its use in cardiology, especially in non-diabetic patients. Limitations include racial variability (higher baseline values in Asians and Africans than Caucasians, lower levels in Japanese than Americans), lack of established cutoffs for microvascular and macrovascular complications, and absence of large cohort studies confirming its utility on a large scale. Future research should focus on standardizing 1,5-AG levels and predicting cardiovascular complications.