Cardi-A1C (LPP + A1C)

Haemoglobin A1c forms through non-enzymatic glycation of haemoglobin in erythrocytes over their 120-day lifespan. The rate and extent of glycation are proportional to mean plasma glucose concentration, making HbA1c an integrated index of glycaemic control over the preceding 8–12 weeks. Because it is a weighted average heavily influenced by the most recent 4–6 weeks, HbA1c tracks changes in glucose control without the daily variation inherent in fasting or random glucose measurements.

HbA1c is the gold-standard marker for long-term glycaemic control, used both to diagnose diabetes and prediabetes and to guide and monitor glycaemic therapy. Unlike glucose, it does not require fasting and is unaffected by acute stress or recent meals, though conditions that alter erythrocyte lifespan or haemoglobin variants can affect its accuracy. Target HbA1c is individualised, typically below 7% for most adults with diabetes, with tighter or more relaxed goals depending on hypoglycaemia risk, life expectancy, and comorbidity.

The LPP panel uses Ion Mobility Analysis to separate lipoprotein particles by size and charge, quantifying particle number and size distribution across VLDL, LDL, and HDL subclasses. Small dense LDL particles are more atherogenic per unit cholesterol than large buoyant LDL because they penetrate the arterial wall more readily, are more susceptible to oxidation, and bind more avidly to arterial proteoglycans. VLDL and IDL particle number reflects hepatic triglyceride-rich lipoprotein secretion and remnant clearance, while HDL particle size and number relate to reverse cholesterol transport capacity and anti-inflammatory function.

LPP subfractionation refines cardiovascular risk assessment beyond standard lipid panels, particularly in patients with discordant LDL-C and apoB or metabolic syndrome, where small dense LDL predominates. Elevated small LDL particle number predicts cardiovascular events independently of LDL-C and can guide statin intensity, whereas large HDL particle predominance and low HDL particle number may unmask residual risk despite normal HDL-C. The pattern of VLDL and LDL particle size helps identify insulin resistance and guide lifestyle or pharmacological intervention.

The LP-IR score is a multivariate algorithm derived from lipoprotein particle concentrations and sizes measured by Ion Mobility Analysis. Insulin resistance shifts lipoprotein metabolism toward increased hepatic VLDL secretion, delayed triglyceride-rich particle clearance, smaller denser LDL via cholesteryl ester transfer protein-mediated lipid exchange, and reduced large HDL particles. The LP-IR score integrates these particle metrics into a single index that correlates with fasting insulin, HOMA-IR, and clamp-derived insulin sensitivity, offering a lipid-based proxy for insulin resistance without requiring glucose or insulin measurement.

LP-IR identifies insulin resistance in patients whose fasting glucose and HbA1c are still normal or only mildly elevated, capturing the dyslipidaemia of prediabetes and metabolic syndrome before overt hyperglycaemia. An elevated LP-IR score prompts earlier lifestyle intervention, consideration of insulin-sensitising therapy, and closer cardiovascular risk monitoring. Because it is derived from lipoproteins already being measured for cardiovascular assessment, it adds metabolic context without additional specimen or cost, though its proprietary nature means it cannot be compared across different laboratories or LPP methods.