SPECIAL REPORT :: LIPID PROFILING Size matters: the true weight of risk in lipid profiling By Emma Callaghan C
ardiovascular disease (CVD) is a leading cause of premature death worldwide, accounting for approximately 17.7 million deaths per year, repre-
senting 31 percent of all deaths worldwide. The under- lying pathology is atherosclerosis (arteriosclerosis) which develops and progresses over many years and is usually in the advanced stages by the time the symp- toms are expressed.1
Globally, the mortality rate for
CVD has dramatically declined over the past 20 years, however, in low- and middle-income regions, the num- ber of lives lost to CVD is increasing. This highlights the growing necessity for the assessment of CVD risk to include methods that account for uncertainty and heterogeneity.2,3
The National Lipid Association The mission of the National Lipid Associa- tion (NLA) is “... to enhance the practice of lipid management in clinical medicine.” NLA advocates advancing the current lipid test- ing profile. The current lipid panel consists of testing LDL cholesterol, HDL cholesterol, total cholesterol, and triglycerides, which only detects approximately 20 percent of all atherosclerotic cardiovascular disease patients. Advanced lipid testing is recom- mended to optimize patient treatment.4
Clinical significance of sdLDL-C
LDL cholesterol (LDL-C) is a low-density lipoprotein involved in cholesterol and triglyceride transfer from the liver to peripheral tissues. LDL-C consists of two parts:
1. The bigger part with phenotypic pattern A is light and almost rich in cholesterol (Large Buoyant LDL Cholesterol (LBLDL-C)) and
2. The smaller part with more special weight and phenotypic pattern B (sdLDL-C) composed of less cholesterol.
The two types of LDL-C vary in size through genetic determination and dietary lipid intake. All LDLs transport triglycerides and cholesterol to the tissues but their atherogenesis varies according to size. sdLDL-C is therefore a subtype of LDL-C, and these smaller particles can more readily permeate the inner arterial wall and are more susceptible to oxidation.5
sdLDL-C in clinical practice Research indicates that individuals with sdLDL-C predominance have a three-fold increased risk of myocardial infarction.6
A sedentary lifestyle, a
diet high in saturated fat, insulin resistance, pre- diabetes, and genetic disposition are all con- tributing factors to elevated sdLDL-C levels. Measuring sdLDL-C levels enables clinicians to gain a more comprehensive overview of lipid risk factors allowing treatment to be tailored
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accordingly. In addition, the high prevalence of sdLDL-C levels are commonly observed in individuals with familial hyperlipidemia, non-insulin dependent diabetes mellitus, and central obesity and insulin syndromes.7
Size matters
The diagram below highlights that although the over- all LDL cholesterol levels are 140mg/dl in both patients, the patient with coronary artery disease (CAD) has 50mg/dl more sdLDL-C particles that the healthy indi- vidual. Therefore, there are more cholesterol particles in the body, increasing the CAD patients’ risk of myocardial infarction.8
Figure 1. Assessment of LDL cholesterol levels in two patients.8
Denka Seiken method for sdLDL-C detection Until recently, the primary methods of assessing a patient’s sdLDL-C levels were based on the laborious and time-consuming ultracentrifugation and electro- phoresis methods. The “Denka Seiken” method pro- duces results in as little as ten minutes, facilitating faster patient diagnosis and treatment plan implementation.9 The diagram below indicates that the Denka Seiken method correlates with the gold standard ultracentri- fugation method. For this study, 64 samples were used from healthy individuals, CAD patients, and diabetic patients.10
Figure 2. Correlation between the ultracentrifugation and Denka Seiken methods10
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